BRADYKININ-INDUCED MESENTERIC VASODILATION IS MEDIATED BY B2-SUBTYPE RECEPTORS AND NITRIC-OXIDE

We investigated mechanisms mediating bradykinin (BK)-induced anterior mesenteric artery (AMA) vasodilation in anesthetized rats. The velocity of blood flowing (VBF) in the AMA was measured with pulsed Doppler velocimetry, and arterial pressure (BP) was measured with a pressure transducer. Drugs were infused through an intra-aortic catheter positioned proximal to the AMA origin. AMA conductance (C) was calculated from mean VBF/BP and expressed as percent of control C. BK infusion (10-1,000 ng . kg-1 . min-1) increased C significantly (C(max) = 201 +/- 18%, ED50 = 100 ng . kg-1 . min-1, P < 0.0 1 for all doses). A B2-subtype receptor antagonist, D-Arg, [Hyp3,Thi5,8,D-Phe7]BK, administered at 10(5) ng . kg . min-1 before or during BK infusion, inhibited the vasodilation by 73 +/- 7 and 103 +/- 7%, respectively. A nitric oxide (NO) synthesis inhibitor, N(G)-nitro-L-arginine, administered at 5.0 mg/kg 15 min before BK, inhibited the hyperemia by 61 +/-8%. Neither a B1-receptor antagonist nor intrajejunal capsaicin inhibited BK-induced vasodilation. BK-evoked, dose-dependent, mesenteric vasodilation in rats appears to be mediated partly by B2-receptors and endogenous NO generation.