Next Article in Journal
Role of Cardiac Natriuretic Peptides in Heart Structure and Function
Next Article in Special Issue
Impact of Heated Tobacco Products, E-Cigarettes, and Cigarettes on Inflammation and Endothelial Dysfunction
Previous Article in Journal
Synthetic Pathways and the Therapeutic Potential of Quercetin and Curcumin
Previous Article in Special Issue
Intersection of the Ubiquitin–Proteasome System with Oxidative Stress in Cardiovascular Disease
 
 
Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
Journals
IJMS
Volume 23
Issue 22
10.3390/ijms232214414
ijms-logo
Submit to this Journal Review for this Journal Propose a Special Issue
► Article Menu

Article Menu

share Share announcement Help format_quote Cite question_answer Discuss in SciProfiles thumb_up
...
Endorse textsms
...
Comment
first_page
settings
Order Article Reprints
Font Type:
Arial Georgia Verdana
Font Size:
Aa Aa Aa
Line Spacing:
Column Width:
Background:
Review

The Heart as a Target of Vasopressin and Other Cardiovascular Peptides in Health and Cardiovascular Diseases

by
Ewa Szczepanska-Sadowska
Department of Experimental and Clinical Physiology, Laboratory of Center for Preclinical Research, The Medical University of Warsaw, Banacha 1B, 02-097 Warsaw, Poland
Int. J. Mol. Sci. 2022, 23(22), 14414; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232214414
Submission received: 21 September 2022 / Revised: 9 November 2022 / Accepted: 17 November 2022 / Published: 20 November 2022
(This article belongs to the Special Issue Abnormal Regulation of Cellular Actions of Cardiovascular Factors)
Browse Figures
Review Reports Versions Notes

Abstract

:
The automatism of cardiac pacemaker cells, which is tuned, is regulated by the autonomic nervous system (ANS) and multiple endocrine and paracrine factors, including cardiovascular peptides. The cardiovascular peptides (CPs) form a group of essential paracrine factors affecting the function of the heart and vessels. They may also be produced in other organs and penetrate to the heart via systemic circulation. The present review draws attention to the role of vasopressin (AVP) and some other cardiovascular peptides (angiotensins, oxytocin, cytokines) in the regulation of the cardiovascular system in health and cardiovascular diseases, especially in post-infarct heart failure, hypertension and cerebrovascular strokes. Vasopressin is synthesized mostly by the neuroendocrine cells of the hypothalamus. There is also evidence that it may be produced in the heart and lungs. The secretion of AVP and other CPs is markedly influenced by changes in blood volume and pressure, as well as by other disturbances, frequently occurring in cardiovascular diseases (hypoxia, pain, stress, inflammation). Myocardial infarction, hypertension and cardiovascular shock are associated with an increased secretion of AVP and altered responsiveness of the cardiovascular system to its action. The majority of experimental studies show that the administration of vasopressin during ventricular fibrillation and cardiac arrest improves resuscitation, however, the clinical studies do not present consisting results. Vasopressin cooperates with the autonomic nervous system (ANS), angiotensins, oxytocin and cytokines in the regulation of the cardiovascular system and its interaction with these regulators is altered during heart failure and hypertension. It is likely that the differences in interactions of AVP with ANS and other CPs have a significant impact on the responsiveness of the cardiovascular system to vasopressin in specific cardiovascular disorders.

1. Introduction

Effective function of the heart is necessary for circulation of the blood in the cardiovascular system in a manner adjusted to actual needs. Action of the heart depends on the automatism of cardiac pacemaker cells, which is precisely tuned by the autonomic nervous system (ANS), and multiple endocrine and paracrine factors. The cardiac muscle forms a functional syncytium, allowing the rapid transmission of signals that are generated in the cardiac conduction system. Under physiological conditions, cells of the cardiac muscle are excited by action potentials generated in the sinoatrial node and transmitted to the atrioventricular node and other parts of the conductive system. In cardiovascular diseases, they may also be initiated in other cardiac cells, serving as ectopic pacemakers.
It is well known that the ANS plays a crucial role in the adaptation of the cardiovascular system to challenges associated with stress, anxiety, ischemia, pain, inflammation and other pathologies. Under resting conditions, the heart and the coronary vessels receive excitatory inputs from the presympathetic neurons of the ANS, which are located mainly in the rostral ventrolateral medulla (RVLM). The signals are transmitted to the sympathetic ganglia of the spinal cord, and subsequently to the heart and vessels. In addition, the heart is innervated by the parasympathetic projections from the nucleus ambiguous and the dorsal motor nucleus of the vagus (DMVNc, AmbNc). Efficient coordination of abundant excitatory and inhibitory inputs from the medullary and supramedullary regions occurs in the RVLM and the nucleus of the solitary tract (NTS) of the brainstem [1,2]. The dysregulation of the interplay between the sympathetic and parasympathetic components of the ANS plays an important role in the generation of the cardiac arrhythmias. The destruction of connections between the supramedullary regions and the NTS significantly reduces baseline activity of the NTS neurons and diminishes their activation by the afferent projections [3,4].
The endogenous cardiovascular peptides (CPs), particularly vasopressin, angiotensins, oxytocin and cytokines, belong to essential paracrine factors affecting the function of the heart. They may be synthesized either in the heart itself or in other organs, including the brain, the kidneys and the digestive system, and have access to the cardiac cells from systemic circulation [5,6,7,8,9]. In the heart, the cardiovascular peptides operate through direct actions exerted on cells of the heart and coronary vessels, and indirectly, through modulation of the activity of the ANS and through interaction with other neuroendocrine and humoral factors. At the cellular level, the cardiovascular peptides act by means of specific receptors and a wide range of intracellular mechanisms, engaging the transport of ions, cellular metabolic processes and the release of neurotransmitters [1,2,9,10]. Plurality of these effects enables precise adjustment of cardiac functions to different challenges.
The purpose of the present review is to draw attention to the specific role of vasopressin (AVP) in the regulation of cardiac functions in health and disease and the interaction of vasopressin with other CP. The present survey is focused on the cooperation of vasopressin with angiotensins (Ang), oxytocin (OT) and cytokines, because thus far the interaction of these peptides in the heart has been most intensely explored.

2. General Overview of the Vasopressin System

Vasopressin synthetizing, cells, vasopressin peptides and vasopressin receptors belong to the vasopressin system (VPS), which regulates blood pressure, water and electrolyte balance, as well as sensitivity to stress and other emotional challenges [8,9]. Most mammal species release arginine vasopressin, and only some of them use lysine vasopressin (LVP). The AVP gene is composed of exons encoding the sequence of a 145-amino acid polypeptide precursor composed of an N-terminal signal peptide, a sequence of vasopressin (the chief component), a sequence of neurophysin II (NPII) and a sequence of a C-terminal peptide, copeptin. Copeptin, which is a 39-amino acid glycopeptide, is released in equimolar quantities with AVP and is frequently used as a biomarker of vasopressin because it is more stable than the chief peptide [11,12]. Measurements of copeptin have been included in ESC guidelines for the management of non-ST-elevation myocardial infarctions [13].
AVP is synthesized mainly in neuroendocrine cells of the supraoptic nucleus (SON), the paraventricular nucleus (PVN) and the suprachiasmatic nucleus (SCN) of the hypothalamus. In addition, immunocytochemical and functional studies provide evidence for its synthesis in cells of the heart and lungs [14,15,16,17,18,19]. Some studies suggest the presence of a local cardiac vasopressin system [20].
Cellular actions of AVP are mediated by V1a receptors (V1aR), V1b receptors (V1bR) and V2 receptors (V2R), which are located in several organs and tissues with specific representation [5,14,17,21,22,23,24,25,26,27]. In addition, AVP can bind to oxytocin receptors (OTR), whereas oxytocin (OT) interacts with V1aR [28].V1aR have been identified at all levels of the brain and the spinal cord, as well as in the heart, vessels, kidneys, lungs and digestive system (including the liver and the pancreas) [26,29,30,31,32,33]. V1bR have been found in the pituitary, brain, pancreatic gland and lungs [34,35,36]. V2R are located mainly in the kidneys [27,37], however, in the neonate rat V2R were also detected in the heart [17]. In addition, the functional studies provide evidence for the presence of V2R in vessels of the brain, skin and skeletal muscles, as well as in cells releasing Factor VIII [38,39,40]. The cardiovascular and neuroregulatory processes are mediated mainly by V1aR [10,41,42,43,44,45,46,47]. Overexpression of V1aR in mouse heart causes cardiac dysfunction, cardiac hypertrophy, ventricular dilation and overactivation of the Gαq/11–mediated pathway [48]. The vasopressin system cooperates closely with the autonomic nervous system in the regulation of blood pressure [46]. The general overview of the vasopressin system is shown in Figure 1.
Multiple studies demonstrate that AVP plays a crucial role in the regulation of cardiovascular homeostasis. AVP secretion is inhibited by increases in blood volume and pressure, and stimulated by hypotension, hypoxia, pain, stress and inflammation—the disturbances that frequently occur during acute and/or chronic cardiovascular diseases. It has been well established that altered regulation of AVP release may have a significant impact on cardiovascular regulation [8,10,22,41,43,44,48,49,50,51,52]. Early studies performed on isolated hearts of dogs showed that the infusion of vasopressin into the left atrium decreased the coronary blood flow and caused myocardial dysfunction [53]. Subsequent investigations provided evidence that intravenous administration of vasopressin in pigs with normal sinus rhythm exerted some positive effects in their cardiovascular systems that were manifested by an increase of the mean arterial blood pressure and elevation of the left anterior descending (LAD) coronary artery cross sectional area. At the same time, the authors noted that application of vasopressin reduced the cardiac index [54,55]. Experiments performed on cardiomyocytes of rats revealed that the stimulation of V1aR causes a dose-dependent increase in myocyte contractile function, [Ca2+]i and IP3 [56].

3. Role of Vasopressin in Cardiovascular Disturbances

As discussed below, hypoxia, ischemia, pain and stress, which are frequent attributes of cardiovascular diseases, are also effective stimuli for vasopressin release.

3.1. Hypoxia and Vasopressin

Many studies provide evidence that hypoxia and/or ischemia provoke the significant release of vasopressin and its surrogate, copeptin [57,58,59,60,61,62]. Moreover, it has been shown that intermittent hypoxia induces direct activation of vasopressinergic neurons in the PVN [63,64] and that its effect is strongly potentiated by the central administration of Ang II [65].
Release of AVP into the systemic circulation during hypoxia is associated with vasoconstriction, which is mediated by V1aR and accounts for generation of significant pressor response [60,66]. However, in some vascular beds (cerebral and pulmonary circulation) AVP can cause vasodilation, which is presumably mediated by the release of nitric oxide [38,67,68]. The pressor effect of AVP during hypoxia is also exerted by the stimulation of the presympathetic neurons located in the PVN and RVLM. The blockade of V1aR within the RVLM modulates the cardiovascular responses evoked by chronic intermittent hypoxia (CIH) and reduces baseline blood pressure in CIH-conditioned rats [69]. It should be noted that acting on V1aR vasopressin modulates function of the carotid chemoreflex and causes a decrease in the respiratory rate [33]. It is likely that the regulation of the carotid chemoreflex by AVP is related to changes of glucose metabolism. Central and systemic application of AVP causes hyperglycemia, which is similar to that observed during hypoxia. Moreover, both the hypoxic and the hyperglycemic responses can be abolished by administration of the V1aR antagonist [70].
There is evidence that AVP plays a positive role in the regulation of the pulmonary blood flow during hypoxia. Chronic administration of AVP in moderate concentration induced a significant reduction of the mean pulmonary arterial pressure and prevented the development of pulmonary hypertension [71].

