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Renal brush border membrane Na/Pi-cotransport: molecular aspects in PTH-dependent and dietary regulation.


Murer, H; Lötscher, M; Kaissling, B; Levi, M; Kempson, S A; Biber, J (1996). Renal brush border membrane Na/Pi-cotransport: molecular aspects in PTH-dependent and dietary regulation. Kidney International, 49(6):1769-1773.

Abstract

Inorganic phosphate (Pi) is reabsorbed in renal proximal tubules in a sodium (Na)-dependent manner involving brush border Na/Pi-cotransporter(s). Regulation of renal Pi-reabsorption, such as by parathyroid hormone (PTH) and/or by dietary Pi-deprivation, involves alterations in the rate of Na/Pi-cotransport. Two structurally different Na/Pi-cotransporters have been identified: type I-transporter and type II-transporter. The related mRNAs and proteins are located in the proximal tubule and in the brush border membrane. In heterologous expression systems type I and type II Na/Pi-cotransporters mediate Na/Pi-cotransport. Characterization of the transport properties suggested that the type II transporter is "responsible' for brush border membrane Na/Pi-cotransport (as observed in isolated vesicles). Administration of PTH to rats resulted in an inhibition of brush border membrane Na/Pi-cotransport (vesicles) and in a reduced brush border membrane content of the type II transporter. Feeding low Pi-diets resulted in an up-regulation of Na/Pi-cotransport (vesicles) and of type II transporter content; only after a prolonged exposure to low Pi-diets (more than 4 hr) was an increase in specific mRNA content observed. Refeeding high Pi diets had the opposite effects on Na/Pi-cotransport activity and on type II transporter protein. It is currently the task of future experiments to define the specific mechanisms leading to protein-synthesis-independent (PTH, acute Pi-deprivation, Pi-refeeding) and to protein-synthesis-dependent (prolonged Pi-deprivation) regulation of the type II Na/Pi-cotransporter.

Inorganic phosphate (Pi) is reabsorbed in renal proximal tubules in a sodium (Na)-dependent manner involving brush border Na/Pi-cotransporter(s). Regulation of renal Pi-reabsorption, such as by parathyroid hormone (PTH) and/or by dietary Pi-deprivation, involves alterations in the rate of Na/Pi-cotransport. Two structurally different Na/Pi-cotransporters have been identified: type I-transporter and type II-transporter. The related mRNAs and proteins are located in the proximal tubule and in the brush border membrane. In heterologous expression systems type I and type II Na/Pi-cotransporters mediate Na/Pi-cotransport. Characterization of the transport properties suggested that the type II transporter is "responsible' for brush border membrane Na/Pi-cotransport (as observed in isolated vesicles). Administration of PTH to rats resulted in an inhibition of brush border membrane Na/Pi-cotransport (vesicles) and in a reduced brush border membrane content of the type II transporter. Feeding low Pi-diets resulted in an up-regulation of Na/Pi-cotransport (vesicles) and of type II transporter content; only after a prolonged exposure to low Pi-diets (more than 4 hr) was an increase in specific mRNA content observed. Refeeding high Pi diets had the opposite effects on Na/Pi-cotransport activity and on type II transporter protein. It is currently the task of future experiments to define the specific mechanisms leading to protein-synthesis-independent (PTH, acute Pi-deprivation, Pi-refeeding) and to protein-synthesis-dependent (prolonged Pi-deprivation) regulation of the type II Na/Pi-cotransporter.

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Additional indexing

Item Type:Journal Article, refereed
Communities & Collections:04 Faculty of Medicine > Institute of Physiology
07 Faculty of Science > Institute of Physiology
Dewey Decimal Classification:570 Life sciences; biology
Language:English
Date:1 June 1996
Deposited On:11 Feb 2008 12:22
Last Modified:05 Apr 2016 12:18
Publisher:Nature Publishing Group
ISSN:0085-2538
Publisher DOI:10.1038/ki.1996.264
PubMed ID:8743494

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