The Na(+)-independent taurine influx in flounder erythrocytes and its association with the volume regulatory taurine efflux.

95% of the Na(+)-independent influx of taurine in flounder erythrocytes at normal osmolality (330 mosmol kg-1) and 0.30 mmol l-1 taurine was mediated by a saturable system (Vmax = 0.689 nmol g-1 dry mass min-1; Km = 0.47 mmol l-1). The influx was inhibited by taurine analogues, but was not significantly affected by reduced osmolality. This saturable influx of taurine was probably mediated by the so-called Na(+)-dependent influx system for taurine operating in the 0 Na+: 1 taurine mode. The remaining 5% of the Na(+)-independent influx was mediated by a diffusional pathway (Kd = 0.050 microliter g-1 dry mass min-1), since it did not show saturation kinetics, was not inhibited by taurine analogues and did not mediate counter-exchange. This non-saturable influx system for taurine was strongly, but transiently, stimulated by reduction of osmolality. The time course for this stimulatory effect was the same as that for the system that mediates the volume regulatory efflux of taurine. The relative inhibitory effect of bumetanide, furosemide, DIDS and quinine on the fluxes mediated by these two transport systems were also the same. We suggest that these unidirectional fluxes of taurine were mediated by only one transport system: a taurine channel. The effect of reduction of osmolality on the rate coefficient for efflux of beta-alanine was equal to the effect on the efflux of taurine, but greater than the effect on the efflux of choline. This difference probably reflects structural and/or electrical restrictions on the substrates to be transported by the taurine channel. The volume regulatory efflux of taurine was inhibited in the presence of the anti-calmodulin drug trifluoperazine and, in a Ca(2+)-free medium, added EGTA. The 5-lipoxygenase inhibitor nordihydroguaiaretic acid completely blocked the volume regulatory efflux of taurine. We suggest that both Ca2+/calmodulin and leukotrienes contribute to the control of the transport mediated by the taurine channel.