Abstract

A preparation employing direct observation of the marginal ear vein of the rabbit in vivo was used to study the venoconstrictive action of bradykinin (BK). By means of this preparation several hypotheses concerning BK mechanism of action were examined. An indirect mechanism mediated by the venoconstrictor amines norepinephrine or histamine was ruled out by the use of the alpha adrenergic blocking drug phentolamine and an antihistamine, tripelennamine. That is, neither blocking drug reduced the BK-induced venoconstriction. 5-Hydroxytryptamine, tyramine and acetylcholine were studied for their possible venoconstrictive effects but were found to be inactive in this regard. Similarly, an indirect mechanism mediated by reflex reactions to BK-evoked pain or systemic hypotension was ruled out by studies in animals with denervated ears. That is, BK was equiactive in normal and denervated ears. It is therefore suggested that, until endogenous venoconstrictor substances not considered here are shown to be released by BK, it may be assumed that BK causes a direct action on venous smooth muscle.