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Journal Article

Lactate-sodium cotransport in rat renal brush border membranes

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Murer,  Heini
Department of Physiology, Max Planck Institute of Biophysics, Max Planck Society;

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Kinne,  Rolf
Department of Physiology, Max Planck Institute of Biophysics, Max Planck Society;

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Citation

Barac-Nieto, M., Murer, H., & Kinne, R. (1980). Lactate-sodium cotransport in rat renal brush border membranes. American Journal of Physiology-Renal Physiology, 239(5), F496-F506. doi:10.1152/ajprenal.1980.239.5.F496.


Cite as: https://hdl.handle.net/21.11116/0000-0008-4AD7-3
Abstract
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.