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1. Administration of bradykinin caused dose-dependent vasoconstriction in rat isolated perfused mesenteric arteries precontracted with noradrenaline. 2. The vasoconstrictor response was not mediated by BK1-bradykinin receptors. 3. Inhibition of cyclo-oxygenase with indomethacin, aspirin or meclofenamate abolished the vasoconstrictor effect of bradykinin, showing that a member of the arachidonic acid cascade may be involved. 4. Inhibitors of thromboxane synthesis (imidazole and UK 38485) did not affect or only reduced the bradykinin-induced vasoconstriction. 5. The endoperoxide H2/thromboxane A2 receptor antagonist SQ 29548 significantly reduced the vasoconstrictor effect of bradykinin, but did not affect the vasoconstrictor response to noradrenaline, adrenaline, vasopressin, 5-hydroxytryptamine or prostaglandins. 6. The eicosanoid(s) that mediate bradykinin-induced vasoconstriction appear to be synthesized outside the arterial endothelium. 7. The data suggest that the vasoconstrictor effect of bradykinin in the rat isolated mesenteric artery is mediated by vasoconstrictor arachidonic acid metabolites including the cyclic endoperoxides and/or the thromboxanes.

The plasma globulins which produce the vasoactive polypeptides, bradykinin, kallidin and angiotensin, have been compared. After incubation of plasma with kallikrein and exhaustion of its kallidinogen, subsequent incubation with trypsin did not result in formation of bradykinin, showing that bradykininogen had also been exhausted and suggesting that kallikrein and trypsin use the same substrate. Kallidin and bradykinin formation was not prevented by acid-treatment of plasma, though heat-denatured substrate produced kallidin less readily. Kallikrein could exhaust plasma bradykininogen without affecting levels of angiotensinogen. Following nephrectomy of dogs, plasma angiotensinogen levels rose whereas bradykininogen levels did not. These results confirm the belief that bradykininogen differs from angiotensinogen but not from kallidinogen.