1. Pelvic nerve stimulation in atropinized cats elicits a sustained contraction of the proximal colon and a relaxation of the rectum. Concomitantly there is an immediate but transient vasodilatation which is followed by recurrent increases and a slight post-stimulatory hyperaemia. Direct stimulation of the pelvic nerve produces secretion of colonic kallikrein and activation of the plasma kinin system. The present study examines whether Trasylol, which inhibits the kinin system, affects the atropine-resistant responses observed on pelvic nerve stimulation. 2. After I.V. or close I.A. administration of Trasylol, the initial vasodilatation on pelvic nerve stimulation was markedly reduced and in a few experiments completely blocked. The recurrent blood flow increases and the post-stimulatory hyperaemia observed on prolonged stimulation were completely abolished. In contrast the proximal colonic contraction and the rectal relaxation appeared unchanged after Trasylol. 3. The reactivity of the vascular bed after Trasylol injection was studied by recording the changes of vascular resistance following sympathetic vasoconstrictor fibre activation and infusion of bradykinin before and after Trasylol injection. The responses were quantitatively unchanged excluding an unspecific interference with nervous transmission or vascular smooth muscle reactivity. 4. The results show that the atropine-resistant vasodilatation in the cat colon as elicited by pelvic nerve stimulation is partly abolished by a kallikrein inhibitor. This observation lends further support to the hypothesis that kinins might be involved in this response. The motor response, however, appears not be dependent on such a mechanism.
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