The unidirectional fluxes of Cl- and Na+ across the frog gastric mucosa in vitro were investigated with radioactive isotopes, and related to the secretory and electrical properties of the normal, and metabolically inhibited, mucosa. The flux of Cl- from nutrient to secretory surface of the mucosa was observed to rise sharply with increasing acid secretion, while the corresponding flux of Na+ did not change appreciably. Lowering [NaCl] in the secretory solution caused a proportional drop in the fluxes from secretory to nutrient surface, of both Cl- and Na+. Under the same conditions, the flux of Cl- from nutrient to secretory surface fell by nearly the same amount as did the flux of Cl- in the opposite direction, while the flux of Na+ from nutrient to secretory surface remained essentially unchanged. Electrical and hydrodynamic causes for this observation could be excluded. Metabolic inhibitors, including cyanide, azide, DNP, and anaerobiosis depressed Cl- flux in both directions distinctly below the corresponding values observed with the normal, non-secreting mucosa. At the same time, a decrease in electrical potential difference and conductance was observed under inhibition. The flux of Na+ was little changed by metabolic inhibition. The relationship between fluxes and conductance of Cl- during metabolic inhibition differs markedly from that observed under normal conditions, and is consistent with the view that during metabolic inhibition most of the Cl- moving across the mucosa does so as a free ion. From the above data it is concluded that Cl- is normally transported across the mucosa in combination with a carrier, the supply of which is impaired under metabolic inhibition. According to the behavior of the Na+ flux, the passive permeability of the mucosa appeared to be little affected by the metabolic inhibition applied, but seemed to rise considerably after death of the mucosa, probably due to structural damage.

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