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.
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References
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© 1994 Springer-Verlag Berlin Heidelberg
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Cuppoletti, J., Baker, A.M., Malinowska, D.H. (1994). Acidophylic CI- and K+ Channels of the Gastric Parietal Cell: A New Model of Regulated HCI Secretion. In: Hirst, B.H. (eds) Molecular and Cellular Mechanisms of H+ Transport. NATO ASI Series, vol 89. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-79301-1_44
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DOI: https://doi.org/10.1007/978-3-642-79301-1_44
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