Adaptive and maladaptive remodeling of cardiomyocyte excitation-contraction coupling by angiotensin II.
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.
Department of Physiology, University of Bern, CH-3012 Bern, Switzerland. egger@pyl.unibe.ch
Marcel
M
Egger
Andrea A
AA
Domenighetti
D000222:Adaptation, Physiological; D000804:Angiotensin II / Q000378:metabolism*; D000818:Animals; D006332:Cardiomegaly / Q000378:metabolism* / Q000503:physiopathology; D056966:Excitation Contraction Coupling; D006333:Heart Failure / Q000378:metabolism* / Q000503:physiopathology; D006801:Humans; D051379:Mice; D018345:Mice, Knockout; D032383:Myocytes, Cardiac / Q000378:metabolism*; D012084:Renin-Angiotensin System / Q000235:genetics; D020257:Ventricular Remodeling
D000804:Angiotensin II