HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 286/4/F647    most recent 00354.2002v2 00354.2002v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (14) Citing Articles via Google Scholar Google Scholar Articles by Mulroney, S. E. Articles by Levi, M. Search for Related Content PubMed PubMed Citation Articles by Mulroney, S. E. Articles by Levi, M.

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

This article has been cited by other articles:

				B. S. Levine, C. R. Kleeman, and A. J. Felsenfeld The Journey From Vitamin D-Resistant Rickets to the Regulation of Renal Phosphate Transport Clin. J. Am. Soc. Nephrol., November 1, 2009; 4(11): 1866 - 1877. [Abstract] [Full Text] [PDF]

				L. S. Alexander, A. Qu, S. A. Cutler, A. Mahajan, S. M. Lonergan, M. F. Rothschild, T. E. Weber, B. J. Kerr, and C. H. Stahl Response to dietary phosphorus deficiency is affected by genetic background in growing pigs J Anim Sci, October 1, 2008; 86(10): 2585 - 2595. [Abstract] [Full Text] [PDF]

				L. V. Virkki, J. Biber, H. Murer, and I. C. Forster Phosphate transporters: a tale of two solute carrier families Am J Physiol Renal Physiol, September 1, 2007; 293(3): F643 - F654. [Abstract] [Full Text] [PDF]

				S. Y. Breusegem, N. Halaihel, M. Inoue, H. Zajicek, E. Lederer, N. P. Barry, V. Sorribas, and M. Levi Acute and chronic changes in cholesterol modulate Na-Pi cotransport activity in OK cells Am J Physiol Renal Physiol, July 1, 2005; 289(1): F154 - F165. [Abstract] [Full Text] [PDF]