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Proximal tubular lactate transport in rat kidney: a micropuncture study

MPS-Authors
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Höhmann,  Bernhard
Department of Physiology, Max Planck Institute of Biophysics, Max Planck Society;

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Frohnert,  Peter P.
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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Baumann,  Karl
Department of Physiology, Max Planck Institute of Biophysics, Max Planck Society;

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Citation

Höhmann, B., Frohnert, P. P., Kinne, R., & Baumann, K. (1974). Proximal tubular lactate transport in rat kidney: a micropuncture study. Kidney International, 5(4), 261-270. doi:10.1038/ki.1974.35.


Cite as: https://hdl.handle.net/21.11116/0000-0008-9E54-8
Abstract
Proximal tubular lactate transport in rat kidney: A micropuncture study. Micropuncture studies of renal lactate behavior in the rat showed free filtration across the glomerular membrane. Under free-flow conditions, 95% of the filtered load was reabsorbed by the proximal tubule, thus generating a transtubular concentration gradient. In the absence of volume changes, an intratubular steady-state concentration of lactate was established irrespective of the presence or absence of lactate in the initial test solution, indicating a passive “leak” along the transtubular concentration gradient which increased with higher serum lactate levels. Although proximal tubular hydrogen ion secretion could explain this lactate gradient on the basis of nonionic diffusion, studies in chronic alkalotic rats showed that lactate was reabsorbed even in the absence of a hydrogen ion gradient. Inhibition of intracellular gluconeogenesis from lactate, by alkalosis and through administration of an inhibitor (MICA), abolished development of the transtubular concentration gradient in the proximal tubule. It is concluded that lactate reabsorption in the proximal tubule is caused by simple diffusion across the luminal membrane in response to a concentration gradient created by intracellular utilization of lactate for gluconeogenesis.