Abstract
Frog (Rana temporaria) fundic mucosae in vitro were pretreated with the histamine H2 receptor antagonist Metiamide (10(-3)M, 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.
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