KCl cotransport: a mechanism for basolateral chloride exit in Necturus gallbladder.
K+ and Cl--selective double-barreled microelectrodes were used to study the effect of changes in external K+ concentration on intracellular Cl- activity (aiCl) in epithelial cells of Necturus gallbladder. Decreasing the K+ concentration simultaneously in both bathing solutions produced a decrease in aiCl. Steady-state values of aiCl were related to the values of the chemical potential gradient for K+ (delta microK) across either the apical or the basolateral cell membrane. A similar dependence between aiCl and delta microK appeared when the K+ concentration was changed in the serosal solution only. This indicates that aiCl depends on delta microK across the basolateral membrane. aiCl was virtually independent of the membrane potential. This supports the idea that both the mucosal and the basolateral membranes of Necturus gallbladder cells have very low passive permeabilities to Cl-. These results indicate that the exit of Cl- from Necturus gallbladder cells is driven by delta microK across the basolateral membrane, and suggest that KCl electroneutral coupled mechanism in this membrane plays an important role in transcellular Cl- transport.
D000818:Animals; D001693:Biological Transport, Active; D002462:Cell Membrane / Q000378:metabolism; D002463:Cell Membrane Permeability; D002712:Chlorides / Q000378:metabolism*; D005704:Gallbladder / Q000378:metabolism*; D066298:In Vitro Techniques; D008564:Membrane Potentials; D009338:Necturus maculosus / Q000378:metabolism; D011188:Potassium / Q000378:metabolism*
D002712:Chlorides; D011188:Potassium