3.2. Role of Vasopressin in Pain and Stress

Pain frequently informs on pathological processes developing in the cardiovascular system. Strong pain is a symptom of the coronary ischemia and may provoke stress and anxiety that intensify the discomfort of the disease and cause activation of the sympathetic nervous system and the release of cardiovascular peptides [72]. Cardiac pain is transmitted to the spinal cord by sympathetic nociceptors and afferents possessing cell bodies located in the thoracic spinal ganglia. It is also generated in parasympathetic nociceptors conveying impulses by means of vagal afferents to the inferior nucleus of the vagus nerve [73,74].
Pain belongs to non-osmotic factors potently stimulating the release of AVP [74]. Exposure to pain elevates AVP content in perfusates of the PVN and of some other brain structures involved in the regulation of pain (e.g., the periaqueductal gray—PAG; the raphe nuclei; the caudate nucleus—CdN) [72,73,74,75,76,77,78,79]. On the other hand, systemic, intraventricular, intrathecal or topical application of this peptide into specific regions of the brain alleviates pain [72,80,81,82,83,84]. It appears that the analgesic effect of AVP is associated with the stimulation of neurons in the CdN, PAG, raphe magnus nucleus (RMN) and spinal cord, which is caused by the stimulation of V1aR [72,80,81,82,85,86,87]. Systemic administrations of AVP or oxytocin (OT) also exert analgesic effects [72,81]. It is possible that the pain alleviating action of OT is mediated by V1aR because it is mimicked by AVP and can be completely blocked by the V1aR antagonist (SR49059), but not by the OT receptor antagonist (L-368899). The analgesic effect of AVP requires the activation of acid-sensing ion channels in the dorsal root ganglia and it cannot be induced in V1aR knockout mice [88].
Neurogenic stress is frequently present in cardiovascular diseases, especially in cardiac ischemia, and has a significant negative effect on the course of the disease. Experimental studies show that the neurogenic stress provokes the release of AVP, and that the stimulation of V1aR by AVP plays a significant role in the potentiation of the magnitude of the cardiovascular and behavioral responses to stress in hypertension and heart failure [43,44,45,89,90].

4. Role of Vasopressin in Cardiovascular Diseases

4.1. Vasopressin in Myocardial Infarction

A myocardial infarction (MI) stimulates VPS, causing the significant activation of vasopressinergic magnocellular neurons in the SON and the elevation of plasma AVP levels [91,92,93]. Studies on human beings revealed that acute MI results in a significant increase in the concentration of vasopressin and/or copeptine in blood samples collected from patients with acute myocardial infarction [94,95,96,97,98]. In addition, experiments performed on rats showed that heart failure causes activation of the cardiac vasopressin system [20].
Experimental studies suggest that the elevated release of AVP during cardiovascular disturbances may play a positive role during the recovery from ischemia. For instance, in the rat model of cardiac ischemia-reperfusion injury, intravenous administration of AVP prevented the post-ischemic bradycardia and diminished the incidence of ventricular arrhythmia. Furthermore, administration of AVP reduced the size of the infarct and decreased the expression of some biochemical parameters, which are used as measures of cardiac ischemia (lactate dehydrogenase—LDH; creatine kinase-MB—CK-MB). These effects were significantly reduced by the administration of SR49059, which is a V1R antagonist [99]. In the porcine model of ischemic ventricular fibrillation induced by occlusion of the left coronary artery, the administration of AVP more effectively augmented the coronary perfusion pressure than the administration of epinephrine [100]. On the other hand, in experiments on dogs, it was found that the ischemia of the left ventricular myocardium is associated with enhanced contractile response of the coronary microvessels to AVP [101]. Thus, the mechanism for action of VPS in the post-infarct state is not yet sufficiently elucidated, and it is likely that AVP may engage different processes, depending on its concentration and interaction with other factors.
It appears that the influence of vasopressin on the heart is significantly altered in diabetes mellitus, as it has been shown that AVP exerts a greater vasoconstrictive effect in coronary vessels obtained from patients with diabetes mellitus who underwent cardioplegic arrest and cardiopulmonary bypass than in vessels obtained from patients undergoing the same procedures but not suffering from diabetes [102]. The enhanced contractility of the coronary vessels in diabetic patients was mediated by increased stimulation of V1aR because it was significantly diminished in the presence of the specific V1aR antagonist (SR 4059). The diabetic patients also had a higher expression of V1aR in their atrial tissue samples [102].

4.2. Vasopressin in Cardiovascular Shock and Cardiopulmonary Resuscitation

Several studies suggest that the administration of vasopressin may exert beneficial effects during the recovery period in some forms of heart failure. Studies performed on the porcine model of cardiac arrest induced by ventricular fibrillation revealed that vasopressin applied alone, or in association with epinephrine, exerted positive cardiovascular effects, such as elevations of coronary perfusion pressure and cerebral blood flow [103,104]. In studies on pigs exposed to hemorrhagic shock and cardiac arrest administration of vasopressin resulted in prolonged survival, reduced acidosis and improved renal blood flow [105]. In a swine resuscitation model, intravenous administration of AVP a few minutes prior to ventricular fibrillation elicited a significant increase in the mid left anterior descending coronary artery cross sectional area and normalized the sinus rhythm [55].
Studies performed on a porcine cardiopulmonary resuscitation model, in which the animals were treated with different combinations of placebo, AVP and epinephrine, the successful restoration of spontaneous circulation was possible in the group treated with a combination of AVP and epinephrine, but not in the group treated with epinephrine alone [104]. In the same cardiopulmonary resuscitation model, the joined application of epinephrine, AVP and nitroglycerine significantly increased the left ventricular blood flow and global cerebral blood flow. Moreover, combined administration of AVP and epinephrine produced a greater elevation of the cerebral blood flow than the infusion of epinephrine alone [106]. Analysis of data from 7 studies comparing the efficiency of various vasopressors used for the return of spontaneous circulation (ROSC) revealed that AVP significantly improved ROSC during ventricular fibrillation evoked by severe hypothermia [107].
Cardiopulmonary resuscitation in human patients with cardiac arrest is associated with a significant elevation in blood levels for AVP, ACTH, cortisol and renin concentration [108,109]. Positive effects of intravenous administration of 40 U of AVP on the survival of patients with cardiac arrest induced by ventricular fibrillation or vasodilatory shock were reported [110,111,112]. In addition, investigations performed on patients with septic shock revealed that administration of AVP in relatively low doses increases blood pressure and urine output and enhances the responsiveness to catecholamines. However, it should be noted that in some patients with vasodilatory shock, application of vasopressin elicited adverse effects (e.g., Russell [113]). A survey of studies analyzing effects of different vasopressors and their combinations indicated that application of AVP or V1aR agonist (selpressin) permits a reduction in the dose of norepinephrine, which is necessary for cardiovascular stabilization in patients with vasodilatory shocks resulting from sepsis, acute myocardial infarction or cardiovascular surgery [7,113]. AVP and V1R agonist (terlipressin) have been successfully used for the treatment of gastrointestinal bleeding, although some patients responded with arrhythmic complications, manifested by a prolonged QT interval and torsade de pointes [114,115]. Retrospective analysis of adult patients admitted to the medical intensive care unit because of arrhythmia revealed that the early (within 6 h) administration of AVP significantly reduced the new onset arrhythmias and decreased the requirements for catecholamine therapy [116].
A triple-blind randomized trial, analyzing the survival of patients with cardiac arrest admitted to Canadian emergency departments, critical care units and hospitals, did not show an advantage in favor of vasopressin over epinephrine [117]. Similar conclusions can be drawn from a meta-analysis of 1519 patients with cardiac arrest in USA hospitals [118].

5. Cooperation of Vasopressin with Other Cardiovascular Peptides

5.1. Vasopressin and Angiotensins

The renin-angiotensin system (RAS) acts on the cardiovascular system directly through effects exerted locally in cardiac and vascular cells and indirectly by means of the presympathetic neurons of the brain and sympathetic neurons of the heart [119,120,121,122,123]. In addition, acting on AT1 receptors, Ang II may modulate function of the heart by means of the parasympathetic neurons, as it has been shown that it inhibits the release of Ach induced by vagal stimulation of the left cardiac ventricle [124].
Several studies have shown that cardiovascular disorders significantly influence activity of the RAS and that the cardiovascular effects of the RAS are markedly altered in cardiovascular diseases [10,125,126,127,128,129,130]. The most effective components of the RAS that participate in the cardiovascular regulation include angiotensin II (Ang II), angiotensin III (Ang III), Ang-(1–7), AT1 receptors (AT1R), AT2 receptors (AT2R) and Mas receptors (MasR). The cardiovascular effects of angiotensins may be mediated either by central effects initiated in the brain or through systemic actions exerted in the heart and vessels [10,125,130]. Analysis of cardiac ventricle samples taken during biopsies from patients with stable and unstable angina revealed that the patients with unstable angina synthesize more Ang II and have higher expressions of angiotensinogen, angiotensin converting enzyme (ACE) and AT1R genes. Besides, in cardiac myocytes and fibroblasts, they manifest upregulation of the iNOS gene and inflammatory cytokine genes (TNF-α, IL-6, IFN-γ, TGF-β) [131,132]. It has been shown that knockout of AT1R in mice with an experimental model of aortic constriction that fibrosis and hypertrophy of the cardiac muscle were significantly reduced and incidence of arrhythmia declined [133].
Acute cardiac failure and hypertension cause parallel activation of the angiotensinergic and vasopressinergic systems [10,123]. For instance, occlusion of the left coronary artery in Sprague Dawley rats resulted in a significant increase in plasma concentration of Ang II, AVP and TNF-α [134]. Most likely, the increase of plasma AVP levels in these experiments was mediated by activation of the hypothalamic angiotensin receptors, i.e., knockdown of AT1R in the subfornical organ (SFO) significantly reduced the increase of plasma AVP provoked by coronary constriction [134].

