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Molecular Basis of Cardiovascular Diseases: Implications of Natriuretic Peptides

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 June 2019) | Viewed by 102762

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Special Issue Editors

Dr. Speranza Rubattu

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Guest Editor

1. IRCCS Neuromed, 86077 Pozzilli, Italy
2. Department of Clinical and Molecular Medicine, School of Medicine and Psychology, Sapienza University, 00185 Rome, Italy
Interests: cardiovascular medicine
Special Issues, Collections and Topics in MDPI journals

Prof. Dr. Massimo Volpe

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Guest Editor

Cardiology Unit, Department of Clinical and Molecular Medicine, Sapienza University of Rome, Sant’Andrea Hospital, Via di Grottarossa 1035, 00189 Rome, Italy
Interests: hypertension; heart failure; neurohormonal systems; cardiovascular prevention
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The natriuretic peptides (NPs) family includes a class of hormones and their receptors needed for the physiological control of cardiovascular functions. The discovery of NPs provided a fundamental contribution into our understanding of the physiological regulation of blood pressure, of heart and kidney functions. NPs have also been implicated in the pathogenesis of several cardiovascular diseases (CVDs), including hypertension, atherosclerosis, heart failure and stroke. A fine comprehension of the molecular mechanisms dependent from NPs and underlying the promotion of cardiovascular damage has contributed to improve our understanding of the molecular basis of all major CVDs. Finally, the opportunity to target NPs in order to develop new therapeutic tools for a better treatment of CVDs has been developed over the years.

This Special Issue will cover all major aspects of the molecular implications of NPs in physiology and pathology of the cardiovascular system, including natriuretic peptide-based therapeutic approaches.

Dr. Speranza Rubattu
Dr. Massimo Volpe
Guest Editors

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Published Papers (14 papers)

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Editorial

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7 pages, 197 KiB

Open AccessEditorial

Natriuretic Peptides in the Cardiovascular System: Multifaceted Roles in Physiology, Pathology and Therapeutics

by Speranza Rubattu and Massimo Volpe

Int. J. Mol. Sci. 2019, 20(16), 3991; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20163991 - 16 Aug 2019

Cited by 28 | Viewed by 4176

Abstract

The natriuretic peptides (NPs) family includes a class of hormones and their receptors needed for the physiological control of cardiovascular functions. The discovery of NPs provided a fundamental contribution into our understanding of the physiological regulation of blood pressure, and of heart and kidney functions. NPs have also been implicated in the pathogenesis of several cardiovascular diseases (CVDs), including hypertension, atherosclerosis, heart failure, and stroke. A fine comprehension of the molecular mechanisms dependent from NPs and underlying the promotion of cardiovascular damage has contributed to improve our understanding of the molecular basis of all major CVDs. Finally, the opportunity to target NPs in order to develop new therapeutic tools for a better treatment of CVDs has been developed over the years. The current Special Issue of the Journal covers all major aspects of the molecular implications of NPs in physiology and pathology of the cardiovascular system, including NP-based therapeutic approaches. Full article

(This article belongs to the Special Issue Molecular Basis of Cardiovascular Diseases: Implications of Natriuretic Peptides)

Research

Jump to: Editorial, Review

14 pages, 3929 KiB

Open AccessArticle

The Expression of BNP, ET-1, and TGF-β1 in Myocardium of Rats with Ventricular Arrhythmias

by Meihui Tian, Ying Xiao, Jiajia Xue, Yuan Zhang, Yuqing Jia, Xinyi Luo, Tianqi Wang, Baoli Zhu and Zhipeng Cao

Int. J. Mol. Sci. 2019, 20(23), 5845; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20235845 - 21 Nov 2019

