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Dual Vasopressin V1a/V2 Antagonism: The Next Step in Neurohormonal Modulation in Patients With Heart Failure?

Abstract
Stimulation of the V1a receptor for arginine vasopressin produces myocardial and vascular effects similar to those of angiotensin II while stimulation of the V2 receptor causes fluid retention. There are no data with sustained blockade of the V1a receptor while single-dose experiments suggest benefit. Acute and chronic administration of selective V2 receptor antagonists reliably relieves dyspnea and produces diuresis without adverse effects on renal function or neurohormonal stimulation, either as adjunctive or alternative therapy to loop diuretics, but has not been shown to improve outcomes as adjunctive therapy. Combined antagonism has been tried only in single-dose studies in stable patients or over the short-term in acute heart failure, with encouraging results. Based on the both the pathophysiologic rationale for additional neurohormonal blockade and these results, chronically blocking both receptors, particularly in more congested patients, may offer significant benefit either as adjunctive or alternative therapy to standard diuretics.
AuthorsSteven R Goldsmith, James E Udelson, Mihai Gheorghiade
JournalJournal of cardiac failure (J Card Fail) Vol. 24 Issue 2 Pg. 112-114 (02 2018) ISSN: 1532-8414 [Electronic] United States
PMID29329950 (Publication Type: Journal Article, Review)
CopyrightCopyright © 2018 Elsevier Inc. All rights reserved.
Chemical References
  • Antidiuretic Hormone Receptor Antagonists
  • Receptors, Vasopressin
Topics
  • Antidiuretic Hormone Receptor Antagonists (therapeutic use)
  • Heart Failure (drug therapy, metabolism, physiopathology)
  • Hormone Replacement Therapy (methods)
  • Humans
  • Receptors, Vasopressin (drug effects)

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