Abstract
To determine the mechanism of endothelium-dependent relaxation by bradykinin, we simultaneously measured changes in cytosolic calcium concentrations ([Ca 2+] i) and force of fura-2-loaded strips of porcine coronary artery. We also examined effects of captopril, an angiotensin converting enzyme inhibitor, on bradykinin-induced relaxation. Bradykinin, in a concentration-dependent manner (10 −10 to 10 −7 M), decreased both [Ca 2+] i and force to resting levels, during 10 −5 M prostaglandin F 2α-induced contractions, only when endothelium was intact. Treatment with 10 −5 M captopril enhanced the bradykinin-induced decreases in [Ca 2+] i and force and shifted the concentration-response bradykinin induced a greater relaxation than that expected from the reduction in [Ca 2+] i. Captopril had no effects on the relationship between reduction in [Ca 2+] i and relaxation induced by bradykinin. Bradykinin relaxes porcine coronary artery in an endothelium-dependent manner, by decreasing [Ca 2+] i and also by controlling the Ca 2+ sensitivity of the contractile apparatus of smooth muscle. Captopril enhanced the bradykinin-induced relaxation, with no apparent direct effect on Ca 2+ sensitivity of the contractile apparatus.
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