Next Article in Journal
Microwave-Assisted Synthesis of Potential Bioactive Benzo-, Pyrido- or Pyrazino-thieno[3,2-d]pyrimidin-4-amine Analogs of MPC-6827
Next Article in Special Issue
Kinins and Their Receptors in Infectious Diseases
Previous Article in Journal
The Application of Inosine 5′-Monophosphate Dehydrogenase Activity Determination in Peripheral Blood Mononuclear Cells for Monitoring Mycophenolate Mofetil Therapy in Children with Nephrotic Syndrome
Previous Article in Special Issue
A Systematic Review of Molecular Imaging Agents Targeting Bradykinin B1 and B2 Receptors
Review

In Vitro Modeling of Bradykinin-Mediated Angioedema States

1
Centre de Recherche du CHU de Québec-Université Laval, Québec, QC G1V 4G2, Canada
2
Service D’allergie, CHU de Québec-Université Laval, Québec, QC G1V 4G2, Canada
3
CHU Sainte-Justine, Université de Montréal, Montréal, QC H3T 1C5, Canada
*
Author to whom correspondence should be addressed.
Pharmaceuticals 2020, 13(9), 201; https://0-doi-org.brum.beds.ac.uk/10.3390/ph13090201
Received: 17 July 2020 / Revised: 14 August 2020 / Accepted: 17 August 2020 / Published: 19 August 2020
Kinins (peptides related to bradykinin, BK) are formed from circulating substrates, the kininogens, by the action of two proteases, the kallikreins. The only clinical application of a BK receptor ligand, the B2 receptor antagonist icatibant, is the treatment of the rare hereditary angioedema (HAE) caused by the deficiency of C1-esterase inhibitor (C1-INH). Less common forms of HAE (genetic variants of factor XII, plasminogen, kininogen) are presumably mediated by increased BK formation. Acquired forms of BK-mediated angioedema, such as that associated with angiotensin-I converting enzyme (ACE) inhibition, are also known. Antibody-based analytical techniques are briefly reviewed, and support that kinins are extremely short-lived, prominently cleared by ACE. Despite evidence of continuous activation of the kallikrein–kinin system in HAE, patients are not symptomatic most of the time and their blood or plasma obtained during remission does not generate excessive immunoreactive BK (iBK), suggesting effective homeostatic mechanisms. HAE-C1-INH and HAE-FXII plasmas are both hyperresponsive to fibrinolysis activation. On another hand, we suggested a role for the alternate tissue kallikrein–kinin system in patients with a plasminogen mutation. The role of the BK B1 receptor is still uncertain in angioedema states. iBK profiles under in vitro stimulation provide fresh insight into the physiopathology of angioedema. View Full-Text
Keywords: hereditary angioedema; bradykinin; acquired angioedema; kallikrein–kinin system; analytical techniques for kinins hereditary angioedema; bradykinin; acquired angioedema; kallikrein–kinin system; analytical techniques for kinins
Show Figures

Figure 1

MDPI and ACS Style

Marceau, F.; Bachelard, H.; Charest-Morin, X.; Hébert, J.; Rivard, G.E. In Vitro Modeling of Bradykinin-Mediated Angioedema States. Pharmaceuticals 2020, 13, 201. https://0-doi-org.brum.beds.ac.uk/10.3390/ph13090201

AMA Style

Marceau F, Bachelard H, Charest-Morin X, Hébert J, Rivard GE. In Vitro Modeling of Bradykinin-Mediated Angioedema States. Pharmaceuticals. 2020; 13(9):201. https://0-doi-org.brum.beds.ac.uk/10.3390/ph13090201

Chicago/Turabian Style

Marceau, François, Hélène Bachelard, Xavier Charest-Morin, Jacques Hébert, and Georges E. Rivard 2020. "In Vitro Modeling of Bradykinin-Mediated Angioedema States" Pharmaceuticals 13, no. 9: 201. https://0-doi-org.brum.beds.ac.uk/10.3390/ph13090201

Find Other Styles
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Back to TopTop