Cited by 6 | Viewed by 3053

Abstract

Ventricular arrhythmia (VA) is a major component of sudden cardiac death (SCD). To investigate the expression of brain natriuretic peptide (BNP), endothelin-1 (ET-1), and transforming growth factor-beta 1 (TGF-β1) during VA, we established a rat model of VA induced by BaCl₂ solution through a microinjector pump. PD142893 (ET-1 receptor blocker) and SB431542 (TGF-β1 receptor type I blocker) were used to explore the effect of ET-1 and TGF-β1 on BNP expression in the myocardium after VA. BNP, ET-1, and TGF-β1 in rat myocardium were assayed by western blot and immunohistochemical staining for proteins, and real-time quantitative polymerase chain reaction for mRNAs. We found increased expression of BNP and ET-1 in rat myocardium that was associated with the duration of VA. However, TGF-β1 protein expression remained unchanged. Such early increases in BNP and ET-1 may be attributed to fatal arrhythmias associated with SCD, suggesting these may be novel biomarkers of this disease. After intraperitoneal injection of PD142893 and SB431542, respectively, BNP was downregulated in the myocardium of the left ventricle; however, this was abrogated by co-application of the two inhibitors. These results suggested that both ET-1 and TGF-β1, by specifically binding to their receptors, might be involved in the myocardial synthesis of BNP during VA in vivo. Full article

(This article belongs to the Special Issue Molecular Basis of Cardiovascular Diseases: Implications of Natriuretic Peptides)

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15 pages, 3850 KiB

Open AccessArticle

PCSK9 is Expressed in Human Visceral Adipose Tissue and Regulated by Insulin and Cardiac Natriuretic Peptides

by Marica Bordicchia, Francesco Spannella, Gianna Ferretti, Tiziana Bacchetti, Arianna Vignini, Chiara Di Pentima, Laura Mazzanti and Riccardo Sarzani

Int. J. Mol. Sci. 2019, 20(2), 245; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20020245 - 09 Jan 2019

Cited by 32 | Viewed by 4606

Abstract

Proprotein convertase subtilisin/kexin type 9 (PCSK9) binds to and degrades the low-density lipoprotein receptor (LDLR), contributing to hypercholesterolemia. Adipose tissue plays a role in lipoprotein metabolism, but there are almost no data about PCSK9 and LDLR regulation in human adipocytes. We studied PCSK9 and LDLR regulation by insulin, atrial natriuretic peptide (ANP, a potent lipolytic agonist that antagonizes insulin), and LDL in visceral adipose tissue (VAT) and in human cultured adipocytes. PCSK9 was expressed in VAT and its expression was positively correlated with body mass index (BMI). Both intracellular mature and secreted PCSK9 were abundant in cultured human adipocytes. Insulin induced PCSK9, LDLR, and sterol-regulatory element-binding protein-1c (SREBP-1c) and -2 expression (SREBP-2). ANP reduced insulin-induced PCSK9, especially in the context of a medium simulating hyperglycemia. Human LDL induced both mature and secreted PCSK9 and reduced LDLR. ANP indirectly blocked the LDLR degradation, reducing the positive effect of LDL on PCSK9. In conclusion, PCSK9 is expressed in human adipocytes. When the expression of PCSK9 is induced, LDLR is reduced through the PCSK9-mediated degradation. On the contrary, when the induction of PCSK9 by insulin and LDL is partially blocked by ANP, the LDLR degradation is reduced. This suggests that NPs could be able to control LDLR levels, preventing PCSK9 overexpression. Full article

(This article belongs to the Special Issue Molecular Basis of Cardiovascular Diseases: Implications of Natriuretic Peptides)

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Review

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21 pages, 640 KiB

Open AccessReview

Genetic Ablation and Guanylyl Cyclase/Natriuretic Peptide Receptor-A: Impact on the Pathophysiology of Cardiovascular Dysfunction

by Kailash N. Pandey

Int. J. Mol. Sci. 2019, 20(16), 3946; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20163946 - 14 Aug 2019

