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