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Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor 48109, USA.

1. We have recently demonstrated that cholecystokinin (CCK) at physiological levels stimulates pancreatic enzyme secretion via gastroduodenal mucosal vagal afferent fibres in the rat. The present study was designed to investigate if non-CCK-mediated pancreatic stimuli which activate duodenal receptors also utilize similar vagal afferent pathways. 2. Intraduodenal administration of maltose (300 mM), hypertonic saline (500 mosmol l-1) and mucosal light stroking in anaesthetized rats evoked 70, 57 and 200% increases, respectively, in pancreatic protein secretion with no changes in plasma CCK concentration. Administration of the CCK receptor antagonist L364,718 did not affect pancreatic secretion evoked by these luminal stimuli. 3. Administration of atropine, acute vagotomy and duodenal mucosal application of capsaicin each completely abolished the pancreatic response to these stimuli. 4. Infusion of a subthreshold dose of the octapeptide of CCK (15 pmol (kg body wt)-1 h-1) potentiated the pancreatic response to duodenal infusion of maltose (300 mM) and hypertonic saline (500 mosmol l-1). 5. In conscious rats, perivagal application of capsaicin abolished the pancreatic response evoked by physiological doses of CCK and intraduodenal administration of maltose or hypertonic saline, confirming the physiological relevance of the observations in anaesthetized rats. 6. These results suggest that like CCK, non-CCK-mediated luminal stimuli evoke pancreatic enzyme secretion via stimulation of a vagal afferent pathway originating from the duodenal mucosa.

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