Adaptive and maladaptive remodeling of cardiomyocyte excitation-contraction coupling by angiotensin II

Trends Cardiovasc Med. 2010 Apr;20(3):78-85. doi: 10.1016/j.tcm.2010.06.001.

Abstract

Chronic elevation of plasma angiotensin II (Ang II) is a major determinant in the pathogenesis of cardiac hypertrophy and congestive heart failure. However, the molecular mechanisms by which the direct actions of Ang II on cardiomyocytes contribute to excitation-contraction coupling (ECC) remodeling are not precisely known. We review this question, as well as acute Ang II-mediated modulation of ECC. In addition, we discuss adaptive/maladaptive modulation of cardiomyocyte ECC under chronic endogenous Ang II overproduction in the heart induced by local overexpression of the of the renin-angiotensin system in the mouse.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adaptation, Physiological
  • Angiotensin II / metabolism*
  • Animals
  • Cardiomegaly / metabolism*
  • Cardiomegaly / physiopathology
  • Excitation Contraction Coupling*
  • Heart Failure / metabolism*
  • Heart Failure / physiopathology
  • Humans
  • Mice
  • Mice, Knockout
  • Myocytes, Cardiac / metabolism*
  • Renin-Angiotensin System* / genetics
  • Ventricular Remodeling*

Substances

  • Angiotensin II