Cytosolic Ca2+ transients in endothelium-dependent relaxation of pig coronary artery, and effects of captopril.

To determine the mechanism of endothelium-dependent relaxation by bradykinin, we simultaneously measured changes in cytosolic calcium concentrations ([Ca2+]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 [Ca2+]i and force to resting levels, during 10(-5) M prostaglandin F2 alpha-induced contractions, only when endothelium was intact. Treatment with 10(-5) M captopril enhanced the bradykinin-induced decreases in [Ca2+]i and force and shifted the concentration-response curve to the left. During 118 mM K+ depolarization, bradykinin induced a greater relaxation than that expected from the reduction in [Ca2+]i. Captopril had no effects on the relationship between reduction in [Ca2+]i and relaxation induced by bradykinin. Bradykinin relaxes porcine coronary artery in an endothelium-dependent manner, by decreasing [Ca2+]i and also by controlling the Ca2+ sensitivity of the contractile apparatus of smooth muscle. Captopril enhanced the bradykinin-induced relaxation, with no apparent direct effect on Ca2+ sensitivity of the contractile apparatus.