Key result
This review discusses the molecular mechanisms by which acute and chronic angiotensin II exposure modulates cardiomyocyte excitation-contraction coupling in cardiac hypertrophy and heart failure.
This review highlights the molecular mechanisms by which acute and chronic Angiotensin II exposure drives adaptive and maladaptive remodeling of cardiomyocyte excitation-contraction coupling in cardiac hypertrophy and heart failure.
Offers no immediate clinical guidance; leaves open targeted interventions against Ang II-mediated ECC remodeling in hypertrophy and HF.
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.
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Egger et al. (2010) conducted a review in Cardiac hypertrophy and congestive heart failure. Angiotensin II was evaluated. This review discusses the molecular mechanisms by which acute and chronic angiotensin II exposure modulates cardiomyocyte excitation-contraction coupling in cardiac hypertrophy and heart failure.
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