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+.
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+.
D000818:Animals; D002034:Bumetanide / Q000494:pharmacology; D002352:Carrier Proteins / Q000378:metabolism*; D002462:Cell Membrane / Q000378:metabolism*; D002712:Chlorides / Q000378:metabolism; D004848:Epithelium / Q000378:metabolism; D005704:Gallbladder / Q000378:metabolism*; D066298:In Vitro Techniques; D007700:Kinetics; D011188:Potassium / Q000494:pharmacology*; D011817:Rabbits; D012964:Sodium / Q000378:metabolism; D049992:Sodium Chloride Symporters; D027981:Symporters
D002352:Carrier Proteins; D002712:Chlorides; D049992:Sodium Chloride Symporters; D027981:Symporters; D002034:Bumetanide; D012964:Sodium; D011188:Potassium