Involvement of cholinergic processes in cholecystokinin (CCK) release by luminal oleic acid

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Cholecystokinin (CCK) is an important bioactive peptide that stimulates pancreatic enzyme secretion. Circulating CCK is secreted from endocrine cells in the upper small intestine in response to various luminal stimuli and to vascular administration of gastrin releasing peptides. However, the mechanism of its release has not been fully elucidated. In the present study, the vascularly perfused duodenojejunum was isolated from male Wistar rats. The effects of luminal infusion of sodium oleate (2 or 0.4%) or intra-arterial infusion of neuromedin C(10(-7) M) with or without atropine and with a recently synthesized specific bombesin antagonist (EABI) were examined. The CCK release produced by intra-arterial infusion of neuromedin C was inhibited by EABI in a dose-dependent manner. The CCK release produced by luminal sodium oleate was inhibited by atropine, but not affected by EABI. The CCK release stimulated by luminal sodium oleate is mediated, at least in part, by a cholinergic mechanism, but neuromedin C directly stimulates CCK release via its receptor on CCK-producing cells.

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