An autocrine/paracrine mechanism triggered by myocardial stretch induces changes in contractility

Abstract

An autocrine/paracrine mechanism is triggered by stretching the myocardium. This mechanism involves release of angiotensin II, release/increased formation of endothelin, activation of the Na(+)/H(+) exchanger, increase in intracellular Na(+), and the increase in the Ca(2+) transient that underlies the slow force response to stretch. The autocrine/paracrine mechanism could explain how changes in afterload alter cardiac contractility.