β-arrestin and the angiotensin II type I receptor act as crucial molecular regulators of the Frank-Starling law of the heart, mediating enhanced contractility in response to biomechanical stretch.
This study identifies β-arrestin and the angiotensin II type I receptor as crucial molecular regulators of the Frank-Starling mechanism of cardiac contractility.
Significance The Frank–Starling law of the heart describes the heart’s ability to enhance contractility in response to increased cardiac filling. This property is fundamental to how humans maintain cardiovascular function in response to changes in circulating blood volume, and is regulated by enhanced calcium sensitivity of myofilaments with biomechanical stretch. The mechanism of how biomechanical stretch leads to changes in the myofilament calcium sensitivity remains poorly understood. Using genetic and pharmacologic approaches, we show that β-arrestin and the angiotensin II type I receptor act as crucial molecular regulators of the Frank–Starling law of the heart. This work identifies β-arrestins as important regulators of this fundamental principle of cardiac contractility.
Abraham et al. (Mon,) conducted a other in Cardiac contractility. Genetic and pharmacologic approaches targeting β-arrestin and angiotensin II type I receptor was evaluated on Frank-Starling mechanism of cardiac contractility. β-arrestin and the angiotensin II type I receptor act as crucial molecular regulators of the Frank-Starling law of the heart, mediating enhanced contractility in response to biomechanical stretch.
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