Enhancement by captopril of bradykinin-induced calcium transients in cultured endothelial cells of the bovine aorta.

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 x 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 x 10(-10) M). In porcine coronary aterial strips with intact endothelium, cumulative applications of bradykinin induced an endothelium-dependent relaxation during prostaglandin F2 alpha-induced contraction (EC50 = 2.0 x 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 x 10(-10) M). Thus, captopril enhances the bradykinin-induced relaxation by mechanisms mainly dependent on the endothelium, namely the inhibition of ACE.