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Articles in PresS, published online ahead of print August 27, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00045.2002
Submitted on February 1, 2002
Accepted on August 23, 2002
1 Necker Medical Faculty, Inserm U.467, University of Paris 5, Paris Cedex 15, Paris Cedex 15, France
* To whom correspondence should be addressed. E-mail: srthomas{at}necker.fr.
We use a mathematical model to explore the possibility that metabolic production of net osmoles in the renal inner medulla (IM) may participate in the urine concentrating mechanism. Anaerobic glycolysis (AG) is an important source of energy for cells of the IM, since this region of the kidney is hypoxic. AG is also a source of net osmoles, since it splits each glucose into two lactates which are not metabolized within the IM. Furthermore, these sugars exert their full osmotic effect across the epithelia of the thin descending limb of Henle and the collecting duct, so they are apt to fulfill the external osmole role previously attributed to interstitial urea (whose role is compromised by the high urea permeability of the LDL). The present simulations show that physiological levels of IM glycolytic lactate production could suffice to significantly amplify the IM accumulation of NaCl. The model predicts that, for this to be effective, IM lactate recycling must be efficient, which requires high lactate permeability of descending vasa recta (DVR) and reduced IM blood flow during antidiuresis, two conditions that are probably fulfilled under normal circumstances. The simulations also suggest that the resulting IM osmotic gradient is virtually insensitive to the urea permeability (Pu) of LDL, thus lifting a longstanding paradox, and that this high Pu may serve for independent regulation of urea balance.
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