Using microscopic fluorometry and fura-2-loaded cultured bovine aortic endothelial cells, we determined the effects of captopril, an angiotensin converting enzyme (ACE) inhibitor, on bradykinin-induced Ca2+ transients in endothelial cells. In the presence of extracellular Ca2+, 10-9 M bradykinin induced an early rise in the transients followed by sustained elevations of cytosolic calcium concentration ([Ca2+]i). Bradykinin concentration-dependently increased [Ca2+]i (EC50 6.7 × 10-9 M). Captopril, 10-5 M, enhanced and prolonged the bradykinin-induced Ca2+ transients and shifted the concentration-response curve to the left (EC50 8.5 × 10-10 M). In porcine coronary aterial strips with intact endothelium, cumulative applications of bradykinin induced an endothelium-dependent relaxation during prostaglandin F2α-induced contraction (EC50 = 2.0 × 10-9 M). Treatment with 10-5 M captopril enhanced the bradykinin-induced relaxation and shifted the concentration-response curve to the left (EC50 = 7.6 × 10-10 M). Thus, captopril enhances the bradykinin-induced relaxation by mechanisms mainly dependent on the endothelium, namely the inhibition of ACE.
|Number of pages||5|
|Journal||European Journal of Pharmacology: Molecular Pharmacology|
|Publication status||Published - Jan 15 1993|
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