The potential as measured in vitro across rat stomach has been examined by substitution, inhibition and flux studies. The effect of choline substitution for sodium on the potential was shown to be immediate, and to act on the mucosal influx, changing it from 1.4 to 0.2 ueq of sodium/hr. Anoxic condition affected mucosal outflux only. The transmembrane potential is linearly dependent on mucosal sodium concentration to 55 molars, where the system apparently becomes saturated. Replacement of chloride by sulfate raises the potential. A potassium requirement could be demonstrated by the elimination of chloride, and a calcium deficiency was noted only in the presence of high concentrations of ETTA. Dinitrophenol was shown to be the most effective of a series of metabolic inhibitors. Gastric mucosa possesses an ATPase, stimulated by sodium and potassium and inhibited by ouabain. All these results point to the conclusion that the potential difference across isolated rat stomach is generated by a sodium transport mechanism, as characterized by others in different issues.
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