Captopril inhibits angiotensin I-induced coronary flow reduction in isolated rat heart but has no effect on contractility or energy metabolism.

Vasoconstriction, caused by activation of the renin-angiotensin system contributes to myocardial damage during ischaemia; the converting enzyme inhibitor, captopril, suppresses angiotensin formation. We investigated the effects of angiotensin I, angiotensin II, and captopril on coronary flow, function and energy metabolism before, during and after ischaemia in 59 Langendorff rat hearts. Angiotensin I (100 nM) and II (10 nM) caused reduction of coronary flow at constant perfusion pressure by 31% (P <0.005) and 27% (P < 0.05), respectively. During reperfusion these compounds decreased flow by 30% (P < 0.005) and 12% (P = 0.40), respectively. Captopril (0.4 mM) inhibited vasoconstriclion caused by angiotensin I, but not by angiotensin II. The drug itself increased flow by 42% (P <0.005). We did not detect significant effects of angiotensin I, angiotensin II, or captopril on cardiac function or high-energy phosphate content. Developed tension in captopril-treated hearts tended to recover faster from ischaemia than controls, with concomitant lower ATP catabolism. We conclude that the isolated rat heart contains an active angiotensin-converting enzyme. Captopril, used at a concen(ration of 0.4 mM, blocks its activity. The drug has no significant effects on myocardial function or energy metabolism but increases coronary flow during normoxic perfusion.