Cl−Dependence of HCO3−Transport in Frog Gastric Mucosa

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 SO₄^2- 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.