K recirculation in A6 cells at increased Na transport rates.

Homocellular regulation of K at increased transcellular Na transport implies an increase in K exit to match the intracellular K load. Increased K conductance, g, was suggested to account for this gain. We tested whether such a mechanism is operational in A6 monolayers. Na transport was increased from 5.1±1.0 μA/cm to 20.7±1.3 μA/cm by preincubation with 0.1 μmol/l dexamethasone for 24 h. Basolateral K conductances were derived from transference numbers of K, t, and basolateral membrane conductances, g, using conventional microelectrodes and circuit analysis with application of amiloride. Activation of Na transport induced an increase in g from 0.333±0.067 mS/ cm to 1.160±0.196 mS/cm and t was reduced to 0.22±0.01 from a value of 0.70±0.05 in untreated control tissues. As a result, g remained virtually unchanged at increased Na transport rates. The increase in g after dexamethasone was due to activation of a conductive leak pathway presumably for Cl. Increased K efflux, I, was a consequence of the larger driving force for K exit due to depolarization at an elevated Na transport rate. The relationship between calculated K fluxes and Na transport rate, measured as the I, is described by the linear function I=0.624× I−0.079, which conforms with a stoichiometry 2∶3 for the fluxes of K and Na in the Na/K-ATPase pathway. Our data show that homocellular regulation of K in A6 cells is not due to up-regulation of g. [ABSTRACT FROM AUTHOR]