Osmotic swelling activates two pathways for K+ efflux in a rat hepatoma cell line.

The pathways for the efflux of K(+) from osmotically-swollen HTC rat hepatoma cells were investigated using (86)Rb(+) as a tracer for K(+). Exposure of HTC cells to a hypotonic solution (<250 mOsm kg(-1)) resulted in a transient efflux of (86)Rb(+) that reached a maximal value after approximately 1 min, and inactivated within 3 min. This initial (86)Rb(+) efflux was inhibited by charybdotoxin, clotrimazole and Ba(2+), but not by apamin or paxilline, consistent with it being via an intermediate-conductance Ca(2+)-activated K(+) channel. For cells exposed to an extracellular osmolality < 180 mOsm kg(-1) there was an additional (86)Rb(+) efflux component which was slower to activate, taking 4 - 6 min to reach a maximum, and remaining active for > 20 min. The second (86)Rb(+) efflux component was not inhibited by K(+) channel blockers but was inhibited by the anion channel blockers, tamoxifen, 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB) and niflumate. The time-courses for its activation and inactivation, as well as its dependence on the extracellular osmolality, were very similar to those observed for the hypotonically-activated efflux of the organic osmolyte, taurine. The data are consistent with the second component of (86)Rb(+) efflux and the efflux of taurine from osmotically-swollen cells occurring via a common pathway having a marked selectivity for taurine over (86)Rb(+).