Cited by 17 | Viewed by 4947

Abstract

Mice bearing targeted gene mutations that affect the functions of natriuretic peptides (NPs) and natriuretic peptide receptors (NPRs) have contributed important information on the pathogenesis of hypertension, kidney disease, and cardiovascular dysfunction. Studies of mice having both complete gene disruption and tissue-specific gene ablation have contributed to our understanding of hypertension and cardiovascular disorders. These phenomena are consistent with an oligogenic inheritance in which interactions among a few alleles may account for genetic susceptibility to hypertension, renal insufficiency, and congestive heart failure. In addition to gene knockouts conferring increased risks of hypertension, kidney disorders, and cardiovascular dysfunction, studies of gene duplications have identified mutations that protect against high blood pressure and cardiovascular events, thus generating the notion that certain alleles can confer resistance to hypertension and heart disease. This review focuses on the intriguing phenotypes of Npr1 gene disruption and gene duplication in mice, with emphasis on hypertension and cardiovascular events using mouse models carrying Npr1 gene knockout and/or gene duplication. It also describes how Npr1 gene targeting in mice has contributed to our knowledge of the roles of NPs and NPRs in dose-dependently regulating hypertension and cardiovascular events. Full article

(This article belongs to the Special Issue Molecular Basis of Cardiovascular Diseases: Implications of Natriuretic Peptides)

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18 pages, 917 KiB

Open AccessReview

Cardiovascular Pleiotropic Effects of Natriuretic Peptides

by Maurizio Forte, Michele Madonna, Sonia Schiavon, Valentina Valenti, Francesco Versaci, Giuseppe Biondi Zoccai, Giacomo Frati and Sebastiano Sciarretta

Int. J. Mol. Sci. 2019, 20(16), 3874; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20163874 - 08 Aug 2019

Cited by 59 | Viewed by 7599

Abstract

Atrial natriuretic peptide (ANP) is a cardiac hormone belonging to the family of natriuretic peptides (NPs). ANP exerts diuretic, natriuretic, and vasodilatory effects that contribute to maintain water–salt balance and regulate blood pressure. Besides these systemic properties, ANP displays important pleiotropic effects in the heart and in the vascular system that are independent of blood pressure regulation. These functions occur through autocrine and paracrine mechanisms. Previous works examining the cardiac phenotype of loss-of-function mouse models of ANP signaling showed that both mice with gene deletion of ANP or its receptor natriuretic peptide receptor A (NPR-A) developed cardiac hypertrophy and dysfunction in response to pressure overload and chronic ischemic remodeling. Conversely, ANP administration has been shown to improve cardiac function in response to remodeling and reduces ischemia-reperfusion (I/R) injury. ANP also acts as a pro-angiogenetic, anti-inflammatory, and anti-atherosclerotic factor in the vascular system. Pleiotropic effects regarding brain natriuretic peptide (BNP) and C-type natriuretic peptide (CNP) were also reported. In this review, we discuss the current evidence underlying the pleiotropic effects of NPs, underlying their importance in cardiovascular homeostasis. Full article

(This article belongs to the Special Issue Molecular Basis of Cardiovascular Diseases: Implications of Natriuretic Peptides)

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17 pages, 1336 KiB

Open AccessReview

BNP as a Major Player in the Heart-Kidney Connection

by Ryuji Okamoto, Yusuf Ali, Ryotaro Hashizume, Noboru Suzuki and Masaaki Ito

Int. J. Mol. Sci. 2019, 20(14), 3581; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20143581 - 22 Jul 2019

Cited by 52 | Viewed by 10375

Abstract

Brain natriuretic peptide (BNP) is an important biomarker for patients with heart failure, hypertension and cardiac hypertrophy. Although it is known that BNP levels are relatively higher in patients with chronic kidney disease and no heart disease, the mechanism remains unknown. Here, we review the functions and the roles of BNP in the heart-kidney interaction. In addition, we discuss the relevant molecular mechanisms that suggest BNP is protective against chronic kidney diseases and heart failure, especially in terms of the counterparts of the renin-angiotensin-aldosterone system (RAAS). The renal medulla has been reported to express depressor substances. The extract of the papillary tips from kidneys may induce the expression and secretion of BNP from cardiomyocytes. A better understanding of these processes will help accelerate pharmacological treatments for heart-kidney disease. Full article

(This article belongs to the Special Issue Molecular Basis of Cardiovascular Diseases: Implications of Natriuretic Peptides)

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11 pages, 511 KiB

Open AccessReview

Atrial Natriuretic Peptide: A Molecular Target of Novel Therapeutic Approaches to Cardio-Metabolic Disease

by Valentina Cannone, Aderville Cabassi, Riccardo Volpi and John C. Burnett, Jr.

