This study describes the contractile action of bradykinin on rat isolated mesenteric arterial rings and a possible mechanism responsible for this action. Bradykinin induced dose-dependent contraction of relaxed mesenteric arterial rings from Holtzman rats, but not from Wistar rats. A second bradykinin challenge in the same ring induced a very small effect or no effect at all. Destruction of the endothelium did not modify the response to bradykinin. des-Arg9-[Leu8]bradykinin failed to antagonize bradykinin's action. HOE 140 (D-Arg- [Hyp3, Thi5,D-Tic7,Oic8]bradykinin) reduced bradykinin-induced contractions. Indomethacin abolished the contractile response to bradykinin; prostaglandin F2 alpha induced a long-lasting contraction, dissimilar from that induced by bradykinin; L-655,240 (3-[1-(4-chlorobenzyl)-5-fluoro-3-methyl-indol-2-yl]-2,2-dimethyl propanoic acid), an antagonist of the thromboxane receptor, inhibited bradykinin-induced contractions. These results suggest that bradykinin-induced contraction in mesenteric arterial rings is indirect, through activation of bradykinin B2 receptors, resulting in liberation of prostanoids from outside the endothelium. Thromboxane A2 is probably an intermediate in this response but we cannot exclude the participation of other prostanoids.