Myocardial stretch induces changes in contractility through an autocrine/paracrine mechanism involving angiotensin II and endothelin, explaining how afterload alters cardiac contractility.
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.
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Cingolani et al. (2001) studied this question.
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