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Title: Peripheral acid inhibitory action of corticotropin releasing factor: mediation by nongastric mechanisms. Author: Todisco A, Park J, Lezoche E, Debas H, Tache Y, Yamada T. Journal: Gastroenterology; 1987 Apr; 92(4):919-24. PubMed ID: 3493937. Abstract: Corticotropin releasing factor (CRF) inhibits gastric acid secretion via both central neural and peripheral mechanisms. We examined whether local gastric factors may mediate the peripheral action of CRF. In pylorus-ligated anesthetized rats, CRF infusion (15 nmol/kg X h) produced roughly 60% inhibition of pentagastrin (16 micrograms/kg X h)-stimulated acid secretion. Similarly, in the gastric fistula dog, CRF (1 nmol/kg X h) inhibited pentagastrin-induced acid secretion by 74%. This action of CRF did not result from direct inhibition of gastric parietal cells, as concentrations of the peptide ranging from 10(-11) to 10(-6) M had no effect on the activity of isolated parietal cells in the unstimulated state or after stimulation with pentagastrin (10(-8) M), histamine (10(-5) M), or carbachol (10(-5) M), against a background of isobutylmethylxanthine (10(-4) M). To determine whether local hormones may mediate CRF-induced acid inhibition, we examined the peptide's effect on the release of somatostatin and gastrin from cultured canine gastric D and G cells and from isolated perfused rat stomachs. Corticotropin releasing factor in doses ranging from 10(-11) to 10(-6) M had no influence on release of either gastric peptide under basal conditions or after stimulation of gastrin with carbachol (10(-6) M) and somatostatin with isoproterenol (10(-8) M). These data suggest that the peripheral acid inhibitory action of CFR is mediated by nongastric mechanisms.[Abstract] [Full Text] [Related] [New Search]