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, gK, 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 microA/cm2 to 20.7 +/- 1.3 microA/cm2 by preincubation with 0.1 mumol/l dexamethasone for 24 h. Basolateral K+ conductances were derived from transference numbers of K+, tK, and basolateral membrane conductances, gb, using conventional microelectrodes and circuit analysis with application of amiloride. Activation of Na+ transport induced an increase in gb from 0.333 +/- 0.067 mS/cm2 to 1.160 +/- 0.196 mS/cm2 and tK was reduced to 0.22 +/- 0.01 from a value of 0.70 +/- 0.05 in untreated control tissues. As a result, gK remained virtually unchanged at increased Na+ transport rates. The increase in gb after dexamethasone was due to activation of a conductive leak pathway presumably for Cl-. Increased K+ efflux, IK, 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 Isc, is described by the linear function IK = 0.624 x INa -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 gK.