It is known that angiotensin converting enzyme (ACE) inhibitors not on
ly prevent the formation of angiotensin II, but also potentiate the ac
tivity of bradykinin. We investigated the effects of the ACE-inhibitor
ramipril in two models of cardiac ischemia. In anesthetized dogs with
a coronary occlusion of 6-h duration, both ramiprilat and bradykinin
significantly reduced infarct-size. This effect was prevented by the c
o-administration of the bradykinin antagonist HOE 140. In rats with a
coronary occlusion of 6-weeks duration, ramipril administration signif
icantly reduced infarct-size and prevented the development of left ven
tricular hypertrophy. Thus, ramipril showed a cardioprotective activit
y in models of acute as well as of chronic myocardial ischemia. These
effects are probably mediated by the potentiation of bradykinin.