A possible relationship between KCl symport and basolateral K(+)-conductance in Necturus gallbladder epithelial cells.

1. Apical membrane potential (Va), transepithelial potential (VT), fractional apical voltage ratio (FVa = delta Va/delta VT), tissue resistance (RT), and intracellular Cl- (aiCl) and K+ (aiK) activities were measured in isolated gallbladders maintained between oxygenated bicarbonate-free physiological media (23 degrees C, pH 7.2 or 8.2) in a divided chamber. The basolateral membrane potential (Vb) was calculated from the measured values of Va and VT. 2. Cl- removal from the serosal medium (which should accelerate coupled basolateral KCl exit) significantly depolarized Vb, decreased aiCl, decreased FVa, increased RT, and attenuated the depolarization of Vb (delta Vb) induced by high K+ added to the serosal side. These changes are consistent with a decrease in the K(+)-conductance of the basolateral membrane (gbK). 3. Addition of furosemide (an inhibitor of KCl cotransport) to the serosal medium induced significant increases in Vb, FVa, and high K(+)-induced delta Vb, indicating an increase in gbK. 4. In the presence of serosal furosemide, Cl- removal from the serosal medium did not significantly alter Vb, aiCl or delta Vb from their corresponding values when serosal Cl- was present. 5. Serosal furosemide had no significant effect on aiK and aiCl measured with double-barreled ion-selective microelectrodes. 6. These results suggest the possibility of a reciprocal relationship between gbK and the rate of basolateral KCl cotransport. This may contribute to the maintenance of aiK in gallbladder epithelial cells.