Gastric Acid Secretion and Neutralization

The primary difficulty with the above model for gastric protection is that the flux of bicarbonate, J, is too small to cause a sufficient reduction of hydrogen ions at the surface of the epithelial cells. A model that addresses this shortcoming by examining the relationship between hydrochloric acid secretion and the release of bicarbonate was constructed by Lacker and his coworkers (de Beus et al., 1993).

Hydrochloric acid is secreted from the parietal cells of the oxyntic glands using a number of reactions. First, water in the cells is dissociated into hydrogen and hydroxyl ions in the cell cytoplasm. The hydrogen ions are actively secreted via a hydrogen-potassium ATPase. In addition, chloride ions are actively secreted and sodium ions are actively absorbed, via separate ATPases. The result is a high concentration of hydrochloric acid in the lumen. At the same time, carbon dioxide combines with hydroxyl ions (catalyzed by carbonic anhydrase) to form carbonic acid and thence bicarbonate. This bicarbonate diffuses out of the cell into the extracellular medium and is transported by the capillary blood flow. The direction of capillary blood flow is from the oxyntic cell in the gastric pit to the epithelial lining of the lumen. Since the epithelial cells are downstream of the oxyntic cells, they absorb bicarbonate from the blood and then secrete it into the mucus. Thus, as acid production increases, so does the rate at which bicarbonate is secreted into the lumen by the epithelial cells. According to de

Beus et al., the lack of this feature in the Engel model caused an underestimation of the rate of bicarbonate secretion from the epithelial layer.

De Beus et al. estimated the model parameters from the available experimental literature and showed that analytic solutions in certain simplified cases agreed well with the full solution. Of particular interest is their reproduction of the alkaline tide. As the rate of H + secretion into the lumen increases, the downstream [H+] (i.e., the gastric venous [H+]) decreases. This reinforces the major idea behind this model, that secretion of HCO- by the epithelial cells is driven by H+ secretion by the oxyntic cells, so that gastric protection is automatically increased as the lumenal H+ increases.

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