Comparison of responses to T-kinin and bradykinin in the mesenteric vascular bed of the cat

Responses to T-kinin and bradykinin were compared in the mesenteric vascular bed of the cat. Under constant-flow conditions, injection of T- kinin and bradykinin into the perfusion circuit induced similar dose-related decreases in perfusion pressure. Responses to T-kinin and bradykinin were inhibited by the kinin B₂ receptor antagonist Hoe-140, but were not altered by the B₁ receptor antagonist des-Arg⁹-[Leu⁸]-BK, the histamine H₁ antagonist pyrilamine, the histamine H₂ receptor antagonist cimetidine, or the H₃ receptor antagonist thioperamide. Vasodilator responses to T-kinin and bradykinin were attenuated by the nitric oxide synthase inhibitor, N(ω) Nitro-L-arginine methyl ester (L-NAME), but were not altered by the cyclooxygenase inhibitor, sodium meclofenamate, or the K⁺(ATP) channel antagonist, U37883A. These data suggest that vasodilator responses to T- kinin and bradykinin are mediated by kinin B₂ receptor stimulated release of nitric oxide from the endothelium, but that the activation of kinin B₁ receptors, the release of vasodilator prostaglandins, or the opening of K⁺(ATP) channels are not involved in the response to T-kinin in the mesenteric vascular bed of the cat.