Effect of intragastric administration of beta-endorphin on thyrotropin-releasing hormone and somatostatin release into gastric lumen of rats

The neuropeptides beta-endorphin (BE), thyrotropin-releasing hormone (TRH), and somatostatin (SOM) in the gastric mucosa have the capacity to regulate gastric function. To clarify the possible role of BE in the interactions of neuropeptides and gastric acid secretion we investigated the effect of the intragastric administration of BE on TRH and SOM release into the gastric lumen. BE (100 ng/kg) induced an immediate decrease in TRH release and a reciprocal increase in SOM release into the gastric lumen, followed by the suppression of gastric acid secretion. When various doses of BE (0-500 ng/kg) were administered, changes in TRH and SOM occurred in a dose-dependent manner. Pretreatment with naloxone dihydrochloride (5 mg/kg, intraperitoneally) completely inhibited the BE-induced changes in the release of these peptides. These findings suggest that BE has a paracrine effect on TRH and SOM release into the gastric lumen through opioid receptors, and that these interactions may be involved in the regulation of gastric acid secretion.