In confluent primary cultures of rat hepatocytes, micromolar concentrations of bromosulfophthalein (BSP) lead to a sizeable hyperpolarization of membrane voltage. The effect is a saturable function of BSP concentration yielding an apparent value of 226 µmol/l and a V_max of 10.3 mV. The BSP-induced membrane hyperpolarization is inhibited by the K⁺ channel blocker Ba²⁺, and in cable-analysis and ion-substitution experiments it becomes evident that the effect is due to a significant increase in cell membrane K⁺ conductance. Voltage changes were attenuated by the simultaneous administration of SO²₄, succinate, and cholate (cis-inhibition) and increased after preincubation with SO²₄ and succinate (trans-stimulation), suggesting that the effect occurs via BSP uptake through the known SO²₄/OH exchanger. Microfluorometric measurements reveal that BSP-induced activation of K⁺ conductance is not mediated by changes in cell pH, cell Ca²⁺, or cell volume. It is concluded that K⁺ channel activation by BSP (as well as by DIDS and indocyanine green) may reflect a physiological mechanism linking the sinusoidal uptake of certain anions to their electrogenic canalicular secretion.

liver; anion transport; membrane voltage; cross-talk

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