Gastric bicarbonate secretion: an update.
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.
D000818:Animals; D001639:Bicarbonates / Q000378:metabolism*; D003864:Depression, Chemical; D004285:Dogs; D004847:Epithelial Cells; D005753:Gastric Mucosa / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D013268:Stimulation, Chemical
D001639:Bicarbonates