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Gastric bicarbonate secretion: an update.

G L Kauffman
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Abstract

In vitro and in vivo studies have demonstrated that gastric fundic and antral mucosa secretes a bicarbonate (HCO3-)-rich fluid under a variety of experimental conditions. Bicarbonate secretion appears to be an active, energy requiring process which is thought to occur at the surface epithelial cell. Transmembrane HCO3- transport, isotopic (H14CO3) flux, pH stat titration and pCO2 measurement has been used to indicate HCO3- secretion. Bicarbonate secretion is stimulated by cholinergic agents, dibutyryl-cGMP, calcium, and 16-16-dimethyl prostaglandin E2. Atropine inhibits carbachol-stimulated HCO3- secretion but has no effect on basal HCO3- secretion. Agents which have been shown to inhibit HCO3- secretion are acetazolamide, O2 deprivation, noradrenalin, aspirin and indomethacin. It is plausible to suppose that HCO3- secretion may play a role in protection of the gastric mucosal epithelium. Although for a given area of gastric mucosa, the amount of HCO3- secreted is only about 5 to 10% of the maximal acid output, the neutralizing capability of the HCO3- rich fluid may be significantly greater at the apical cell membrane of the surface epithelial cells.

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AnimalsBicarbonatesDepression, ChemicalDogsEpithelial CellsGastric MucosaStimulation, ChemicalJournal ArticleReview

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BibTeXRIS

G L Kauffman. 1980. Gastric bicarbonate secretion: an update.. https://doi.org/10.1016/0361-9230(80)90298-1

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