Acidophylic CI^- and K⁺ Channels of the Gastric Parietal Cell: A New Model of Regulated HCI Secretion

Abstract

The gastric parietal cell is responsible for HC1 production. Primary active transport of H⁺ occurs through the action of the Mg²⁺-dependent H⁺/K⁺ ATPase, which catalyses the ATP-dependent inward movement of one extracytosolic K⁺ for each H⁺ produced. Pathways for the movement of K⁺ and CI⁻ are also required for continued action of the H⁺ pump, to provide luminal K⁺ and equivalents of CI⁻ for HCl production. KCl flux across the apical membrane is under regulation (Sachs et al, 1976; Malinowska et al, 1983). The gastric parietal cell also undergoes a morphological reorganization upon stimulation of HCl secretion, whereupon intracellular vesicles containing the H⁺/K⁺ ATPase (tubulovesicles) disappear, and elaborate into the apical membrane. Since HCl concentrations in the primary gastric secretion exceed 0.15 M, the H⁺/K⁺ ATPase and any other proteins (such as ion channels) required for HC1 secretion must function in this harsh environment.