5.2. Vasopressin and Oxytocin

Similar to vasopressin, oxytocin is synthesized mainly by neuroendocrine cells of the SON, PVN and SCN, and is released to the systemic circulation in vessels of the posterior pituitary [9,14]. It can also be released by neural projections in the brain and is synthesized in the heart [14,135,136].
As early as in 1964, it was shown that systemic administration of synthetic oxytocin (OT) decreases blood pressure and reduces cardiac arrhythmias in several species, including humans [137]. Similar to AVP and angiotensins, oxytocin regulates the cardiovascular system through direct actions exerted on OT receptors (OTR) located in the heart and vessels, and via indirect effects exerted on neurons of the cardiovascular regions of the brain [14,138]. There is evidence for synthesis of OT and OTR in the heart, vessels and brain and for involvement of OT and OTR in the modulation of blood pressure, heart rate and behavioral responses [51,136,137,138,139,140,141]. In many instances, AVP and OT are secreted together, which enhances the chance of their nonspecific interaction [28,142,143]. Along these lines, it has been shown that local applications of high doses of vasopressin or oxytocin into the central nucleus of the amygdala accelerates HR and magnifies the release of corticosterone [144]. As the responses to AVP and OT could be abolished by pretreatment with a selective oxytocin antagonist, it has been suggested that high concentrations of AVP may regulate cardiovascular responses by means of OTR [144].
Experiments on rats have shown that, acting in the brain, OT reduces cardiovascular responses to stress, and that its buffering action is significantly attenuated after a myocardial infarction [50]. In addition, studies with blockades of OTR and V1aR in the brain revealed significant differences in the interaction between OT and AVP, in regards to these receptors in the regulation of cardiovascular responses to acute neurogenic stress between WKY and SHR rats [51,52]. The SHR responded with significantly greater pressor responses to neurogenic stress than the WKY rats and found that the augmentation could be abolished by intraventricular administration of oxytocin. The latter finding suggested that the enhanced cardiovascular responses of the SHR to stress may partly result from deficient action of oxytocin in the brain [51].
Systemic administration of oxytocin prior to ischemia/reperfusion of the myocardium prevents hypotension during the early phase of ischemia and reduces the infarct size and ventricular arrhythmias in SD rats [145]. It has been also shown that SD rats with a myocardial infarction manifest elevated concentrations of the OTR protein in the cardiac muscle [146].

5.3. Vasopressin and Cytokines

Cytokines form a big family of specific, biologically active compounds with proinflammatory or anti-inflammatory properties [147,148,149,150]. Several studies provide evidence that cardiovascular diseases, especially myocardial infarction and cerebrovascular stroke initiate inflammatory and anti-inflammatory processes associated with the release of cytokines [147,148,149,150,151,152,153]. There is also evidence that in a myocardial infarction, cytokines play a particularly important role during the early recovery period [154,155,156,157].
Coronary heart disease and heart failure significantly increase the production of potent inflammatory cytokines (interleukin-1—IL-1; interleukin-6—IL-6; tumor necrosis factor-α—TNF-α) in the heart and other organs [147,148,150,156,157,158,159]. It has also been shown that these cytokines play an essential role in the regulation of blood pressure and cardiac remodeling, through cooperation with angiotensins, vasopressin and nitric oxide [158,159,160,161,162,163,164]. The proinflammatory interleukins cooperate with Ang II and AVP by means of central and systemic effects. Acting in the brain, IL-1β and TNF-α exert pressor effects, which are mediated by Ang II and AT1R [157,159,160]. It has also been shown that the central pressor action of TNF-α is intensified in rats with a myocardial infarction [161]. In the heart, the proinflammatory cytokine TGF-β cooperates with Ang II and this cooperation plays an essential role in the development of cardiac fibrosis [131,162].
There are studies showing that the inflammatory cytokines interact with the vasopressinergic system. Administrations of IL-1β- and IL-6 stimulate release of AVP [163,164,165,166,167,168]. On the other hand, reduced V1aR expression was found in aortic smooth muscle cells, and this was associated with attenuated cardiovascular responsiveness to AVP [168]. In SD rats and murine hearts, AVP was found to induce an expression of IL-6 mRNA and IL-6 protein in fibroblasts [168]. Moreover, experiments on cardiac fibroblasts of neonatal SD rats provide evidence that vasopressin promotes the synthesis of TGF-β1 and collagen through actions exerted on V1aR. It is likely that these effects may play an essential role in the development of myocardial fibrosis [169]. The cardiovascular effects of cytokines are at least partly mediated by nitric oxide [170,171].
Altogether, the present evidence indicates that cytokines, acting directly or in cooperation with other cardiovascular factors, may play an essential role in the adaptation of the cardiovascular system to inflammatory injury and in the reparation of injured tissue.

6. Summary and Conclusions

The function of the heart is regulated by the autonomic nervous system and biologically active compounds. The cardiovascular peptides, especially vasopressin, angiotensins, oxytocin and cytokines belong to a family of peptides with a wide range of actions that can regulate hemodynamic parameters through direct actions exerted in cells of the cardiovascular system or indirectly by means of the autonomic nervous system. The cardiac and vascular effects of cardiovascular peptides are significantly altered in cardiovascular disorders induced by a myocardial infarction, hypertension and cardiovascular shock, and by hypoxia, stress, pain and inflammation, which frequently occur in cardiovascular diseases. Putative interaction of vasopressin, angiotensins, oxytocin and cytokines with the autonomic nervous system in the regulation of cardiovascular parameters during stress, anxiety, hypoxia and inflammation is illustrated in Figure 2.
This review is focused on the interaction of vasopressin with the most effective cardiovascular peptides, but it is likely that vasopressin may also interact with other cardiovascular factors. Specifically, the cooperation of vasopressin with aldosterone and pancreatic hormones is worthy of attention [172,173,174,175,176,177].
In conclusion, available evidence indicates that vasopressin effectively interacts with the autonomic nervous system and angiotensin II, Ang(1–7), oxytocin and cytokines in the regulation of the cardiovascular system. Action of these peptides is altered in cardiovascular diseases, as well as during stress, pain and inflammation. Presumably, joint action of these peptides largely determines the responsiveness of the cardiovascular system to pharmacological treatments under pathological conditions.

Funding

This work was supported by the Medical University of Warsaw Scientific Projects (1MA/N/2022) and carried out with the use of CEPT infrastructure financed by the European Union—The European Regional Development Fund. The work did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

Institutional Review Board Statement

Not applicable.

Informed Consent Statement

Not applicable.

Data Availability Statement

Not relevant.

Acknowledgments

The author wish to express gratitude to Marcin Kumosa for graphic preparation of the figures.

Conflicts of Interest

The author declares no conflict of interest.

