The renal transport of taurine and the regulation of renal sodium-chloride-dependent transporter activity.

A model for the beta-amino acid taurine transport is presented to help define the ionic, pH, and voltage requirements for the movement of taurine into the rat proximal tubule brush border membrane vesicle (BBMV). Sodium-(Na+)-taurine symport across the apical surface of the proximal tubule has a highly specific requirement for Cl- and Br-. Active taurine transport operates with a 2 Na+:1 Cl-:1 taurine-carrier complex. Complexes like the one required for maximal taurine transport may be pertinent for many other amino acids whose uptake is Na(+)-dependent. Renal epithelial cell lines LLC-PK and MDCK were used to define the nature of taurine uptake; they express Na(+)-Cl(-)-taurine cotransport that is inhibited by beta-alanine. The cell lines up- or down-regulate taurine transport in response to changes in the taurine concentration of the medium in a manner similar to that seen in BBMV. The adaptation is present by 12 h and depends on new protein synthesis and protein import to the cell membrane. The role of trafficking in the adaptive response was also explored in brush border vesicles. During dietary surfeit, transporter could be down-regulated and transporters could be shifted back into the microtubule system, resulting in taurinuria. Use of continuous renal cell lines allowed a more mechanistic exploration of intracellular trafficking in the up- and down-expression of the Na(+)-Cl(-)-taurine cotransporter. Colchicine appeared to be a more potent inhibitor of the rapid (over hours) adaptive response to a reduction in media and, therefore, intracellular taurine content.(ABSTRACT TRUNCATED AT 250 WORDS)