Aniotensin-Converting Enzyme (ACE) Activity: Aortic ancf Endocardial Endothelium Compared

Publisher Website
Google Scholar
Abstract
Vascular endothelial cells release bradykinin (BK), which acts in an autocrine manner to raise intracellular calcium concentrations ([Ca2+]i) and release NO, effects which can be modified by angiotensin-converting enzyme (ACE) inhibitors. Little is known of the effects of BK and ACE inhibitors on endocardial endothelium however. In this study, we investigated the effects of the ACE inhibitors captopril and ramiprilat on (a) BK-degrading activity, (b) resting Ca2+ homeostasis and (c) BK-induced changes in [Ca2+]i and cGMP in bovine aortic endothelial (BAE) and right ventricle endocardial (BRVE) cells. Captopril and ramiprilat inhibited the BK-degrading activity of both cell types. Resting levels of [Ca2+]i and cGMP were significantly higher in BRVE than in BAE. Captopril or ramiprilat did not alter resting [Ca*+]i, but caused significant increases in resting cGMP which were reduced by the NO synthase inhibitor L-nitroarginine benzyl ester and the B2-kinin receptor antagonist HOE 140. Captopril and ramiprilat enhanced the peak Ca2+ reponses to exogenous BK in both cell types, while having no effect on BK-induced increases in cGMP. These data demonstrate that endocardial endothelial cells, like vascular endothelial cells, possess ACE activity which may modulate the activity of endogenous kinins.

This publication has 25 references indexed in Scilit: