Mechanism of action of CCK in avian gastroduodenal motility: evidence for nitric oxide involvement.

Our objective was to study the mechanism of action of cholecystokinin (CCK) on the motility of the gastroduodenal area. Chickens were implanted with five electrodes for electromyography in the stomach and duodenum. The effects of CCK (10(-9) mol.kg-1.10 min-1) were studied against the presence of several antagonists and in vagotomized animals. CCK caused inhibition of gastric motility and duodenal hyperactivity. Vagotomy blocked CCK responses in the stomach but not in the duodenum. Hexamethonium partially blocked gastric inhibition induced by CCK. NG-nitro-L-arginine methyl ester blocked the inhibitory response to CCK in the stomach but did not modify duodenum response. L-Arginine did not modify CCK actions. Opioid antagonists naloxone and naltrindole and adrenergic antagonists phentolamine and propranolol did not modify CCK response. Atropine did not modify duodenal response to CCK. Sodium nitroprusside (10(-8)-10(-6) mol/kg) inhibited gastroduodenal activity in a dose-related manner. We suggest that gastric response to CCK is vagally mediated, mainly by the nitric oxide system. Duodenal hyperactivity seems to be a direct action of CCK. Nitric oxide is a putative neurotransmitter in the chicken gut.