References

  1. Agarwal, S.K.; Calaresu, F.R. Supramedullary inputs to cardiovascular neurons of rostral ventrolateral medulla in rats. Am. J. Physiol. 1993, 265, R111–R116. [Google Scholar] [CrossRef]
  2. Dampney, R.A.L.; Horiuchi, J.; Tagawa, T.; Fontes, M.A.P.; Potts, P.D.; Polson, J.W. Medullary and supramedullary mechanisms regulating sympathetic vasomotor tone. Acta Physiol. Scand. 2003, 177, 209–218. [Google Scholar] [CrossRef]
  3. Shen, M.J.; Zipes, D.P. Role of the autonomic nervous system in modulating cardiac arrhythmias. Circ. Res. 2014, 114, 1004–1021. [Google Scholar] [CrossRef] [Green Version]
  4. Cooper, C.M.; Farrand, A.Q.; Andresen, M.C.; Beaumont, E. Vagus nerve stimulation activates nucleus of solitary tract neurons via supramedullary pathways. J. Physiol. 2021, 599, 5261–5279. [Google Scholar] [CrossRef]
  5. Hiroyama, M.; Wang, S.; Aoyagi, T.; Oikawa, R.; Sanbe, A.; Takeo, S.; Tanoue, A. Vasopressin promotes cardiomyocyte hypertrophy via the vasopressin V1A receptor in neonatal mice. Eur. J. Pharmacol. 2007, 559, 89–97. [Google Scholar] [CrossRef]
  6. Jahng, J.W.; Song, E.; Sweeney, G. Crosstalk between the heart and peripheral organs in heart failure. Exp. Mol. Med. 2016, 48, e21. [Google Scholar] [CrossRef] [Green Version]
  7. Russell, J.A.; Gordon, A.C.; Williams, M.D.; Boyd, J.H.; Walley, K.R.; Kissoon, N. Vasopressor therapy in the intensive care unit. Semin. Respir. Crit. Care Med. 2021, 42, 59–77. [Google Scholar] [CrossRef]
  8. Szczepanska-Sadowska, E.; Cudnoch-Jedrzejewska, A.; Ufnal, M.; Zera, T. Brain and cardiovascular diseases: Common neurogenic background of cardiovascular, metabolic and inflammatory diseases. J. Physiol. Pharmacol. 2010, 61, 509–521. [Google Scholar]
  9. Szczepanska-Sadowska, E.; Wsol, A.; Cudnoch-Jedrzejewska, A.; Żera, T. Complementary role of oxytocin and vasopressin in cardiovascular regulation. Int. J. Mol. Sci. 2021, 22, 11465. [Google Scholar] [CrossRef]
  10. Szczepanska-Sadowska, E.; Czarzasta, K.; Cudnoch-Jedrzejewska, A. Dysregulation of the renin-angiotensin system and the vasopressinergic system interactions in cardiovascular disorders. Curr. Hypertens. Rep. 2018, 20, 19. [Google Scholar] [CrossRef] [Green Version]
  11. Morgenthaler, N.G.; Struck, J.; Alonso, C.; Bergmann, A. Assay for the measurement of copeptin, a stable peptide derived from the precursor of vasopressin. Clin. Chem. 2006, 52, 112–119. [Google Scholar] [CrossRef]
  12. Nickel, C.H.; Bingisser, R.; Morgenthaler, N.G. The role of copeptin as a diagnostic and prognostic biomarker for risk stratification in the emergency department. BMC Med. 2012, 10, 7. [Google Scholar] [CrossRef] [Green Version]
  13. Roffi, M.; Patrono, C. CardioPulse: ‘Ten Commandments’ of 2015 European Society of Cardiology Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation (NSTE-ACS). Eur. Heart J. 2016, 37, 208. [Google Scholar] [CrossRef]
  14. Buijs, R.M.; De Vries, G.J.; Van Leeuwen, F.W.; Swaab, D.F. Vasopressin and oxytocin: Distribution and putative functions in the brain. Prog. Brain Res. 1983, 60, 115–122. [Google Scholar] [CrossRef] [Green Version]
  15. Buijs, R.M.; Hurtado-Alvarado, G.; Soto-Tinoco, E. Vasopressin: An output signal from the suprachiasmatic nucleus to prepare physiology and behaviour for the resting phase. J. Neuroendocrinol. 2021, 33, e12998. [Google Scholar] [CrossRef]
  16. Fay, M.J.; Friedmann, A.S.; Yu, X.M.; North, W.G. Vasopressin and vasopressin-receptor immunoreactivity in small-cell lung carcinoma (SCCL) cell lines: Disruption in the activation cascade of V1a-receptors in variant SCCL. Cancer Lett. 1994, 82, 167–174. [Google Scholar] [CrossRef]
  17. Gutkowska, J.; Miszkurka, M.; Danalache, B.; Gassanov, N.; Wang, D.; Jankowski, M. Functional arginine vasopressin system in early heart maturation. Am. J. Physiol. Heart Circ. Physiol. 2007, 293, H2262–H2270. [Google Scholar] [CrossRef] [Green Version]
  18. Hallbeck, M.; Larhammar, D.; Blomqvist, A. Neuropeptide expression in rat paraventricular hypothalamic neurons that project to the spinal cord. J. Comp. Neurol. 2001, 433, 222–238. [Google Scholar] [CrossRef]
  19. Hupf, H.; Grimm, D.; Riegger, G.A.; Schunkert, H. Evidence for a vasopressin system in the rat heart. Circ. Res. 1999, 84, 365–370. [Google Scholar] [CrossRef] [Green Version]
  20. Chen, X.; Lu, G.; Tang, K.; Li, Q.; Gao, X. The secretion patterns and roles of cardiac and circulating arginine vasopressin during the development of heart failure. Neuropeptides 2015, 51, 63–73. [Google Scholar] [CrossRef]
  21. Koshimizu, T.A.; Nakamura, K.; Egashira, N.; Hiroyama, M.; Nonoguchi, H.; Tanoue, A. Vasopressin V1a and V1b receptors: From molecules to physiological systems. Physiol. Rev. 2012, 92, 1813–1864. [Google Scholar] [CrossRef]
  22. Szczepanska-Sadowska, E.; Zera, T.; Sosnowski, P.; Cudnoch-Jedrzejewska, A.; Puszko, A.; Misicka, A. Vasopressin and related peptides; potential value in diagnosis, prognosis and treatment of clinical disorders. Curr. Drug Metab. 2017, 18, 306–345. [Google Scholar] [CrossRef]
  23. Carmosino, M.; Brooks, H.L.; Cai, Q.; Davis, L.S.; Opalenik, S.; Hao, C.; Breyer, M.D. Axial heterogeneity of vasopressin-receptor subtypes along the human and mouse collecting duct. Am. J. Physiol. Renal Physiol. 2007, 292, F351–F360. [Google Scholar] [CrossRef]
  24. Milik, E.; Szczepanska-Sadowska, E.; Cudnoch-Jedrzejewska, A.; Dobruch, J. Down-regulation of V1a vasopressin receptors in the cerebellum after myocardial infarction. Neurosci. Lett. 2011, 499, 119–123. [Google Scholar] [CrossRef]
  25. Milik, E.; Szczepanska-Sadowska, E.; Dobruch, J.; Cudnoch-Jedrzejewska, A.; Maslinski, W. Altered expression of V1a receptors mRNA in the brain and kidney after myocardial infarction and chronic stress. Neuropeptides 2014, 48, 257–266. [Google Scholar] [CrossRef]
  26. Ostrowski, N.L.; Lolait, S.J.; Young, W.S., 3rd. Cellular localization of vasopressin V1a receptor messenger ribonucleic acid in adult male rat brain, pineal, and brain vasculature. Endocrinology 1994, 135, 1511–1528. [Google Scholar] [CrossRef]
  27. Ostrowski, N.L.; Lolait, S.J.; Bradley, D.J.; O’Carroll, A.M.; Brownstein, M.J.; Young, W.S., 3rd. Distribution of V1a and V2 vasopressin receptor messenger ribonucleic acids in rat liver, kidney, pituitary and brain. Endocrinology 1992, 131, 533–535. [Google Scholar] [CrossRef]
  28. Song, Z.; Albers, H.E. Cross-talk among oxytocin and arginine-vasopressin receptors: Relevance for basic and clinical studies of the brain and periphery. Front. Neuroendocrinol. 2018, 51, 14–24. [Google Scholar] [CrossRef]
  29. Góźdź, A.; Szczepańska-Sadowska, E.; Maśliński, W.; Kumosa, M.; Szczepańska, K.; Dobruch, J. Differential expression of vasopressin V1a and V1b receptors mRNA in the brain of renin transgenic TGR(mRen2)27 and Sprague-Dawley rats. Brain Res. Bull. 2003, 59, 399–403. [Google Scholar] [CrossRef]
  30. Góźdź, A.; Szczepańska-Sadowska, E.; Szczepańska, K.; Maśliński, W.; Luszczyk, B. Vasopressin V1a, V1b and V2 receptors mRNA in the kidney and heart of the renin transgenic TGR(mRen2)27 and Sprague Dawley rats. J. Physiol. Pharmacol. 2002, 53, 349–357. [Google Scholar]
  31. Hirasawa, A.; Hashimoto, K.; Tsujimoto, G. Distribution and developmental change of vasopressin V1A and V2 receptor mRNA in rats. Eur. J. Pharmacol. 1994, 267, 71–75. [Google Scholar] [CrossRef]
  32. Young, L.J.; Toloczko, D.; Insel, T.R. Localization of vasopressin (V1a) receptor binding and mRNA in the rhesus monkey brain. J. Neuroendocrinol. 1999, 11, 291–297. [Google Scholar] [CrossRef] [PubMed]
  33. Żera, T.; Przybylski, J.; Grygorowicz, T.; Kasarełło, K.; Podobińska, M.; Mirowska-Guzel, D.; Cudnoch-Jędrzejewska, A. Vasopressin V1a receptors are present in the carotid body and contribute to the control of breathing in male Sprague-Dawley rats. Peptides 2018, 102, 68–74. [Google Scholar] [CrossRef] [PubMed]
  34. Corbani, M.; Marir, R.; Trueba, M.; Chafai, M.; Vincent, A.; Borie, A.M.; Desarménien, M.G.; Ueta, Y.; Tomboly, C.; Olma, A.; et al. Neuroanatomical distribution and function of the vasopressin V1B receptor in the rat brain deciphered using specific fluorescent ligands. Gen. Comp. Endocrinol. 2018, 258, 15–32. [Google Scholar] [CrossRef] [PubMed]
  35. Folny, V.; Raufaste, D.; Lukovic, L.; Pouzet, B.; Rochard, P.; Pascal, M.; Serradeil-Le Gal, C. Pancreatic vasopressin V1b receptors: Characterization in In-R1-G9 cells and localization in human pancreas. Am. J. Physiol. Endocrinol. Metab. 2003, 285, E566–E576. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  36. Monstein, H.J.; Truedsson, M.; Ryberg, A.; Ohlsson, B. Vasopressin receptor mRNA expression in the human gastrointestinal tract. Eur. Surg. Res. 2008, 40, 34–40. [Google Scholar] [CrossRef] [PubMed]
  37. Morel, A.; Lolait, S.J.; Brownstein, M.J. Molecular cloning and expression of rat V1a and V2 arginine vasopressin receptors. Regul. Pept. 1993, 45, 53–59. [Google Scholar] [CrossRef]
  38. Koźniewska, E.; Szczepańska-Sadowska, E. V2-like receptors mediate cerebral blood flow increase following vasopressin administration in rats. J. Cardiovasc. Pharmacol. 1990, 15, 579–585. [Google Scholar] [CrossRef] [PubMed]
