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.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine