Regulation of myocardial contractility: Insights from transgenic mice

O Ben-Yehuda; H A Rockman

doi:10.1016/1050-1738(96)00010-2

Regulation of myocardial contractility: Insights from transgenic mice

Trends Cardiovasc Med. 1996 Apr;6(3):95-9. doi: 10.1016/1050-1738(96)00010-2.

Authors

O Ben-Yehuda¹, H A Rockman

Affiliation

¹ Ori Ben-Yehuda and Howard A. Rockman are at the Division of Cardiology, Department of Medicine, University of California at San Diego, School of Medicine, La Jolla, CA 92093-01613, USA.

PMID: 21232281
DOI: 10.1016/1050-1738(96)00010-2

Abstract

Myocardial contraction occurs when calcium (Ca(2+)) is released from the sarcoplasmic reticulum, binding troponin C and allowing actin and myosin to cross link. Ca(2+) release and uptake is closely regulated by G protein-coupled β-adrenergic receptors through the action of the second messenger cAMP. An increase in cAMP level leads to phosphorylation of key regulatory proteins affecting intracellular Ca(2+) homeostasis. The β-adrenergic receptors themselves are regulated by a set of specific kinases, termed the G-protein-coupled receptor kinases (GRKs). The study of this complex system in vivo has recently been advanced by the development of transgenic and gene-targeted (knockout) mouse models. Combining transgenic technology with sophisticated physiological measurements of cardiac hemodynamics is an extremely powerful approach to the study of myocardial contractility and its regulation. This review focuses on several recent transgenic mouse models that have increased our understanding of the regulation of cardiac contractility.