The regulation of proximal tubular salt transport in hypertension: An update

Document Type

Journal Article

Publication Date

9-1-2009

Journal

Current Opinion in Nephrology and Hypertension

Volume

18

Issue

5

DOI

10.1097/MNH.0b013e32832f5775

Keywords

Hypertension; Kidney; Proximal tubule; Sodium transporter

Abstract

PURPOSE OF REVIEW: Renal proximal tubular sodium reabsorption is regulated by sodium transporters, including the sodium glucose transporter, sodium amino acid transporter, sodium hydrogen exchanger isoform 3 and sodium phosphate cotransporter type 2 located at the luminal/apical membrane, and sodium bicarbonate cotransporter and Na/KATPase located at the basolateral membrane. This review summarizes recent studies on sodium transporters that play a major role in the increase in blood pressure in essential/polygenic hypertension. RECENT FINDINGS: Sodium transporters and Na/KATPase are segregated in membrane lipid and nonlipid raft microdomains that regulate their activities and trafficking via cytoskeletal proteins. The increase in renal proximal tubule ion transport in polygenic hypertension is primarily due to increased activity of NHE3 and Cl/HCO3 exchanger at the luminal/apical membrane and a primary or secondary increase in Na/KATPase activity. SUMMARY: The increase in renal proximal tubule ion transport in hypertension is due to increased actions by prohypertensive factors that are unopposed by antihypertensive factors. © 2009 Lippincott Williams & Wilkins, Inc.

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