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Central control of renal sodium-phosphate (NaPi-2) transporters

¹Department of Physiology and Biophysics, Georgetown University School of Medicine, Washington, D.C. 20057; and ²Division of Renal Diseases and Hypertension, University of Colorado Health Sciences Center, Denver, Colorado 80262

Submitted 3 October 2002 ; accepted in final form 19 November 2003

Regulation of phosphate (P_i) reabsorption occurs through the up- and downregulation of the renal type-II sodium P_i cotransporters (NaPi-2). Recently, renal NaPi2-type expression has been identified in areas of the brain. The present study determined whether brain NaPi-2 is regulated by dietary P_i and whether the behavioral and renal adaptations to low-dietary P_i are controlled centrally. NaPi-2-like expression in the third ventricle (3V) and amygdala of juvenile Wistar rats was regulated by dietary P_i, as in the kidneys. When cerebrospinal fluid (CSF) P_i concentration was elevated by 3V injections of Pi in rats fed low-P_i diet (LPD), the behavioral and renal adaptations to LPD were abolished. Most importantly, NaPi-2 expression was markedly reduced not only in the brain, but also renal proximal tubules, despite the low plasma P_i milieu. This was confirmed by the significant reduction in the transport maximum for P_i (from 8.1 ± 0.2 in LPD + veh 3V to 1.7 ± 0.1 µmol P_i/ml glomerular filtration rate in LPD + 3V P_i, P < 0.001). These findings indicate that NaPi-2-like transporters in the brain are regulated by both dietary P_i and CSF P_i concentrations, and most significantly, that the central P_i milieu can regulate renal NaPi-2 expression. We hypothesize that central 3V NaPi-2 transporters may act as P_i sensors and help regulate both brain and whole body P_i homeostasis.

juvenile rats; behavior; P_i sensors

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