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 ∼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 ⁺ .