Role of angiotensin II in mechanical stress-induced cardiac hypertrophy

Many lines of evidence have suggested that the renin-angiotensin system plays an important role in the development of cardiac hypertrophy. Pressure overload-induced cardiac hypertrophy is prevented by angiotensin-converting enzyme inhibitors in vivo, and mechanical stretch induces secretion and production of angiotensin II (Ang II) from cardiac myocytes in vitro. Ang II induces cardiomyocyte hypertrophy through the Ang II type 1 (AT1) receptor. All these results suggest that the AT1 receptor-mediated signaling is critical for the development of mechanical stress-induced cardiac hypertrophy. However, we have recently obtained results from AT1 knockout mice suggesting that mechanical stress can induce cardiac hypertrophy without AT1 receptor-mediated Ang II signaling.