HYPOTONICITY INCREASES BASOLATERAL TAURINE PERMEABILITY IN RABBIT PROXIMAL CONVOLUTED TUBULE

The permeabilities of the basolateral membrane of rabbit proximal convoluted tubule (PCT) to taurine (P-Tau) and glucose (P-Glc) were estimated under control and hypotonic conditions using the initial rate of increase in cellular volume (CV) induced on isotonic replacement of 40 mM mannitol by one or the other of these substrates. Under control conditions, addition of taurine led to an increase in CV at an initial rate of 7.1 +/- 1.7%/min, leading to a cell swelling of 30.2 +/- 4.8% after 5 min (n = 6). Addition of glucose led to an increase in CV at an initial rate of 30.0 +/- 3.8%/min, leading to a cell swelling of 25.7 +/- 3.1% after 5 min (n = 7). After a period of recovery of 5 min in the absence of taurine or glucose, a 40 mosmol/kg hypotonic shock induced a cell swelling of 14.2 +/- 1.3 and 16.1 +/- 5.2%, respectively, followed by an almost complete volume regulatory decrease after 5 min. At that time, addition of taurine under continuous hypotonicity induced an increase in CV at an initial rate 2.57 +/- 0.17 times larger than that observed under the isotonic condition (p < 0.005), while addition of glucose induced an initial increase in CV identical to that observed under the isotonic condition. The increases in CV observed on addition of taurine were completely abolished in the absence of sodium under both isotonic and hypotonic conditions. The permeability to K+ was also estimated, in the absence of sodium, using the initial rate of increase in CV induced on isotonic replacement of 40 mM N-methyl-D-glucamine by K+. Our results demonstrate that there is an influx of potassium through the basolateral membrane under isotonic and hypotonic conditions, despite the absence of sodium, a situation known to reduce K+ channels activity. Also, addition of taurine in the presence of barium and quinine led to an increase in CV, demonstrating that taurine enters the cells via a pathway different from that for potassium. Together with the previous results, this demonstrates that taurine does not enter the cell through potassium channels. The complete inhibition of P-Tau in sodium-free media can thus be attributed to a direct effect on a sodium-dependent taurine transport. Finally, chloride was shown not to affect the entry of taurine under both isotonic and hypotonic conditions. In conclusion, the present study demonstrates the presence of a sodium-dependent taurine transporter in the basolateral membrane of PCT, activated by hypotonicity.