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

  • John Cuppoletti
  • Ann M. Baker
  • Danuta H. Malinowska
Conference paper
Part of the NATO ASI Series book series (NATO ASI, volume 89)


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.


Apical Membrane Cystic Fibrosis Transmembrane Regulator Discrimination Ratio Gastric Parietal Cell Negative Membrane Potential 
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Copyright information

© Springer-Verlag Berlin Heidelberg 1994

Authors and Affiliations

  • John Cuppoletti
    • 1
  • Ann M. Baker
    • 1
  • Danuta H. Malinowska
    • 1
  1. 1.Department of Physiology and BiophysicsUniversity of Cincinnati College of MedicineCincinnatiUSA

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