Gastric acid inhibition by antral acidification mediated by endogenous prostaglandins.
The effects of indomethacin on the basal and stimulated gastric acid secretion at controlled intragastric pH were examined. Four tests with modified sham feeding were made in nine healthy volunteers on different occasions, twice with acid and twice with alkaline perfusion of the stomach. Blocking of the prostaglandin biosynthesis with indomethacin preceded one of the tests at each pH. Plasma levels of gastrin were measured. Antral acidification suppressed the basal and vagally stimulated gastric secretion rate of H+ and Cl-. The inhibition was associated with a decreased plasma gastrin response. Indomethacin reduced the inhibition of the peak acid output and plasma gastrin levels induced by antral acidification. During alkalinization of the stomach indomethacin had no effect on the acid secretion rate or plasma gastrin levels. The results suggest that the pH-dependent inhibitory regulation of the gastric acid secretion is mediated by locally produced prostaglandins. The mechanism functions at least partially through modifying the release of gastrin.
D000328:Adult; D016861:Cyclooxygenase Inhibitors; D005502:Food; D005744:Gastric Acid / Q000378:metabolism*; D005755:Gastrins / Q000097:blood; D006801:Humans; D006863:Hydrogen-Ion Concentration; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D011453:Prostaglandins / Q000502:physiology*
D016861:Cyclooxygenase Inhibitors; D005755:Gastrins; D011453:Prostaglandins; D007213:Indomethacin