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

• Published in: The Journal of membrane biology 1988-05, Vol.102 (2), p.131-139
• Main Authors: WOLFF, N. A, KINNE, R
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Biological Transport - drug effects; Cell physiology; Chlorides - metabolism; Chlorides - pharmacology; Fundamental and applied biological sciences. Psychology; kidney; Kidney Cortex - physiology; Male; Membrane and intracellular transports; Membrane Potentials - drug effects; Microvilli - metabolism; Molecular and cellular biology; Rabbits; Sodium - metabolism; taurine; Taurine - metabolism
• ISSN: 0022-2631; 1432-1424
• DOI: 10.1007/BF01870451

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 beta-amino acids. It displayed a specific anion requirement (Cl- greater than or equal to Br- much greater than SCN- greater than I- greater than 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 150 mM). 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.