Atropine and naloxone block the colonic contraction elicited by cholecystokinin and pentagastrin.

Abstract

The effects of cholecystokinin (CCK) and gastrin on proximal and distal colonic motility were investigated because of the possible role of these peptides in feeding-induced colonic motility. Experiments were performed using 22 chloralose-urethane anaesthetized cats in which the colon was acutely denervated. The volume changes of the proximal and distal colon were recorded with water-filled flaccid balloons. The venous effluxes from the proximal and distal colon were recorded separately using drop recorder units. CCK-8, I-200 pmol X min-I close i.a., and pentagastrin, I-200 pmol X min-I close i.a., evoked dose-dependent contractions of the colon without altering systemic arterial blood pressure and colonic blood flow. The CCK peptides -8, -33 and -39 produced contractions of similar magnitude in the proximal and distal colon. The stimulatory effect of CCK-8 and pentagastrin on colonic motility was blocked by tetrodotoxin (I microgram X kg-I i.a.) and hexamethonium (I0 mg X kg-I i.v.). Atropine (0.5 mg X kg-I i.v.) completely blocked the responses to CCK-8 and pentagastrin in the distal colon but only partially in the proximal colon. Additional administration of naloxone (I mg X kg-I i.a.) abolished the remaining contractile response to the peptides in the proximal colon. The present results support the idea that CCK and pentagastrin have a stimulatory effect on distal colonic motility mediated via preganglionic and postganglionic cholinergic pathways. The possible role of opioid peptides and cholinergic mechanisms in the proximal colon is discussed.