Int. J. Mol. Sci. 2019, 20(13), 3265; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20133265 - 02 Jul 2019

Cited by 50 | Viewed by 12670

Abstract

Atrial natriuretic peptide (ANP) is a cardiac hormone with pleiotropic cardiovascular and metabolic properties including vasodilation, natriuresis and suppression of the renin-angiotensin-aldosterone system. Moreover, ANP induces lipolysis, lipid oxidation, adipocyte browning and ameliorates insulin sensitivity. Studies on ANP genetic variants revealed that subjects with higher ANP plasma levels have lower cardio-metabolic risk. In vivo and in humans, augmenting the ANP pathway has been shown to exert cardiovascular therapeutic actions while ameliorating the metabolic profile. MANP is a novel designer ANP-based peptide with greater and more sustained biological actions than ANP in animal models. Recent studies also demonstrated that MANP lowers blood pressure and inhibits aldosterone in hypertensive subjects whereas cardiometabolic properties of MANP are currently tested in an on-going clinical study in hypertension and metabolic syndrome. Evidence from in vitro, in vivo and in human studies support the concept that ANP and related pathway represent an optimal target for a comprehensive approach to cardiometabolic disease. Full article

(This article belongs to the Special Issue Molecular Basis of Cardiovascular Diseases: Implications of Natriuretic Peptides)

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8 pages, 595 KiB

Open AccessReview

Pulmonary Arterial Hypertension Due to NPR-C Mutation: A Novel Paradigm for Normal and Pathologic Remodeling?

by Emmanuel Eroume-A Egom

Int. J. Mol. Sci. 2019, 20(12), 3063; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20123063 - 22 Jun 2019

Cited by 12 | Viewed by 2986

Abstract

Idiopathic Pulmonary Arterial Hypertension (IPAH) is a deadly and disabling disease characterized by severe vascular remodeling of small pulmonary vessels by fibroblasts, myofibroblasts and vascular smooth muscle cell proliferation. Recent studies suggest that the Natriuretic Peptide Clearance Receptor (NPR-C) signaling pathways may play a crucial role in the development of IPAH. Reduced expression or function of NPR-C signaling in pulmonary artery smooth muscle cells may contribute to the pulmonary vascular remodeling, which is characteristic of this disease. The likely mechanisms may involve an impaired interaction between NPR-C, specific growth factors and other signal transduction pathways including but not limited to Gqα/mitogen-activated protein kinase (MAPK)/PI3K and AKT signaling. The resulting failure of growth suppression in pulmonary artery smooth muscle cells provides critical clues to the cellular pathobiology of IPAH. The reciprocal regulation of NPR-C signaling in models of tissue remodeling may thus provide new insights to our understanding of IPAH. Full article

(This article belongs to the Special Issue Molecular Basis of Cardiovascular Diseases: Implications of Natriuretic Peptides)

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17 pages, 1295 KiB

Open AccessReview

Clinical Applications of Natriuretic Peptides in Heart Failure and Atrial Fibrillation

by Masako Baba, Kentaro Yoshida and Masaki Ieda

Int. J. Mol. Sci. 2019, 20(11), 2824; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20112824 - 10 Jun 2019

Cited by 30 | Viewed by 4705

Abstract

Natriuretic peptides (NPs) have become important diagnostic and prognostic biomarkers in cardiovascular diseases, particularly in heart failure (HF). Diagnosis and management of coronary artery disease and atrial fibrillation (AF) can also be guided by NP levels. When interpreting NP levels, however, the caveat is that age, sex, body mass index, renal dysfunction, and race affect the clearance of NPs, resulting in different cut-off values in clinical practice. In AF, NP levels have been associated with incident AF in the general population, recurrences after catheter ablation, prediction of clinical prognosis, and the risk of stroke. In this article, we first review and summarize the current evidence and the roles of B-type NP and atrial NP in HF and coronary artery disease and then focus on the increasing utility of NPs in the diagnosis and management of and the research into AF. Full article

