DUODENAL ACID-INDUCED INHIBITION OF GASTRIC-MOTILITY AND EMPTYING IN RATS

The mechanism by which acid in the duodenum inhibits proximal gastric motor function and delays emptying was investigated in urethan-anesthe tized and awake rats. Gastric motility inhibited by duodenal acid (0.2 N HCI) in urethan-anesthetized rats was attenuated by 68 and 54%, res pectively, by functional ablation of the vagal or spinal sensory inner vation with capsaicin. 5-Hydroxytryptamine3 receptor blockade with zac opride (0.2 mg/kg ip) or cholecystokinin (CCK)-A-type receptor blockad e with MK-329 (1 mg/kg ip) had no effect on the motility response to a cid. In awake rats with chronically implanted gastric and duodenal can nulas, perfusion of the duodenum with acid (0.1 and 0.2 N HCI) inhibit ed gastric emptying of a nonnutrient liquid (38 and 59%, respectively) . Blockade of CCK-A-type receptors reduced by 30% inhibition of gastri c emptying induced by 0.1 N HCI. However, functional ablation of the v agal or spinal sensory innervation, 5-hydroxytryptamine3 receptor bloc kade, or immunoneutralization of secretin by systemic administration o f a polyclonal antibody (no. 7842, 1 ml ip) had no effect on acid-indu ced (0.1 N HCl) inhibition of gastric emptying. Perfusion of the duode num with 0.2 N HCI but not 0.1 N HCI inhibited proximal gastric motili ty in awake rats. These results suggest that 1) a duodenal acid load i nhibits gastric emptying in part by a mechanism involving CCK and 2) d ecreased proximal gastric motility plays a minor role in inhibition of gastric emptying in response to acid.