The nature of the neutral Na+−Cl−-coupled entry at the apical membrane of rabbit gallbladder epithelium: II. Na+−Cl− symport is independent of K+

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Abstract
In the epithelium of rabbit gallbladder, in the nominal absence of bicarbonate, intracellular Cl− activity is about 25mm, about 4 times higher than intracellular Cl− activity at the electrochemical equilibrium. It is essentially not affected by 10−4 m acetazolamide and 10−4 m 4-acetamido-4′-isothiocyanostilbene-2,2′-disulfonate (SITS) even during prolonged exposures; it falls to the equilibrium value by removal of Na+ from the lumen without significant changes of the apical membrane potential difference. Both intracellular Cl− and Na+ activities are decreased by luminal treatment with 25mm SCN−; the initial rates of change are not significantly different. In addition, the initial rates of change of intracellular Cl− activity are not significantly different upon Na+ or Cl− entry block by the appropriate reduction of the concentration of either ion in the luminal solution. Luminal K+ removal or 10−5 m bumetanide do not affect intracellular Cl− and Na+ activities or Cl− influx through the apical membrane. It is concluded that in the absence of bicarbonate NaCl entry is entirely due to a Na+−Cl− symport on a single carrier which, at least under the conditions tested, does not cotransport K+.