(This article belongs to the Special Issue Molecular Basis of Cardiovascular Diseases: Implications of Natriuretic Peptides)

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Graphical abstract

23 pages, 726 KiB

Open AccessReview

Natriuretic Peptides in Heart Failure with Preserved Left Ventricular Ejection Fraction: From Molecular Evidences to Clinical Implications

by Daniela Maria Tanase, Smaranda Radu, Sinziana Al Shurbaji, Genoveva Livia Baroi, Claudia Florida Costea, Mihaela Dana Turliuc, Anca Ouatu and Mariana Floria

Int. J. Mol. Sci. 2019, 20(11), 2629; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20112629 - 28 May 2019

Cited by 47 | Viewed by 6444

Abstract

The incidence of heart failure with preserved ejection fraction (HFpEF) is increasing and its challenging diagnosis and management combines clinical, imagistic and biological data. Natriuretic peptides (NPs) are hormones secreted in response to myocardial stretch that, by increasing cyclic guanosine monophosphate (cGMP), counteract myocardial fibrosis and hypertrophy, increase natriuresis and determine vasodilatation. While their role in HFpEF is controversial, most authors focused on b-type natriuretic peptides (BNPs) and agreed that patients may show lower levels. In this setting, newer molecules with an increased specificity, such as middle-region pro-atrial natriuretic peptide (MR-proANP), emerged as promising markers. Augmenting NP levels, either by NP analogs or breakdown inhibition, could offer a new therapeutic target in HFpEF (already approved in their reduced EF counterparts) by increasing the deficient cGMP levels found in patients. Importantly, these peptides also retain their prognostic value. This narrative review focuses on NPs’ physiology, diagnosis, therapeutic and prognostic implication in HFpEF. Full article

(This article belongs to the Special Issue Molecular Basis of Cardiovascular Diseases: Implications of Natriuretic Peptides)

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23 pages, 914 KiB

Open AccessReview

C-Type Natriuretic Peptide: A Multifaceted Paracrine Regulator in the Heart and Vasculature

by Amie J. Moyes and Adrian J. Hobbs

Int. J. Mol. Sci. 2019, 20(9), 2281; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20092281 - 08 May 2019

Cited by 85 | Viewed by 9810

Abstract

C-type natriuretic peptide (CNP) is an autocrine and paracrine mediator released by endothelial cells, cardiomyocytes and fibroblasts that regulates vital physiological functions in the cardiovascular system. These roles are conveyed via two cognate receptors, natriuretic peptide receptor B (NPR-B) and natriuretic peptide receptor C (NPR-C), which activate different signalling pathways that mediate complementary yet distinct cellular responses. Traditionally, CNP has been deemed the endothelial component of the natriuretic peptide system, while its sibling peptides, atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP), are considered the endocrine guardians of cardiac function and blood volume. However, accumulating evidence indicates that CNP not only modulates vascular tone and blood pressure, but also governs a wide range of cardiovascular effects including the control of inflammation, angiogenesis, smooth muscle and endothelial cell proliferation, atherosclerosis, cardiomyocyte contractility, hypertrophy, fibrosis, and cardiac electrophysiology. This review will focus on the novel physiological functions ascribed to CNP, the receptors/signalling mechanisms involved in mediating its cardioprotective effects, and the development of therapeutics targeting CNP signalling pathways in different disease pathologies. Full article

(This article belongs to the Special Issue Molecular Basis of Cardiovascular Diseases: Implications of Natriuretic Peptides)

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13 pages, 248 KiB

Open AccessReview

ARNi: A Novel Approach to Counteract Cardiovascular Diseases

by Massimo Volpe, Speranza Rubattu and Allegra Battistoni

Int. J. Mol. Sci. 2019, 20(9), 2092; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20092092 - 28 Apr 2019

