A Study of Gastric HCl Formation

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Abstract
Sheets of rats stomach are clamped as separating membrane between 2 half cells, each containing test soln., a glass electrode, and bubbling O2. The half cell on the mucosal side becomes acid, that on the serosal side becomes alkaline. Anoxia or addition of either cyanide, fluoride, arsenite, iodoacetate, or tetramethyl-p-phenylenediamine inhibit acid production; benadryl, malonate, or phloridzin have no effect; histamine gives inconstant stimulation. The mechanism postulated to explain gastric acid production involves a stratification of enzyme systems in the mucosal cell. A local high concn. of H+ is produced at the lumen border of the cell by action of pyridine nucleotide dehydrogenase system on some carbohydrate intermediate, and diffuses into the lumen in combination with Cl- from NaCl. Flavoprotein, cytochrome, and cytochrome oxidase are stratified in that order between the pyridine nucleotide and carbonic anhydrase; they produce OH- from O2 and molecular H from dehydrogenase. The OH- combines with CO2 under the influence of carbonic anhydrase stratified at the anti-lumen side of cell to form HCO3- which diffuses into the blood in combination with Na+ from NaCl.

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