  39. Liard, J.F. Cardiovascular effects associated with antidiuretic activity of vasopressin after blockade of its vasoconstrictor action in dehydrated dogs. Circ. Res. 1986, 58, 631–640. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  40. Rosenberg, J.B.; Foster, P.A.; Kaufman, R.J.; Vokac, E.A.; Moussalli, M.; Kroner, P.A.; Montgomery, R.R. Intracellular trafficking of factor VIII to von Willebrand factor storage granules. J. Clin. Investig. 1998, 101, 613–624. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  41. Cowley, A.W., Jr.; Szczepanska-Sadowska, E.; Stepniakowski, K.; Mattson, D. Chronic intravenous administration of V1 arginine vasopressin agonist results in sustained hypertension. Am. J. Physiol. 1994, 267, H751–H756. [Google Scholar] [CrossRef] [PubMed]
  42. Cudnoch-Jedrzejewska, A.; Szczepanska-Sadowska, E.; Dobruch, J.; Puchalska, L.; Ufnal, M.; Kowalewski, S.; Wsół, A. Differential sensitisation to central cardiovascular effects of angiotensin II in rats with a myocardial infarct: Relevance to stress and interaction with vasopressin. Stress 2008, 11, 290–301. [Google Scholar] [CrossRef] [PubMed]
  43. Cudnoch-Jedrzejewska, A.; Szczepanska-Sadowska, E.; Dobruch, J.; Gomolka, R.; Puchalska, L. Brain vasopressin V(1) receptors contribute to enhanced cardiovascular responses to acute stress in chronically stressed rats and rats with myocardial infarction. Am. J. Physiol. Regul. Integr. Comp. Physiol. 2010, 298, R672–R680. [Google Scholar] [CrossRef] [PubMed]
  44. Cudnoch-Jedrzejewska, A.; Puchalska, L.; Szczepanska-Sadowska, E.; Wsol, A.; Kowalewski, S.; Czarzasta, K. The effect of blockade of the central V1 vasopressin receptors on anhedonia in chronically stressed infarcted and non-infarcted rats. Physiol. Behav. 2014, 135, 208–214. [Google Scholar] [CrossRef]
  45. Dobruch, J.; Cudnoch-Jedrzejewska, A.; Szczepanska-Sadowska, E. Enhanced involvement of brain vasopressin V1 receptors in cardiovascular responses to stress in rats with myocardial infarction. Stress 2005, 8, 273–284. [Google Scholar] [CrossRef]
  46. Lozić, M.; Šarenac, O.; Murphy, D.; Japundžić-Žigon, N. Vasopressin, Central Autonomic Control and Blood Pressure Regulation. Curr. Hypertens. Rep. 2018, 26, 11. [Google Scholar] [CrossRef]
  47. Szczepanska-Sadowska, E.; Wsol, A.; Cudnoch-Jedrzejewska, A.; Czarzasta, K.; Żera, T. Multiple aspects of inappropriate action of renin-angiotensin, vasopressin, and oxytocin systems in neuropsychiatric and neurodegenerative diseases. J. Clin. Med. 2022, 11, 908. [Google Scholar] [CrossRef]
  48. Li, X.; Chan, T.O.; Myers, V.; Chowdhury, I.; Zhang, X.Q.; Song, J.; Zhang, J.; Andrel, J.; Funakoshi, H.; Robbins, J.; et al. Controlled and cardiac-restricted overexpression of the arginine vasopressin V1A receptor causes reversible left ventricular dysfunction through Gαq-mediated cell signaling. Circulation 2011, 124, 572–581. [Google Scholar] [CrossRef] [Green Version]
  49. Szczepanska-Sadowska, E.; Stepniakowski, K.; Skelton, M.M.; Cowley, A.W., Jr. Prolonged stimulation of intrarenal V1 vasopressin receptors results in sustained hypertension. Am. J. Physiol. 1994, 267, R1217–R1225. [Google Scholar] [CrossRef]
  50. Wsół, A.; Cudnoch-Jedrzejewska, A.; Szczepanska-Sadowska, E.; Kowalewski, S.; Dobruch, J. Central oxytocin modulation of acute stress-induced cardiovascular responses after myocardial infarction in the rat. Stress 2009, 12, 517–525. [Google Scholar] [CrossRef]
  51. Wsol, A.; Szczepanska-Sadowska, E.; Kowalewski, S.; Puchalska, L.; Cudnoch-Jedrzejewska, A. Oxytocin differently regulates pressor responses to stress in WKY and SHR rats: The role of central oxytocin and V1a receptors. Stress 2014, 17, 117–125. [Google Scholar] [CrossRef] [PubMed]
  52. Wsol, A.; Wojno, O.; Puchalska, L.; Wrzesien, R.; Szczepanska-Sadowska, E.; Cudnoch-Jedrzejewska, A. Impaired hypotensive effects of centrally acting oxytocin in SHR and WKY rats exposed to chronic mild stress. Am. J. Physiol. Regul. Integr. Comp. Physiol. 2020, 318, R160–R172. [Google Scholar] [CrossRef] [PubMed]
  53. Wilson, M.F.; Brackett, D.J.; Archer, L.T.; Hinshaw, L.B. Mechanisms of impaired cardiac function by vasopressin. Ann. Surg. 1980, 191, 494–500. [Google Scholar] [CrossRef]
  54. Mayr, V.D.; Wenzel, V.; Wagner-Berger, H.G.; Stadlbauer, K.H.; Cavus, E.; Raab, H.; Müller, T.H.; Jochberger, S.; Dünser, M.W.; Krismer, A.C.; et al. Arginine vasopressin during sinus rhythm: Effects on haemodynamic variables, left anterior descending coronary artery cross sectional area and cardiac index, before and after inhibition of NO-synthase, in pigs. Resuscitation 2007, 74, 366–371. [Google Scholar] [CrossRef] [PubMed]
  55. Wenzel, V.; Kern, K.B.; Hilwig, R.W.; Berg, R.A.; Schwarzacher, S.; Butman, S.M.; Lindner, K.H.; Ewy, G.A. Effects of intravenous arginine vasopressin on epicardial coronary artery cross sectional area in a swine resuscitation model. Resuscitation 2005, 64, 219–226. [Google Scholar] [CrossRef]
  56. Chandrashekhar, Y.; Prahash, A.J.; Sen, S.; Gupta, S.; Roy, S.; Anand, I.S. The role of arginine vasopressin and its receptors in the normal and failing rat heart. J. Mol. Cell. Cardiol. 2003, 35, 495–504. [Google Scholar] [CrossRef]
  57. Forsling, M.L.; Aziz, L.A. Release of vasopressin in response to hypoxia and the effect of aminergic and opioid antagonists. J. Endocrinol. 1983, 99, 77–86. [Google Scholar] [CrossRef]
  58. Proczka, M.; Przybylski, J.; Cudnoch-Jędrzejewska, A.; Szczepańska-Sadowska, E.; Żera, T. Vasopressin and breathing: Review of evidence for respiratory effects of the antidiuretic hormone. Front. Physiol. 2021, 12, 744177. [Google Scholar] [CrossRef]
  59. Rose, C.E., Jr.; Anderson, R.J.; Carey, R.M. Antidiuresis and vasopressin release with hypoxemia and hypercapnia in conscious dogs. Am. J. Physiol. 1984, 247, R127–R134. [Google Scholar] [CrossRef]
  60. Rose, C.E., Jr.; Godine, R.L., Jr.; Rose, K.Y.; Anderson, R.J.; Carey, R.M. Role of arginine vasopressin and angiotensin II in cardiovascular responses to combined acute hypoxemia and hypercapnic acidosis in conscious dogs. J. Clin. Investig. 1984, 74, 321–331. [Google Scholar] [CrossRef]
  61. Stark, R.I.; Daniel, S.S.; Husain, M.K.; Zubrow, A.B.; James, L.S. Effects of hypoxia on vasopressin concentrations in cerebrospinal fluid and plasma of sheep. Neuroendocrinology 1984, 38, 453–460. [Google Scholar] [CrossRef] [PubMed]
  62. Wang, B.C.; Sundet, W.D.; Goetz, K.L. Vasopressin in plasma and cerebrospinal fluid of dogs during hypoxia or acidosis. Am. J. Physiol. 1984, 247, E449–E455. [Google Scholar] [CrossRef] [PubMed]
  63. Kc, P.; Dick, T.E. Modulation of cardiorespiratory function mediated by the paraventricular nucleus. Respir. Physiol. Neurobiol. 2010, 174, 55–64. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  64. Maruyama, N.O.; Mitchell, N.C.; Truong, T.T.; Toney, G.M. Activation of the hypothalamic paraventricular nucleus by acute intermittent hypoxia: Implications for sympathetic long-term facilitation neuroplasticity. Exp. Neurol. 2019, 314, 1–8. [Google Scholar] [CrossRef]
  65. Wu, Y.; Du, J.Z. Effects of angiotensin II on release of CRH and AVP from hypothalamus during acute hypoxia. Acta Pharmacol. Sin. 2000, 21, 1035–1038. [Google Scholar]
  66. Walker, B.R. Role of vasopressin in the cardiovascular response to hypoxia in the conscious rat. Am. J. Physiol. 1986, 251, H1316–H1323. [Google Scholar] [CrossRef]
  67. Russ, R.D.; Walker, B.R. Role of nitric oxide in vasopressinergic pulmonary vasodilatation. Am. J. Physiol. 1992, 262, H743–H747. [Google Scholar] [CrossRef]
  68. Walker, B.R.; Haynes, J., Jr.; Wang, H.L.; Voelkel, N.F. Vasopressin-induced pulmonary vasodilation in rats. Am. J. Physiol. 1989, 257, H415–H422. [Google Scholar] [CrossRef]
  69. Kc, P.; Balan, K.V.; Tjoe, S.S.; Martin, R.J.; Lamanna, J.C.; Haxhiu, M.A.; Dick, T.E. Increased vasopressin transmission from the paraventricular nucleus to the rostral medulla augments cardiorespiratory outflow in chronic intermittent hypoxia-conditioned rats. J. Physiol. 2010, 588, 725–740. [Google Scholar] [CrossRef]
  70. Montero, S.; Mendoza, H.; Valles, V.; Lemus, M.; Alvarez-Buylla, R.; de Alvarez-Buylla, E.R. Arginine-vasopressin mediates central and peripheral glucose regulation in response to carotid body receptor stimulation with Na-cyanide. J. Appl. Physiol. 2006, 100, 1902–1909. [Google Scholar] [CrossRef]
  71. Jin, H.K.; Yang, R.H.; Chen, Y.F.; Thornton, R.M.; Jackson, R.M.; Oparil, S. Hemodynamic effects of arginine vasopressin in rats adapted to chronic hypoxia. J. Appl. Physiol. 1989, 66, 151–160. [Google Scholar] [CrossRef] [PubMed]
  72. Hisata, Y.; Zeredo, J.L.; Eishi, K.; Toda, K. Cardiac nociceptors innervated by vagal afferents in rats. Auton. Neurosci. 2006, 126–127, 174–178. [Google Scholar] [CrossRef] [PubMed]
  73. Rosen, S.D. From heart to brain: The genesis and processing of cardiac pain. Can. J. Cardiol. 2012, 28, S7–S19. [Google Scholar] [CrossRef] [PubMed]
  74. Kendler, K.S.; Weitzman, R.E.; Fisher, D.A. The effect of pain on plasma arginine vasopressin concentrations in man. Clin. Endocrinol. 1978, 8, 89–94. [Google Scholar] [CrossRef]
  75. Szczepanska-Sadowska, E.; Cudnoch-Jedrzejewska, A.; Sadowski, B. Differential role of specific cardiovascular neuropeptides in pain regulation: Relevance to cardiovascular diseases. Neuropeptides 2020, 81, 102046. [Google Scholar] [CrossRef]
  76. Yang, J.; Yang, Y.; Chen, J.M.; Xu, H.T.; Liu, W.Y.; Wang, C.H.; Lin, B.C. Arginine vasopressin is an important regulator in antinociceptive modulation of hypothalamic paraventricular nucleus in the rat. Neuropeptides 2007, 41, 165–176. [Google Scholar] [CrossRef] [PubMed]
