Lactate-sodium cotransport in rat renal brush border membranes.
Brush border membrane vesicles were obtained from rat kidney cortex through a calcium precipitation method and their transport properties for lactate were studied by a rapid-filtration technique. Transient concentrative uptake of L-lactate was observed in the presence of inwardly directed NaCl gradient, but not in the presence of a KCl, LiCl, RbCl, CsCl, or choline chloride gradient. The sodium-dependent L-lactate uptake was saturable and was inhibited by D-lactate. The activation curve with sodium was hyperbolic. Maneuvers that render the inside of the vesicle more negative stimulated sodium-dependent L-lactate uptake, suggesting an electrogenic transfer of L-lactate and sodium. An L-lactate gradient also accelerates the sodium movement across the brush border membrane. Studies on the pH dependency of L-lactate transport and on the effect of L-lactate on proton movements across the brush border membrane indicate that there is little contribution of nonionic diffusion and/or of lactate-H+ cotransport to the transfer of L-lactate across the renal brush border membrane. In summary, sodium-lactate cotransport is the major mechanism for L-lactate transfer across the renal brush border membrane.
D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects; D002474:Cell-Free System; D005947:Glucose / Q000378:metabolism; D006096:Gramicidin / Q000494:pharmacology; D006863:Hydrogen-Ion Concentration; D007672:Kidney Cortex / Q000378:metabolism*; D007773:Lactates / Q000378:metabolism*; D008297:Male; D008564:Membrane Potentials; D008871:Microvilli / Q000378:metabolism; D051381:Rats; D012964:Sodium / Q000378:metabolism*
D007773:Lactates; D006096:Gramicidin; D012964:Sodium; D005947:Glucose