Heterogeneity in mechanisms of bradykinin action in canine isolated blood vessels.

The relaxation induced by bradykinin in helical strips of coronary arteries contracted with prostaglandin (PG) F2 alpha was abolished by removal of the endothelium and was markedly suppressed by treatment with methylene blue or AA861, a lipoxygenase inhibitor. Indomethacin did not alter the response. Renal arterial relaxation by bradykinin was partially reduced by removal of the endothelium. Indomethacin moderately attenuated the response in the strips with endothelium and additional treatment with methylene blue or AA861 suppressed the response further. Tranylcypromine or diphloretin phosphate, an antagonist of PGI2, attenuated the peptide-induced relaxation. In mesenteric veins, the relaxation induced by bradykinin was slightly reduced by removal of the endothelium; indomethacin reversed the relaxation to a contraction in the strips with or without endothelium. Des-Arg9-[Leu8]bradykinin, a bradykinin B1 antagonist, did not alter the relaxation due to bradykinin in coronary arteries but reduced the response of mesenteric veins. It appears that bradykinin-induced relaxation is associated exclusively with EDRF in dog coronary arteries, with both PGI2 and EDRF in the renal arteries, and only with PGI2 liberated from endothelial and subendothelial tissues in the mesenteric veins. The release of PGI2 and EDRF may be mediated by activation of B1 and B2 receptor subtypes, respectively.