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.