Background and aims: 

The bicarbonate secretion by the duodenal mucosa protects this epithelium against acid discharged from the stomach. Cholecystokinin (CCK) released postprandially from the duodenum is an interesting potential stimulus of the protective secretion. The aim of this study was to characterize effects of CCK-8, ghrelin and some related peptides on duodenal bicarbonate secretion in vivo and evaluated CCK-induced calcium signaling in acutely isolated duodenal enterocytes

Methods: 

A segment of duodenum was cannulated in situ in anaesthetized rats and mucosal bicarbonate secretion recorded (pH-stat). Peptides were administrated to the duodenal segment by close intra-arterial infusion. Clusters of duodenal enterocytes were isolated and attached to the bottom of a perfusion chamber. The intracellular calcium concentration ([Ca²⁺]i) was examined by dual-wavelength imaging.

Results: 

CCK-8 caused dose-dependent increases in duodenal alkaline secretion. Findings in overnight fasted and continuously fed animals were similar, and the CCK1R-antagonist devazepide and atropine but not the CCK2-antagonist YMM022 reduced the rise in secretion. Ghrelin and galanin were without effect on the duodenal secretion in fasted as well as in fed animals.

Conclusion: 

Low doses of CCK-8 stimulate duodenal bicarbonate secretion and induce enterocyte [Ca²⁺]i signaling by an action at CCK-1 receptors. The increase in alkaline secretion most likely provides postprandial protection of the duodenal mucosa.