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

Abstract

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