Katsuhiko Ito, Yi-Zhun Zhu, Yi-Chun Zhu, Peter Gohlke and Thomas Unger
Department of Pharmacology, Christian-Albrechts University of Kiel, Hospitalstrasse 4, 24105 Kiel, and German Institute for High Blood Pressure Research, Heidelberg, Germany
Abstract: 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.
Keywords: Bradykinin, Angiotensin converting enzyme, Angiotensin II receptor antagonist, B2 receptor antagonist, Myocardial infarction, Cardioprotective action