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β-adrenergic receptor-mediated cardiac contractility is inhibited via vasopressin type 1A-receptor-dependent

Douglas G Tilley1, Weizhong Zhu2, Valerie D Myers2

  • 1From the Center for Translational Medicine (D.G.T., E.G., J.S, R.L.C., L.A.G., W.J.K., J.Y.C.), Department of Pharmacology (D.G.T., W.J.K.), Cardiovascular Research Center (W.Z., V.D.M., L.A.B., C.A.M., C.D.T., R.C.C., S.R.H.), Department of Physiology (L.A.B., C.A.M., S.R.H., A.M.F.), Department of Clinical Sciences (D.Y.), and Department of Medicine (J.Y.C., A.M.F.), Temple University School of Medicine, Philadelphia, PA; and the Division of Cardiology, Fourth Military Medical University, Xian, People's Republic of China (X.L.). douglas.tilley@temple.edu arthur.feldman@tuhs.temple.edu.

Circulation
|September 11, 2014
PubMed
Abstract

Keywords:
cardiomyopathiesmyocardial failuremyocardiumreceptors, adrenergic, betavasopressin type 1A receptor

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