Decreased transport in renal basolateral membrane vesicles from hypertaurinuric mice.

Basolateral membrane vesicles were prepared from mouse kidney by use of a Percoll density gradient method. The preparation was enriched ninefold in Na+-K+-ATPase with minimal contamination by other cellular membranes. The basolateral membranes were a mixture of sealed inside-out and right-side-out vesicles (30%) and leaky vesicles or sheets (70%). Taurine uptake into basolateral membrane vesicles was osmotically sensitive, sodium dependent, temperature sensitive, inhibited by beta-alanine, and saturable (apparent Km, 360 microM; Vmax, 25.4 pmol.mg protein-1.15 s-1), indicating transport by a carrier-mediated process. The function of this transporter was examined in an inbred mouse strain, C57BL/6J, which has selective hypertaurinuria, presumably a result of decreased basolateral membrane permeability to taurine [Rozen et al., Am. J. Physiol. 244 (Renal Fluid Electrolyte Physiol. 13): F150-F155, 1983]. The sodium-dependent component of taurine uptake was significantly lower in C57BL/6J vesicles relative to control (C3H/HeJ strain): 2.9 +/- 0.7 vs. 9.4 +/- 0.3 (SE) pmol.mg protein-1.15 s-1, respectively; P less than 0.001. The interstrain difference in uptake was specific for taurine and could not be ascribed to differences in vesicle purification, integrity, orientation, or size. These findings indicate that the renal basolateral membrane is the site of a transport defect, which explains decreased net taurine reabsorption in vivo in the C57BL/6J strain, and corroborate earlier observations in the renal cortical slice preparation.