Endothelium-derived bradykinin is responsible for the increase in calcium produced by angiotensin-converting enzyme inhibitors in human endothelial cells |
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Authors: | Rudi Busse Daniel Lamontagne |
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Affiliation: | (1) Institut für Angewandte Physiologie, Universität Freiburg, Hermann-Herder-Strasse 7, W-7800 Freiburg i. Br., Federal Republic of Germany |
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Abstract: | Summary The effects of angiotensin-converting enzyme (ACE) inhibitors on intracellular calcium concentration ([Ca2+]i) were examined under resting conditions and after stimulation with bradykinin in cultured human umbilical vein endothelial cells. The ACE inhibitors ramiprilat and enalaprilat (0.3 M) enhanced the increase in [Ca2+]i elicited by bradykinin (3 nM) and also caused an increase in resting [Ca2+]i when given alone. This increase in resting [Ca2+]i was long-lasting and accompanied by an increased formation of nitric oxide, as assessed by a NG-nitro-l-arginine-sensitive cyclic GMP accumulation in the cells. Both increases in resting [Ca2+]i and nitric oxide production by ACE inhibitors were inhibited by preincubation of the cells with the B2-receptor antagonist Hoe 140. These data indicate that ACE inhibitors are able to unmask a release of bradykinin from cultured human endothelial cells. This endothelium-derived bradykinin can exert an autocrine function by stimulating endothelial B2-receptors with a subsequent increase in [Ca2+]i and nitric oxide formation.Send offprint requests to R. Busse at the above address |
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Keywords: | Angiotensin-converting enzyme B2-kinin receptor antagonist Vascular endothelium Nitric oxide Cyclic GMP |
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