In the epithelium of rabbit gallbladder, in the nominal absence of bicarbonate, intracellular Cl- activity is about 25 mM, 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 25 mM 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+.
Animals Bumetanide