Cited by 23 | Viewed by 10867

Abstract

Cardiovascular diseases (CVDs) still represent the greatest burden on healthcare systems worldwide. Despite the enormous efforts over the last twenty years to limit the spread of cardiovascular risk factors, their prevalence is growing and control is still suboptimal. Therefore, the availability of new therapeutic tools that may interfere with different pathophysiological pathways to slow the establishment of clinical CVDs is important. Previously, the inhibition of neurohormonal systems, namely the renin–angiotensin–aldosterone system (RAAS) and the sympathetic nervous system, has proven to be useful in the treatment of many CVDs. Attempts have recently been made to target an additional hormonal system, that of the natriuretic peptides (NPs), which, when dysregulated, can also play a role in the development CVDs. Indeed, a new class of drug, the angiotensin receptor–neprilysin inhibitors (ARNi), has the ability to counteract the effects of angiotensin II as well as to increase the activity of NPs. ARNi have already been proven to be effective in the treatment of heart failure with reduced ejection fraction. New evidence has suggested that, in the next years, the field of ARNi application will widen to include other CVDs, such as heart failure, with preserved ejection fraction and hypertension. Full article

(This article belongs to the Special Issue Molecular Basis of Cardiovascular Diseases: Implications of Natriuretic Peptides)

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16 pages, 792 KiB

Open AccessReview

BNP and NT-proBNP as Diagnostic Biomarkers for Cardiac Dysfunction in Both Clinical and Forensic Medicine

by Zhipeng Cao, Yuqing Jia and Baoli Zhu

Int. J. Mol. Sci. 2019, 20(8), 1820; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20081820 - 12 Apr 2019

Cited by 163 | Viewed by 14061

Abstract

Currently, brain natriuretic peptide (BNP) and N-terminal proBNP (NT-proBNP) are widely used as diagnostic biomarkers for heart failure (HF) and cardiac dysfunction in clinical medicine. They are also used as postmortem biomarkers reflecting cardiac function of the deceased before death in forensic medicine. Several previous studies have reviewed BNP and NT-proBNP in clinical medicine, however, few articles have reviewed their application in forensic medicine. The present article reviews the biological features, the research and application status, and the future research prospects of BNP and NT-proBNP in both clinical medicine and forensic medicine, thereby providing valuable assistance for clinicians and forensic pathologists. Full article

(This article belongs to the Special Issue Molecular Basis of Cardiovascular Diseases: Implications of Natriuretic Peptides)

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12 pages, 764 KiB

Open AccessReview

Molecular Implications of Natriuretic Peptides in the Protection from Hypertension and Target Organ Damage Development

by Speranza Rubattu, Maurizio Forte, Simona Marchitti and Massimo Volpe

Int. J. Mol. Sci. 2019, 20(4), 798; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20040798 - 13 Feb 2019

Cited by 42 | Viewed by 5383

Abstract

The pathogenesis of hypertension, as a multifactorial trait, is complex. High blood pressure levels, in turn, concur with the development of cardiovascular damage. Abnormalities of several neurohormonal mechanisms controlling blood pressure homeostasis and cardiovascular remodeling can contribute to these pathological conditions. The natriuretic peptide (NP) family (including ANP (atrial natriuretic peptide), BNP (brain natriuretic peptide), and CNP (C-type natriuretic peptide)), the NP receptors (NPRA, NPRB, and NPRC), and the related protease convertases (furin, corin, and PCSK6) constitute the NP system and represent relevant protective mechanisms toward the development of hypertension and associated conditions, such as atherosclerosis, stroke, myocardial infarction, heart failure, and renal injury. Initially, several experimental studies performed in different animal models demonstrated a key role of the NP system in the development of hypertension. Importantly, these studies provided relevant insights for a better comprehension of the pathogenesis of hypertension and related cardiovascular phenotypes in humans. Thus, investigation of the role of NPs in hypertension offers an excellent example in translational medicine. In this review article, we will summarize the most compelling evidence regarding the molecular mechanisms underlying the physiological and pathological impact of NPs on blood pressure regulation and on hypertension development. We will also discuss the protective effect of NPs toward the increased susceptibility to hypertensive target organ damage. Full article

(This article belongs to the Special Issue Molecular Basis of Cardiovascular Diseases: Implications of Natriuretic Peptides)

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