Sodium and potassium transport in trout (Salmo gairdneri) erythrocytes.

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Abstract
The principal pathways of Na+ and K+ transport in trout erythrocyte were characterized. Of K+ influx in steady-state erythrocytes, .apprx. 50% was inhibited by ouabain (1 mM) and 46% by furosemide (1 mM). Furosemide-sensitive K+ influx was a saturable function of external K+ concentration with a Km of 25 mM. This flux component was also inhibited by SITS (4-acetamido-4''-isothiocyanatostilbene-2 2''-disulfonate) (concentration required for 50% inhibition, I50 = 7.6 .times. 10-6 M) and by the removal of external Cl-. An increase in cell volume stimulated furosemide-sensitive K+ influx and cell shrinkage inhibited this flux. K+ efflux was mainly furosemide-sensitive (64% of total). This pathway was unaffected by variations in extracellular K+ concentration and is not exchange diffusion. It was affected by variations in cell volume in a similar way to the furosemide-sensitive K+ influx. Na+ influx was only slightly sensitive to furosemide (13% of total) but this component was very sensitive to changes in cell volume; decreased cell volume increased Na+ influx while increased cell volume inhibited Na+ influx. Furosemide-sensitive K+ influx was unaffected by variations in external Na+ concentration. Similarly, furosemide-sensitive Na+ influx was unaffected by variations in external K+ concentration. This indicates that the passive influxes of Na+ and K+ were not coupled, in contrast to the situation in avian erythrocytes. The opposite effects of cell volume upon passive Na+ and K+ fluxes are in good agreement with the net movements of these cations during volume regulation in erythrocytes of the flounder and the toadfish.

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