  77. Yang, J.; Yang, Y.; Xu, H.T.; Chen, J.M.; Liu, W.Y.; Lin, B.C. Arginine vasopressin induces periaqueductal gray release of enkephalin and endorphin relating to pain modulation in the rat. Regul. Pept. 2007, 142, 29–36. [Google Scholar] [CrossRef]
  78. Yang, J.; Yuan, H.; Chu, J.; Yang, Y.; Xu, H.; Wang, G.; Liu, W.Y.; Lin, B.C. Arginine vasopressin antinociception in the rat nucleus raphe magnus is involved in the endogenous opiate peptide and serotonin system. Peptides 2009, 30, 1355–1361. [Google Scholar] [CrossRef]
  79. Yang, J.; Yuan, H.; Liu, W.; Song, C.; Xu, H.; Wang, G.; Song Cai Ni, N.; Yang, D.; Lin, B. Arginine vasopressin in hypothalamic paraventricular nucleus is transferred to the nucleus raphe magnus to participate in pain modulation. Peptides 2009, 30, 1679–1682. [Google Scholar] [CrossRef]
  80. Colloca, L.; Pine, D.S.; Ernst, M.; Miller, F.G.; Grillon, C. Vasopressin boosts placebo analgesic effects in women: A randomized trial. Biol. Psychiatry 2016, 79, 794–802. [Google Scholar] [CrossRef]
  81. Juif, P.E.; Poisbeau, P. Neurohormonal effects of oxytocin and vasopressin receptor agonists on spinal pain processing in male rats. Pain 2013, 154, 1449–1456. [Google Scholar] [CrossRef] [PubMed]
  82. Kordower, J.H.; Bodnar, R.J. Vasopressin analgesia: Specificity of action and non-opioid effects. Peptides 1984, 5, 747–756. [Google Scholar] [CrossRef]
  83. Yang, J.; Lu, L.; Wang, H.C.; Zhan, H.Q.; Hai, G.F.; Pan, Y.J.; Lv, Q.Q.; Wang, D.X.; Wu, Y.Q.; Li, R.R.; et al. Effect of intranasal arginine vasopressin on human headache. Peptides 2012, 38, 100–104. [Google Scholar] [CrossRef]
  84. Zhao, X.Y.; Zhang, Q.S.; Yang, J.; Sun, F.J.; Wang, D.X.; Wang, C.H.; He, W.Y. The role of arginine vasopressin in electroacupuncture treatment of primary sciatica in human. Neuropeptides 2015, 52, 61–65. [Google Scholar] [CrossRef]
  85. Ahn, D.K.; Kim, K.H.; Ju, J.S.; Kwon, S.; Park, J.S. Microinjection of arginine vasopressin into the central nucleus of amygdala suppressed nociceptive jaw opening reflex in freely moving rats. Brain Res. Bull. 2001, 55, 117–121. [Google Scholar] [CrossRef]
  86. Kordower, J.H.; Bodnar, R.J. Differential effects of dPTyr(Me)AVP, a vasopressin antagonist, upon foot shock analgesia. Int. J. Neurosci. 1985, 28, 269–278. [Google Scholar] [CrossRef]
  87. Peng, F.; Qu, Z.W.; Qiu, C.Y.; Liao, M.; Hu, W.P. Spinal vasopressin alleviates formalin-induced nociception by enhancing GABAA receptor function in mice. Neurosci. Lett. 2015, 593, 61–65. [Google Scholar] [CrossRef]
  88. Qiu, F.; Qiu, C.Y.; Cai, H.; Liu, T.T.; Qu, Z.W.; Yang, Z.; Li, J.D.; Zhou, Q.Y.; Hu, W.P. Oxytocin inhibits the activity of acid-sensing ion channels through the vasopressin, V1A receptor in primary sensory neurons. Br. J. Pharmacol. 2014, 171, 3065–3076. [Google Scholar] [CrossRef] [Green Version]
  89. Caldwell, H.K.; Aulino, E.A.; Rodriguez, K.M.; Witchey, S.K.; Yaw, A.M. Social context, stress, neuropsychiatric disorders, and the vasopressin 1b receptor. Front. Neurosci. 2017, 11, 567. [Google Scholar] [CrossRef]
  90. Siegenthaler, J.; Walti, C.; Urwyler, S.A.; Schuetz, P.; Christ-Crain, M. Copeptin concentrations during psychological stress: The PsyCo study. Eur. J. Endocrinol. 2014, 171, 737–742. [Google Scholar] [CrossRef] [Green Version]
  91. Brown, C.H. Magnocellular neurons and posterior pituitary function. Compr. Physiol. 2016, 6, 1701–1741. [Google Scholar] [CrossRef] [PubMed]
  92. Brown, C.H.; Ludwig, M.; Tasker, J.G.; Stern, J.E. Somato-dendritic vasopressin and oxytocin secretion in endocrine and autonomic regulation. J. Neuroendocrinol. 2020, 32, e12856. [Google Scholar] [CrossRef] [PubMed]
  93. Roy, R.K.; Augustine, R.A.; Brown, C.H.; Schwenke, D.O. Acute myocardial infarction activates magnocellular vasopressin and oxytocin neurones. J. Neuroendocrinol. 2019, 31, e12808. [Google Scholar] [CrossRef] [PubMed]
  94. Boeckel, J.N.; Oppermann, J.; Anadol, R.; Fichtlscherer, S.; Zeiher, A.M.; Keller, T. Analyzing the release of copeptin from the heart in acute myocardial infarction using a transcoronary gradient model. Sci. Rep. 2016, 6, 20812. [Google Scholar] [CrossRef] [PubMed]
  95. Donald, R.A.; Crozier, I.G.; Foy, S.G.; Richards, A.M.; Livesey, J.H.; Ellis, M.J.; Mattioli, L.; Ikram, H. Plasma corticotrophin releasing hormone, vasopressin, ACTH and cortisol responses to acute myocardial infarction. Clin. Endocrinol. 1994, 40, 499–504. [Google Scholar] [CrossRef]
  96. McAlpine, H.M.; Cobbe, S.M. Neuroendocrine changes in acute myocardial infarction. Am. J. Med. 1988, 84, 61–66. [Google Scholar] [CrossRef]
  97. Möckel, M.; Searle, J. Copeptin-marker of acute myocardial infarction. Curr. Atheroscler. Rep. 2014, 16, 421. [Google Scholar] [CrossRef] [Green Version]
  98. Schill, F.; Timpka, S.; Nilsson, P.M.; Melander, O.; Enhörning, S. Copeptin as a predictive marker of incident heart failure. ESC Heart Fail. 2021, 8, 3180–3188. [Google Scholar] [CrossRef]
  99. Nazari, A.; Sadr, S.S.; Faghihi, M.; Imani, A.; Moghimian, M. The cardioprotective effect of different doses of vasopressin (AVP) against ischemia-reperfusion injuries in the anesthetized rat heart. Peptides 2011, 32, 2459–2466. [Google Scholar] [CrossRef]
  100. Youngquist, S.T.; Shah, A.; McClung, C.; Thomas, J.L.; Rosborough, J.P.; Niemann, J.T. Does prearrest adrenergic integrity affect pressor response? A comparison of epinephrine and vasopressin in a spontaneous ventricular fibrillation swine model. Resuscitation 2011, 82, 228–231. [Google Scholar] [CrossRef] [Green Version]
  101. Sellke, F.; Quillen, J. Altered effects of vasopressin on the coronary circulation after ischemia. J. Thorac. Cardiovasc. Surg. 1992, 104, 357–363. [Google Scholar] [CrossRef]
  102. Sellke, N.; Kuczmarski, A.; Lawandy, I.; Cole, V.L.; Ehsan, A.; Singh, A.K.; Liu, Y.; Sellke, F.W.; Feng, J. Enhanced coronary arteriolar contraction to vasopressin in patients with diabetes after cardiac surgery. J. Thorac. Cardiovasc. Surg. 2018, 156, 2098–2107. [Google Scholar] [CrossRef] [PubMed]
  103. Mulligan, K.A.; McKnite, S.H.; Lindner, K.H.; Lindstrom, P.J.; Detloff, B.; Lurie, K.G. Synergistic effects of vasopressin plus epinephrine during cardiopulmonary resuscitation. Resuscitation 1997, 35, 265–271. [Google Scholar] [CrossRef]
  104. Stadlbauer, K.H.; Wagner-Berger, H.G.; Wenzel, V.; Voelckel, W.G.; Krismer, A.C.; Klima, G.; Rheinberger, K.; Pechlaner, S.; Mayr, V.D.; Lindner, K.H. Survival with full neurologic recovery after prolonged cardiopulmonary resuscitation with a combination of vasopressin and epinephrine in pigs. Anesth. Analg. 2003, 96, 1743–1749. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  105. Voelckel, W.G.; Lurie, K.G.; Lindner, K.H.; Zielinski, T.; McKnite, S.; Krismer, A.C.; Wenzel, V. Vasopressin improves survival after cardiac arrest in hypovolemic shock. Anesth. Analg. 2000, 91, 627–634. [Google Scholar] [CrossRef] [PubMed]
  106. Lurie, K.G.; Voelckel, W.G.; Iskos, D.N.; McKnite, S.H.; Zielinski, T.M.; Sugiyama, A.; Wenzel, V.; Benditt, D.; Lindner, K.H. Combination drug therapy with vasopressin, adrenaline (epinephrine) and nitroglycerin improves vital organ blood flow in a porcine model of ventricular fibrillation. Resuscitation 2002, 54, 187–194. [Google Scholar] [CrossRef]
  107. Wira, C.R.; Becker, J.U.; Martin, G.; Donnino, M.W. Anti-arrhythmic and vasopressor medications for the treatment of ventricular fibrillation in severe hypothermia: A systematic review of the literature. Resuscitation 2008, 78, 21–29. [Google Scholar] [CrossRef]
  108. Lindner, K.H.; Haak, T.; Keller, A.; Bothner, U.; Lurie, K.G. Release of endogenous vasopressors during and after cardiopulmonary resuscitation. Heart 1996, 75, 145–150. [Google Scholar] [CrossRef]
  109. Lindner, K.H.; Strohmenger, H.U.; Ensinger, H.; Hetzel, W.D.; Ahnefeld, F.W.; Georgieff, M. Stress hormone response during and after cardiopulmonary resuscitation. Anesthesiology 1992, 77, 662–668. [Google Scholar] [CrossRef]
  110. Krismer, A.C.; Wenzel, V.; Mayr, V.D.; Voelckel, W.G.; Strohmenger, H.U.; Lurie, K.; Lindner, K.H. Arginine vasopressin during cardiopulmonary resuscitation and vasodilatory shock: Current experience and future perspectives. Curr. Opin. Crit. Care 2001, 7, 157–169. [Google Scholar] [CrossRef]
  111. Lindner, K.H.; Dirks, B.; Strohmenger, H.U.; Prengel, A.W.; Lindner, I.M.; Lurie, K.G. Randomised comparison of epinephrine and vasopressin in patients with out-of-hospital ventricular fibrillation. Lancet 1997, 349, 535–537. [Google Scholar] [CrossRef]
  112. Lindner, K.H.; Prengel, A.W.; Brinkmann, A.; Strohmenger, H.U.; Lindner, I.M.; Lurie, K.G. Vasopressin administration in refractory cardiac arrest. Ann. Inter. Med. 1996, 124, 1061–1064. [Google Scholar] [CrossRef] [PubMed]
  113. Russell, J.A. Vasopressin in vasodilatory and septic shock. Curr. Opin. Crit. Care 2007, 13, 383–391. [Google Scholar] [CrossRef]
  114. Faigel, D.O.; Metz, D.C.; Kochman, M.L. Torsade de pointes complicating the treatment of bleeding esophageal varices: Association with neuroleptics, vasopressin, and electrolyte imbalance. Am. J. Gastroenterol. 1995, 90, 822–824. [Google Scholar] [PubMed]
  115. Urge, J.; Sincl, F.; Procházka, V.; Urbánek, K. Terlipressin-induced ventricular arrhythmia. Scand. J. Gastroenterol. 2008, 43, 1145–1148. [Google Scholar] [CrossRef] [PubMed]
