Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Todisco, A. et al.

Peripheral acid inhibitory action of corticotropin releasing factor: mediation by nongastric mechanisms.

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.[1]

References

Peripheral acid inhibitory action of corticotropin releasing factor: mediation by nongastric mechanisms. Todisco, A., Park, J., Lezoche, E., Debas, H., Tache, Y., Yamada, T. Gastroenterology (1987) [Pubmed]

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