Why the study?
Does the potentiation of endogenous kinins contribute to the cardioprotective actions of ACE inhibition in hypertension and myocardial infarction?
Does the potentiation of endogenous kinins contribute to the cardioprotective actions of ACE inhibition in hypertension and myocardial infarction?
This review highlights that the cardioprotective benefits of ACE inhibitors in hypertension and post-myocardial infarction are mediated not only by reducing angiotensin II but also by potentiating endogenous bradykinin.
ACEI benefits may involve kinin potentiation beyond angiotensin II reduction; leaves open whether this mechanism warrants targeted trials in hypertension or post-MI.
Angiotensin converting enzyme (ACE) is identical with kininase II. Besides reducing the production of angiotensin II, inhibition of ACE potentiates the biological actions of endogenous kinins. In hypertension-induced left ventricular hypertrophy, potentiation of endogenous kinins contributes to the improvement of cardiac function and energy metabolism and to capillary proliferation effected by ACE inhibitors. In myocardial infarction (MI), the potentiation of kinins has been shown to be involved in the reduction of infarct size and improvement of cardiac function by ACE inhibition. The cardioprotective actions of ACE inhibition in MI seem to be, in part, mediated by the augmentation of myocardial blood flow, especially in the ischemic region of the heart.
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Ito et al. (1997) studied this question.
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