β-Adrenergic Receptor–Mediated Cardiac Contractility Is Inhibited via Vasopressin Type 1A-Receptor–Dependent Signaling
Author(s) -
Douglas G. Tilley,
Weizhong Zhu,
Valerie D. Myers,
Larry A. Barr,
Erhe Gao,
Xue Li,
Jianliang Song,
Rhonda L. Carter,
Catherine A. Makarewich,
Daohai Yu,
Constantine D. Troupes,
Laurel A. Grisanti,
Ryan C. Coleman,
Walter J. Koch,
Steven R. Houser,
Joseph Y. Cheung,
Arthur M. Feldman
Publication year - 2014
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.114.010434
Subject(s) - medicine , heart failure , endocrinology , vasopressin , contractility , receptor , cardiac function curve , cardiomyopathy , receptor antagonist , g protein coupled receptor kinase , vasopressin receptor , antagonist , g protein
Enhanced arginine vasopressin levels are associated with increased mortality during end-stage human heart failure, and cardiac arginine vasopressin type 1A receptor (V1AR) expression becomes increased. Additionally, mice with cardiac-restricted V1AR overexpression develop cardiomyopathy and decreased β-adrenergic receptor (βAR) responsiveness. This led us to hypothesize that V1AR signaling regulates βAR responsiveness and in doing so contributes to development of heart failure.
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