  116. Reardon, D.P.; DeGrado, J.R.; Anger, K.E.; Szumita, P.M. Early vasopressin reduces incidence of new onset arrhythmias. J. Crit. Care 2014, 29, 482–485. [Google Scholar] [CrossRef]
  117. Stiell., I.G.; Hébert, P.C.; Wells, G.A.; Vandemheen, K.L.; Tang, A.S.; Higginson, L.A.; Dreyer, J.F.; Clement, C.; Battram, E.; Watpool, I.; et al. Vasopressin versus epinephrine for in hospital cardiac arrest: A randomised controlled trial. Lancet 2001, 358, 105–109. [Google Scholar] [CrossRef]
  118. Aung, K.; Htay, T. Vasopressin for cardiac arrest: A systematic review and meta-analysis. Arch. Intern. Med. 2005, 165, 17–24. [Google Scholar] [CrossRef] [Green Version]
  119. Acosta, E.; Mendoza, V.; Castro, E.; Cruzblanca, H. Modulation of a delayed-rectifier K+ current by angiotensin II in rat sympathetic neurons. J. Neurophysiol. 2007, 98, 79–85. [Google Scholar] [CrossRef] [Green Version]
  120. Dendorfer, A.; Thornagel, A.; Raasch, W.; Grisk, O.; Tempel, K.; Dominiak, P. Angiotensin II induces catecholamine release by direct ganglionic excitation. Hypertension 2002, 40, 348–354. [Google Scholar] [CrossRef] [Green Version]
  121. Luft, F.C. Cardiac angiotensin is upregulated in the hearts of unstable angina patients. Circ. Res. 2004, 94, 1530–1532. [Google Scholar] [CrossRef] [PubMed]
  122. Xia, H.; Lazartigues, E. Angiotensin-converting enzyme 2: Central regulator for cardiovascular function. Curr. Hypertens. Rep. 2010, 12, 170–175. [Google Scholar] [CrossRef] [PubMed]
  123. Szczepanska-Sadowska, E.K.; Zera, T.; Cudnoch-jedrzejewska, A. The contribution of angiotensin peptides to cardiovascular regulation in health and disease. In Angiotensin: From the Kidney to Coronavirus; Pilowsky, P.M., Ed.; Elsevier: Amsterdam, The Netherlands, 2022; ISBN 10:0323996183. [Google Scholar]
  124. Kawada, T.; Yamazaki, T.; Akiyama, T.; Li, M.; Zheng, C.; Shishido, T.; Mori, H.; Sugimachi, M. Angiotensin II attenuates myocardial interstitial acetylcholine release in response to vagal stimulation. Am. J. Physiol. Heart Circ. Physiol. 2007, 293, H2516–H2522. [Google Scholar] [CrossRef] [PubMed]
  125. Chen, A.; Huang, B.S.; Wang, H.W.; Ahmad, M.; Leenen, F.H. Knockdown of mineralocorticoid or angiotensin II type 1 receptor gene expression in the paraventricular nucleus prevents angiotensin II hypertension in rats. J. Physiol. 2014, 592, 3523–3536. [Google Scholar] [CrossRef] [PubMed]
  126. Fischer, R.; Dechend, R.; Gapelyuk, A.; Shagdarsuren, E.; Gruner, K.; Gruner, A.; Gratze, P.; Qadri, F.; Wellner, M.; Fiebeler, A.; et al. Angiotensin II-induced sudden arrhythmic death and electrical remodeling. Am. J. Physiol. Heart Circ. Physiol. 2007, 293, H1242–H1253. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  127. Iravanian, S.; Dudley, S.C., Jr. The renin-angiotensin-aldosterone system (RAAS) and cardiac arrhythmias. Heart Rhythm 2008, 5, S12–S17. [Google Scholar] [CrossRef] [Green Version]
  128. Li, X.C.; Zhang, J.; Zhuo, J.L. The vasoprotective axes of the renin-angiotensin system: Physiological relevance and therapeutic implications in cardiovascular, hypertensive and kidney diseases. Pharmacol. Res. 2017, 125, 21–38. [Google Scholar] [CrossRef]
  129. Mackins, C.J.; Kano, S.; Seyedi, N.; Schäfer, U.; Reid, A.C.; Machida, T.; Silver, R.B.; Levi, R. Cardiac mast cell-derived renin promotes local angiotensin formation, norepinephrine release, and arrhythmias in ischemia/reperfusion. J. Clin. Investig. 2006, 116, 1063–1070. [Google Scholar] [CrossRef]
  130. Dobruch, J.; Paczwa, P.; Łoń, S.; Khosla, M.C.; Szczepańska-Sadowska, E. Hypotensive function of the brain angiotensin-(1-7) in Sprague Dawley and renin transgenic rats. J. Physiol. Pharmacol. 2003, 54, 371–381. [Google Scholar]
  131. Neri Serneri, G.G.; Boddi, M.; Modesti, P.A.; Coppo, M.; Cecioni, I.; Toscano, T.; Papa, M.L.; Bandinelli, M.; Lisi, G.F.; Chiavarelli, M. Cardiac angiotensin II participates in coronary microvessel inflammation of unstable angina and strengthens the immunomediated component. Circ. Res. 2004, 94, 1630–1637. [Google Scholar] [CrossRef] [Green Version]
  132. Rosenkranz, S. TGF-beta1 and angiotensin networking in cardiac remodeling. Cardiovasc. Res. 2004, 63, 423–432. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  133. Yasuno, S.; Kuwahara, K.; Kinoshita, H.; Yamada, C.; Nakagawa, Y.; Usami, S.; Kuwabara, Y.; Ueshima, K.; Harada, M.; Nishikimi, T.; et al. Angiotensin II type 1a receptor signalling directly contributes to the increased arrhythmogenicity in cardiac hypertrophy. Br. J. Pharmacol. 2013, 170, 1384–1395. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  134. Yu, Y.; Wei, S.G.; Weiss, R.M.; Felder, R.B. Angiotensin II type 1a receptors in the subfornical organ modulate neuroinflammation in the hypothalamic paraventricular nucleus in heart failure rats. Neuroscience 2018, 381, 46–58. [Google Scholar] [CrossRef] [PubMed]
  135. Katz, R.L. Antiarrhythmic and cardiovascular effects of synthetic oxytocin. Anesthesiology 1964, 25, 653–661. [Google Scholar] [CrossRef] [PubMed]
  136. Jankowski, M.; Bissonauth, V.; Gao, L.; Gangal, M.; Wang, D.; Danalache, B.; Wang, Y.; Stoyanova, E.; Cloutier, G.; Blaise, G.; et al. Anti-inflammatory effect of oxytocin in rat myocardial infarction. Basic Res. Cardiol. 2010, 105, 205–218. [Google Scholar] [CrossRef] [PubMed]
  137. Jankowski, M.; Broderick, T.L.; Gutkowska, J. The role of oxytocin in cardiovascular protection. Front. Psychol. 2020, 11, 2139. [Google Scholar] [CrossRef]
  138. Gutkowska, J.; Jankowski, M.; Lambert, C.; Mukaddam-Daher, S.; Zingg, H.H.; McCann, S.M. Oxytocin releases atrial natriuretic peptide by combining with oxytocin receptors in the heart. Proc. Natl. Acad. Sci. USA 1997, 94, 11704–11709. [Google Scholar] [CrossRef] [Green Version]
  139. Jankowski, M.; Danalache, B.; Wang, D.; Bhat, P.; Hajjar, F.; Marcinkiewicz, M.; Paquin, J.; McCann, S.M.; Gutkowska, J. Oxytocin in cardiac ontogeny. Proc. Natl. Acad. Sci. USA 2004, 101, 13074–13079. [Google Scholar] [CrossRef] [Green Version]
  140. Jankowski, M.; Hajjar, F.; Kawas, S.A.; Mukaddam-Daher, S.; Hoffman, G.; McCann, S.M.; Gutkowska, J. Rat heart: A site of oxytocin production and action. Proc. Natl. Acad. Sci. USA 1998, 95, 14558–14563. [Google Scholar] [CrossRef] [Green Version]
  141. Quagliotto, E.; Casali, K.R.; Dal Lago, P.; Rasia-Filho, A.A. Neuropeptides in the posterodorsal medial amygdala modulate central cardiovascular reflex responses in awake male rats. Braz. J. Med. Biol. Res. 2015, 48, 128–139. [Google Scholar] [CrossRef] [Green Version]
  142. Wang, D.; Gutkowska, J.; Marcinkiewicz, M.; Rachelska, G.; Jankowski, M. Genistein supplementation stimulates the oxytocin system in the aorta of ovariectomized rats. Cardiovasc. Res. 2003, 57, 186–194. [Google Scholar] [CrossRef] [Green Version]
  143. Song, Z.; Larkin, T.E.; Malley, M.O.; Albers, H.E. Oxytocin (OT) and arginine-vasopressin (AVP) act on OT receptors and not AVP V1a receptors to enhance social recognition in adult Syrian hamsters (Mesocricetus auratus). Horm. Behav. 2016, 81, 20–27. [Google Scholar] [CrossRef] [Green Version]
  144. Song, Z.; McCann, K.E.; McNeill, J.K., 4th; Larkin, T.E., 2nd; Huhman, K.L.; Albers, H.E. Oxytocin induces social communication by activating arginine-vasopressin V1a receptors and not oxytocin receptors. Psychoneuroendocrinology 2014, 50, 14–19. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  145. Roozendaal, B.; Schoorlemmer, G.H.; Koolhaas, J.M.; Bohus, B. Cardiac, neuroendocrine, and behavioral effects of central amygdaloid vasopressinergic and oxytocinergic mechanisms under stress-free conditions in rats. Brain Res. Bull. 1993, 32, 573–579. [Google Scholar] [CrossRef]
  146. Faghihi, M.; Alizadeh, A.M.; Khori, V.; Latifpour, M.; Khodayari, S. The role of nitric oxide, reactive oxygen species, and protein kinase C in oxytocin-induced cardioprotection in ischemic rat heart. Peptides 2012, 37, 314–319. [Google Scholar] [CrossRef]
  147. Wsol, A.; Gondek, A.; Podobinska, M.; Chmielewski, M.; Sajdel-Sułkowska, E.; Cudnoch-Jędrzejewska, A. Increased oxytocinergic system activity in the cardiac muscle in spontaneously hypertensive SHR rats. Arch. Med. Sci. 2019, 18, 1088–1094. [Google Scholar] [CrossRef]
  148. Bartekova, M.; Radosinska, J.; Jelemensky, M.; Dhalla, N.S. Role of cytokines and inflammation in heart function during health and disease. Heart Fail. Rev. 2018, 23, 733–758. [Google Scholar] [CrossRef] [PubMed]
  149. Lambertsen, K.L.; Biber, K.; Finsen, B. Inflammatory cytokines in experimental and human stroke. J. Cereb. Blood Flow Metab. 2012, 32, 1677–1698. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  150. Maida, C.D.; Norrito, R.L.; Daidone, M.; Tuttolomondo, A.; Pinto, A. Neuroinflammatory Mechanisms in Ischemic Stroke: Focus on Cardioembolic Stroke, Background, and Therapeutic Approaches. Int. J. Mol. Sci. 2020, 21, 6454. [Google Scholar] [CrossRef]
  151. Zhu, H.; Hu, S.; Li, Y.; Sun, Y.; Xiong, X.; Hu, X.; Chen, J.; Qiu, S. Interleukins and Ischemic Stroke. Front. Immunol. 2022, 13, 828447. [Google Scholar] [CrossRef]
  152. Baci, D.; Bosi, A.; Parisi, L.; Buono, G.; Mortara, L.; Ambrosio, G.; Bruno, A. Innate Immunity Effector Cells as Inflammatory Drivers of Cardiac Fibrosis. Int. J. Mol. Sci. 2020, 21, 7165. [Google Scholar] [CrossRef] [PubMed]
