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 implan ted.with five electrodes for electromyography in the stomach and duode num. The effects of CCK (10(-9) mol.kg-1.10 min-1) were studied agains t the presence of several antagonists and in vagotomized animals. CCK caused inhibition of gastric motility and duodenal hyperactivity. Vago tomy blocked CCK responses in the stomach but not in the duodenum. Hex amethonium partially blocked gastric inhibition induced by CCK. NG-nit ro-L-arginine methyl ester blocked the inhibitory response to CCK in t he stomach but did not modify duodenum response. L-Arginine did not mo dify CCK actions. Opioid antagonists naloxone and naltrindole and adre nergic antagonists phentolamine and propranolol did not modify CCK res ponse. Atropine did not modify duodenal response to CCK. Sodium nitrop russide (10(-8)-10(-6) mol/kg) inhibited gastroduodenal activity in a dose-related manner. We suggest that gastric response to CCK is vagall y mediated, mainly by the nitric oxide system. Duodenal hyperactivity seems to be a direct action of CCK. Nitric oxide is a putative neurotr ansmitter in the chicken gut.