Taurine transport by rabbit kidney brush-border membranes: Coupling to sodium, chloride, and the membrane potential

Abstract

Ion dependence and electrogenicity of taurine uptake were studied in rabbit renal outer cortical brush-border membrane vesicles isolated by differential precipitation. Na⁺-d-glucose cotransport was followed in parallel to monitor changes in the membrane potential. Concentrative taurine flux was dependent on a chemical and/or an electrical Na⁺ gradient (K⁺ diffusion potential) and could be completely inhibited by other β-amino acids. It displayed a specific anion requirement (Cl⁻≥Br⁻≫SCN⁻>I⁻>NO ₃ ⁻ ). At chemical Na⁺ equilibrium, Cl⁻ gradients, depending on their orientation, stimulated or inhibited taurine uptake more than could be attributed solely to electrical anion effects, although a Cl⁻ gradient alone could not energize an overshoot. Furthermore, taurine tracer exchange was significantly stimulated by Cl⁻ as well as Br⁻. The Cl⁻ stoichiometry was found to be one, whereas taurine transport, in the presence of Cl⁻, was sigmoidally related to the Na⁺ concentration, resulting in a coupling ratio of 2 to 3 Na⁺: 1 taurine. Upon Cl⁻ replacement with gluconate, taurine uptake showed a reduced potential sensitivity and was no longer detectably affected by the Na⁺ concentration (up to 150mm). These results suggest a 2 to 3 Na⁺:1 Cl⁻:1 taurine cotransport mechanism driven mainly by the Na⁺ gradient, which is sensitive to the membrane potential due to a negatively charged empty carrier. Cl⁻ appears to stimulate taurine flux primarily by facilitating the formation of the translocated solute-carrier complex.