Mechanisms underlying bradykinin-induced vasoconstriction were investigated in rat perfused mesenteric vascular beds with active tone. In preparations with intact endothelium, bolus injections of bradykinin (1 to 1,000 pmol) dose-dependently produced three-phase vascular effects, which consisted of a first-phase vasodilation followed by a second-phase vasoconstriction and a subsequent third-phase vasodilation; these effects were abolished by FR172357 (bradykinin B₂-receptor antagonist), but not by des-Arg⁹-[Leu⁸]-bradykinin (bradykinin B₁-receptor antagonist). In preparations with intact endothelium, indomethacin (cyclooxygenase inhibitor), seratrodast (thromboxane A₂ (TXA₂)-receptor antagonist), ONO-3708 (TXA₂/prostaglandin H₂ (PGH₂)-receptor antagonist) or ozagrel (TXA₂ synthesis inhibitor) markedly inhibited the bradykinin-induced vasoconstriction. In preparations without endothelium, the bradykinin-induced vasoconstriction was abolished by indomethacin and ONO-3708, while seratrodast and ozagrel had no effect. These results suggest that the endothelium-dependent vasoconstriction of bradykinin is mainly mediated by TXA₂ and that prostanoids other than TXA₂, probably PGH₂, in mesenteric vascular smooth muscle are responsible for bradykinin-induced endothelium-independent vasoconstriction.