RELEASE OF ACETYLCHOLINE MEDIATED BY CHOLECYSTOKININ RECEPTOR FROM THE GUINEA-PIG SPHINCTER OF ODDI

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Abstract
Mechanism involved in the action of cholecystokinin octapeptide (CCK-8) on the isolated circular muscle of the quinea pig sphincter of Oddi were investigated. CCK-8 (10-9 to 10-6 M) caused a concentration-dependent contraction of the sphincter. Angiotensin II, bethanechol and serotonin also contracted this tissue. CCK-8 exerted the most potent effect. However, bradykinin, porcine motilin and norepinephrine failed to elicit any contraction. The CCK-8-induced contraction was inhibited by about 60% by atropine (3 .times. 10-7 M) or tetrodotoxin (3 .times. 10-7 M) but was not affected by hexamethonium (3 .times. 10-5 to 10-4 M) or phentolamine (3 .times. 10-6 to 10-5 M). Proglumide (3 .times. 10-4 to 3 .times. 10-3 M), a derivative of glutaramic acid, inhibited competitively the contraction by CCK-8. However, proglumide influenced neither the electrically elicited twitch contraction nor the bethanechol-induced contraction. CCK-8 evoked a concentration-related release of [3H]acetylcholine (ACh) from previously labeled stores. The CCK-8-evoked release of [3H]ACh was eliminated by tetrodotoxin and was inhibited, in a concentration-dependent manner, by proglumide. These results suggest that the contractile response to CCK-8 of the guinea pig sphincter of Oddi consists of a direct effect on the smooth muscle and an indirect effect mediated by ACh release from postganglionic parasympathetic neurons.

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