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ENaC, renal sodium excretion and extracellular ATP.

Wildman, Scott S.P., Kang, Esther S-K, King, Brian F. (2009) ENaC, renal sodium excretion and extracellular ATP. Purinergic Signalling, 5 (4). pp. 481-489. ISSN 1573-9538. E-ISSN 1573-9546. (doi:10.1007/s11302-009-9150-6) (Access to this publication is currently restricted. You may be able to access a copy if URLs are provided)

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Abstract

Sodium balance determines the extracellular fluid volume and sets arterial blood pressure (BP). Chronically raised BP (hypertension) represents a major health risk in Western societies. The relationship between BP and renal sodium excretion (the pressure/natriuresis relationship) represents the key element in defining the BP homeostatic set point. The renin-angiotensin-aldosterone system (RAAS) makes major adjustments to the rates of renal sodium secretion, but this system works slowly over a period of hours to days. More rapid adjustments can be made by the sympathetic nervous system, although the kidney can function well without sympathetic nerves. Attention has now focussed on regulatory mechanisms within the kidney, including extracellular nucleotides and the P2 receptor system. Here, we discuss how extracellular ATP can control renal sodium excretion by altering the activity of epithelial sodium channels (ENaC) present in the apical membrane of principal cells. There remains considerable controversy over the molecular targets for released ATP, although the P2Y(2) receptor has received much attention. We review the available data and reflect on our own findings in which ATP-activated P2Y and P2X receptors make adjustments to ENaC activity and therefore sodium excretion.

Item Type: Article
DOI/Identification number: 10.1007/s11302-009-9150-6
Uncontrolled keywords: P2X(4) receptor – P2Y(2) receptor – Amiloride-sensitive currents – ATP – Nucleotide – Kidney – Blood pressure
Subjects: R Medicine > RM Therapeutics. Pharmacology
Divisions: Faculties > Sciences > Medway School of Pharmacy
Depositing User: Scott S.P. Wildman
Date Deposited: 10 Dec 2015 14:49 UTC
Last Modified: 29 May 2019 16:41 UTC
Resource URI: https://kar.kent.ac.uk/id/eprint/53055 (The current URI for this page, for reference purposes)
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