Basolateral KCl co-transport in a NaCl-absorbing epithelium.
In NaCl-absorbing epithelia such as proximal renal tubule, small intestine and gallbladder, Na+-dependent Cl- entry across the luminal membrane is an electroneutral transport process that has been attributed to Na-Cl symport, Na-K-Cl symport, or a double (Na-H, Cl-HCO3) antiport. At the basolateral (antiluminal) membrane, Na+ extrusion can be attributed to the Na+-K+ pump, and Cl- transport could be explained in principle by electrodiffusion since the intracellular Cl- activity is higher than predicted for equilibrium distribution. However, in Necturus gallbladder, as in other epithelia, the electrodiffusional Cl- permeability of the membrane (PCl) is too low to account for the transepithelial Cl- transport rate. Because K+ is at a higher chemical potential in the cell than in the extracellular fluid, and because serosal Cl- substitutions have only small effects on membrane potential, the hypothesis of carrier-mediated electroneutral KCl co-transport was proposed. The experiments reported here were designed to test this hypothesis in Necturus gallbladder epithelium. Intracellular Cl- and K+ activities (aCli, aKi) were measured with ion-sensitive intracellular microelectrodes before, during and after ionic substitutions of the serosal (basolateral) bathing medium. The results demonstrate a Na+-independent basolateral membrane KCl symport.
D001693:Biological Transport, Active; D004848:Epithelium / Q000378:metabolism; D005704:Gallbladder / Q000166:cytology*; D008564:Membrane Potentials; D008839:Microelectrodes; D011189:Potassium Chloride / Q000378:metabolism*; D012965:Sodium Chloride / Q000378:metabolism*
D012965:Sodium Chloride; D011189:Potassium Chloride