Cl−Dependence of HCO3−Transport in Frog Gastric Mucosa

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Abstract
Frog (Rana temporaria) fundic mucosae in vitro were pretreated with the histamine H2 receptor antagonist Metiamide (10−3M, nutrient side) until net H+ secretion had ceased and a steady rate of HCO3− transport (luminal alkalinization) was titrated. Removal of Cl− with SO42- or isethionate replacement from solutions bathing both sides of the mucosa abolished luminal alkalinization. Readdition of Cl− to the luminal side only reestablished full rates of HCO3− transport. Nutrient (serosal) side Cl− had no effect in this aspect. The results support the previous suggestion that the gastric HCO3− transport process is located at the luminal membrane of the surface epithelial cells and indicate that it occurs by (electroneutral) HCO3−/Cl− exchange.