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    American Physiological Society ; 1999
    In:  American Journal of Physiology-Gastrointestinal and Liver Physiology Vol. 276, No. 6 ( 1999-06-01), p. G1380-G1390
    In: American Journal of Physiology-Gastrointestinal and Liver Physiology, American Physiological Society, Vol. 276, No. 6 ( 1999-06-01), p. G1380-G1390
    Abstract: 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 Ba 2+ , 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 [Formula: see text], succinate, and cholate ( cis-inhibition) and increased after preincubation with [Formula: see text] and succinate ( trans-stimulation), suggesting that the effect occurs via BSP uptake through the known[Formula: see text]/OH − exchanger. Microfluorometric measurements reveal that BSP-induced activation of K + conductance is not mediated by changes in cell pH, cell Ca 2+ , 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.
    Type of Medium: Online Resource
    ISSN: 0193-1857 , 1522-1547
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1999
    detail.hit.zdb_id: 1477329-6
    SSG: 12
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