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Autocrine release of angiotensin II mediates stretch-induced hypertrophy of cardiac myocytes in vitro

1993; Cell Press; Volume: 75; Issue: 5 Linguagem: Inglês

10.1016/0092-8674(93)90541-w

1097-4172

Junichi Sadoshima, Yuhui Xu, Henry S. Slayter, Seigo Izumo,

Muscle Physiology and Disorders

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 cardiac hypertrophy, we demonstrate that mechanical stretch causes release of angiotensin II (Ang II) from cardiac myocytes and that Ang II acts as an initial mediator of the stretch-induced hypertrophic response. The results not only provide direct evidence for the autocrine mechanism in load-induced growth of cardiac muscle cells, but also define the pathophysiological role of the local (cardiac) renin-angiotensin system.