  153. Kumar, V.; Prabhu, S.D.; Bansal, S.S. CD4+ T-lymphocytes exhibit biphasic kinetics post-myocardial infarction. Front. Cardiovasc. Med. 2022, 9, 992653. [Google Scholar] [CrossRef] [PubMed]
  154. Kumar, V.; Rosenzweig, R.; Asalla, S.; Nehra, S.; Prabhu, S.D.; Bansa, S.S. TNFR1 Contributes to Activation-Induced Cell Death of Pathological CD4+ T Lymphocytes During Ischemic Heart Failure. J. Am. Coll. Cardiol. Basic to Trans Science 2022, 7, 1038–1049. [Google Scholar]
  155. Meyer, I.S.; Li, X.; Meyer, C.; Voloshanenko, O.; Pohl, S.; Boutros, M.; Katus, H.A.; Frey, N.; Leuschner, F. Blockade of Wnt Secretion Attenuates Myocardial Ischemia-Reperfusion Injury by Modulating the Inflammatory Response. Int. J. Mol. Sci. 2022, 23, 12252. [Google Scholar] [CrossRef] [PubMed]
  156. Besse, S.; Nadaud, S.; Balse, E.; Pavoine, C. Early protective role of inflammation in cardiac remodeling and heart failure: Focus on TNFα and resident macrophages. Cells 2022, 11, 1249. [Google Scholar] [CrossRef] [PubMed]
  157. Feng, Y.; Ye, D.; Wang, Z.; Pan, H.; Lu, X.; Wang, M.; Xu, Y.; Yu, J.; Zhang, J.; Zhao, M.; et al. The role of interleukin-6 family members in cardiovascular diseases. Front. Cardiovasc. Med. 2022, 9, 818890. [Google Scholar] [CrossRef] [PubMed]
  158. Hanna, A.; Frangogiannis, N.G. Inflammatory cytokines and chemokines as therapeutic targets in heart failure. Cardiovasc. Drugs Ther. 2020, 34, 849–863. [Google Scholar] [CrossRef]
  159. Sun, K.; Li, Y.Y.; Jin, J. A double-edged sword of immuno-microenvironment in cardiac homeostasis and injury repair. Signal. Transduct. Target Ther. 2021, 6, 79. [Google Scholar] [CrossRef]
  160. Szabo, T.M.; Frigy, A.; Nagy, E.E. Targeting mediators of inflammation in heart failure: A short synthesis of experimental and clinical results. Int. J. Mol. Sci. 2021, 22, 13053. [Google Scholar] [CrossRef]
  161. Hirota, H.; Yoshida, K.; Kishimoto, T.; Taga, T. Continuous activation of gp130, a signal-transducing receptor component for interleukin 6-related cytokines, causes myocardial hypertrophy in mice. Proc. Natl. Acad. Sci. USA 1995, 92, 4862–4866. [Google Scholar] [CrossRef] [Green Version]
  162. Ufnal, M.; Dudek, M.; Zera, T.; Szczepańska-Sadowska, E. Centrally administered interleukin-1 beta sensitizes to the central pressor action of angiotensin II. Brain Res. 2006, 1100, 64–72. [Google Scholar] [CrossRef] [PubMed]
  163. Ufnal, M.; Dudek, M.; Szczepańska-Sadowska, E. Inhibition of brain nitric oxide synthesis enhances and prolongs the hypertensive effect of centrally administered interleukin-1beta in rats. Cytokine 2006, 33, 166–170. [Google Scholar] [CrossRef] [PubMed]
  164. Ufnal, M.; Zera, T.; Szczepańska-Sadowska, E. Blockade of angiotensin II AT1 receptors inhibits pressor action of centrally administered interleukin-1beta in Sprague Dawley rats. Neuropeptides 39, 581–585. [CrossRef] [PubMed]
  165. Żera, T.; Ufnal, M.; Szczepańska-Sadowska, E. TNF and angiotensin type 1 receptors interact in the brain control of blood pressure in heart failure. Cytokine 2015, 71, 272–277. [Google Scholar] [CrossRef]
  166. Yao, L.; Shao, W.; Chen, Y.; Wang, S.; Huang, D. Suppression of ADAM8 attenuates angiotensin II-induced cardiac fibrosis and endothelial-mesenchymal transition via inhibiting TGF-β1/Smad2/Smad3 pathways. Exp. Anim. 2022, 71, 90–99. [Google Scholar] [CrossRef]
  167. Kimura, T.; Yamamoto, T.; Ota, K.; Shoji, M.; Inoue, M.; Sato, K.; Ohta, M.; Funyu, T.; Yoshinaga, K. Central effects of interleukin-1 on blood pressure, thermogenesis, and the release of vasopressin, ACTH, and atrial natriuretic peptide. Ann. N. Y. Acad. Sci. 1993, 689, 330–345. [Google Scholar] [CrossRef]
  168. Takahashi, H.; Nishimura, M.; Sakamoto, M.; Ikegaki, I.; Nakanishi, T.; Yoshimura, M. Effects of interleukin-1 beta on blood pressure, sympathetic nerve activity, and pituitary endocrine functions in anesthetized rats. Am. J. Hypertens. 1992, 5, 224–229. [Google Scholar] [CrossRef]
  169. Xu, F.; Sun, S.; Wang, X.; Ni, E.; Zhao, L.; Zhu, W. GRK2 mediates arginine vasopressin-induced interleukin-6 production via nuclear factor-κB signaling neonatal rat cardiac fibroblast. Mol. Pharmacol. 2017, 92, 278–284. [Google Scholar] [CrossRef]
  170. Yan-Hong, F.; Hui, D.; Qing, P.; Lei, S.; Hai-Chang, W.; Wei, Z.; Yan-Jie, C. Effects of arginine vasopressin on differentiation of cardiac fibroblasts into myofibroblasts. J. Cardiovasc. Pharmacol. 2010, 55, 489–495. [Google Scholar] [CrossRef]
  171. Finkel, M.S.; Oddis, C.V.; Jacob, T.D.; Watkins, S.C.; Hattler, B.G.; Simmons, R.L. Negative inotropic effects of cytokines on the heart mediated by nitric oxide. Science 1992, 257, 387–389. [Google Scholar] [CrossRef]
  172. Yamamoto, K.; Ikeda, U.; Okada, K.; Saito, T.; Kawahara, Y.; Okuda, M.; Yokoyama, M.; Shimad, K. Arginine vasopressin increases nitric oxide synthesis in cytokine-stimulated rat cardiac myocytes. Hypertension 1997, 30, 1112–1120. [Google Scholar] [CrossRef] [PubMed]
  173. Hems, D.A.; Whitton, P.D.; Ma, G.Y. Metabolic actions of vasopressin, glucagon and adrenalin in the intact rat. Biochim. Biophys. Acta 1975, 411, 155–164. [Google Scholar] [CrossRef]
  174. Lee, B.; Yang, C.; Chen, T.H.; al-Azawi, N.; Hsu, W.H. Effect of AVP and oxytocin on insulin release: Involvement of V1b receptors. Am. J. Physiol. 1995, 269, E1095–E1100. [Google Scholar] [CrossRef] [PubMed]
  175. Sztechman, D.; Czarzasta, K.; Cudnoch-Jedrzejewska, A.; Szczepanska-Sadowska, E.; Zera, T. Aldosterone and mineralocorticoid receptors in regulation of the cardiovascular system and pathological remodelling of the heart and arteries. J. Physiol. Pharmacol. 2018, 69, 829–845. [Google Scholar] [CrossRef]
  176. Taveau, C.; Chollet, C.; Bichet, D.G.; Velho, G.; Guillon, G.; Corbani, M.; Roussel, R.; Bankir, L.; Melander, O.; Bouby, N. Acute and chronic hyperglycemic effects of vasopressin in normal rats: Involvement of V1A receptors. Am. J. Physiol. Endocrinol. Metab. 2017, 312, E127–E135. [Google Scholar] [CrossRef]
  177. Yibchok-anun, S.; Hsu, W.H. Effects of arginine vasopressin and oxytocin on glucagon release from clonal alpha-cell line In-R1-G9: Involvement of V1b receptors. Life Sci. 1998, 63, 1871–1878. [Google Scholar] [CrossRef]
Ijms 23 14414 g001 550
Figure 1. Components of the vasopressin system involved in the regulation of blood flow in the brain, heart, vessels, kidney, lungs and digestive system. AVP—arginine vasopressin; SNS—sympathetic nervous system; V1aR—vasopressin V1a receptors; V1bR—vasopressin V1b receptors; V2R—vasopressin V2 receptors.
Figure 1. Components of the vasopressin system involved in the regulation of blood flow in the brain, heart, vessels, kidney, lungs and digestive system. AVP—arginine vasopressin; SNS—sympathetic nervous system; V1aR—vasopressin V1a receptors; V1bR—vasopressin V1b receptors; V2R—vasopressin V2 receptors.
Ijms 23 14414 g001
Ijms 23 14414 g002 550
Figure 2. Interaction of vasopressin, angiotensins, oxytocin and cytokines with the autonomic nervous system in the regulation of cardiovascular parameters. Stress, anxiety, pain, hypoxia and inflammation enhance the release of vasopressin, oxytocin, angiotensins and cytokines in the brain, heart and vessels, and these peptides regulate the function of the heart and vessels through central and intracardiac effects. Ang II—angiotensin II; Ang (1–7)—angiotensin-(1–7); AT1R—AT1 receptors, AVP—arginine vasopressin; IL-1β—interleukin 1-β; OTR—oxytocin receptors; OXY—oxytocin; TGF-β—transforming growth factor β; TNF-α—tumor necrosis factor α; V1aR—vasopressin V1a receptors. → sequence of events, ↑- increased activation, ↓ - decreased activation.
Figure 2. Interaction of vasopressin, angiotensins, oxytocin and cytokines with the autonomic nervous system in the regulation of cardiovascular parameters. Stress, anxiety, pain, hypoxia and inflammation enhance the release of vasopressin, oxytocin, angiotensins and cytokines in the brain, heart and vessels, and these peptides regulate the function of the heart and vessels through central and intracardiac effects. Ang II—angiotensin II; Ang (1–7)—angiotensin-(1–7); AT1R—AT1 receptors, AVP—arginine vasopressin; IL-1β—interleukin 1-β; OTR—oxytocin receptors; OXY—oxytocin; TGF-β—transforming growth factor β; TNF-α—tumor necrosis factor α; V1aR—vasopressin V1a receptors. → sequence of events, ↑- increased activation, ↓ - decreased activation.
Ijms 23 14414 g002
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Share and Cite

MDPI and ACS Style

Szczepanska-Sadowska, E. The Heart as a Target of Vasopressin and Other Cardiovascular Peptides in Health and Cardiovascular Diseases. Int. J. Mol. Sci. 2022, 23, 14414. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232214414

AMA Style

Szczepanska-Sadowska E. The Heart as a Target of Vasopressin and Other Cardiovascular Peptides in Health and Cardiovascular Diseases. International Journal of Molecular Sciences. 2022; 23(22):14414. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232214414

Chicago/Turabian Style

Szczepanska-Sadowska, Ewa. 2022. "The Heart as a Target of Vasopressin and Other Cardiovascular Peptides in Health and Cardiovascular Diseases" International Journal of Molecular Sciences 23, no. 22: 14414. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232214414

Note that from the first issue of 2016, this journal uses article numbers instead of page numbers. See further details here.

Article Metrics

Back to TopTop