Controlled and Cardiac-Restricted Overexpression of the Arginine Vasopressin V1A Receptor Causes Reversible Left Ventricular Dysfunction Through Gα q -Mediated Cell Signaling
Author(s) -
Xue Li,
Tung O. Chan,
Valerie D. Myers,
Ibrul Chowdhury,
Xue-Qian Zhang,
Jianliang Song,
Jin Zhang,
Jocelyn Andrel,
Hajime Funakoshi,
Jeffrey Robbins,
Walter J. Koch,
Terry Hyslop,
Joseph Y. Cheung,
Arthur M. Feldman
Publication year - 2011
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.111.021352
Subject(s) - endocrinology , medicine , vasopressin , arginine vasopressin receptor 2 , heart failure , receptor , transgene , cardiac function curve , biology , antagonist , biochemistry , gene
[Arg8]-vasopressin (AVP) activates 3 G-protein-coupled receptors: V1A, V2, and V1B. The AVP-V1A receptor is the primary AVP receptor in the heart; however, its role in cardiac homeostasis is controversial. To better understand AVP-mediated signaling in the heart, we created a transgenic mouse with controlled overexpression of the V1A receptor.
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