AUTOCRINE RELEASE OF ANGIOTENSIN-II MEDIATES STRETCH-INDUCED HYPERTROPHY OF CARDIAC MYOCYTES IN-VITRO

Hypertrophy is a fundamental adaptive process employed by postmitotic cardiac and skeletal muscle in response to mechanical load. How muscle cells convert mechanical stimuli into growth signals has been a long- standing question. Using an in vitro model of load (stretch)-induced c ardiac hypertrophy, we demonstrate that mechanical stretch causes rele ase of angiotensin II (Ang II) from cardiac myocytes and that Ang II a cts as an initial mediator of the stretch-induced hypertrophic respons e. The results not only provide direct evidence for the autocrine mech anism in load-induced growth of cardiac muscle cells, but also define the pathophysiological role of the local (cardiac) renin-angiotensin s ystem.