Regulation of blood pressure and renal function by NCC and ENaC: lessons from genetically engineered mice.

Autor: Verouti SN; Department of Pharmacology and Toxicology, University of Lausanne, Lausanne, Switzerland., Boscardin E; Department of Pharmacology and Toxicology, University of Lausanne, Lausanne, Switzerland., Hummler E; Department of Pharmacology and Toxicology, University of Lausanne, Lausanne, Switzerland. Electronic address: Edith.Hummler@unil.ch., Frateschi S; Department of Pharmacology and Toxicology, University of Lausanne, Lausanne, Switzerland. Electronic address: Simona.Frateschi@unil.ch.
Jazyk: angličtina
Zdroj: Current opinion in pharmacology [Curr Opin Pharmacol] 2015 Apr; Vol. 21, pp. 60-72. Date of Electronic Publication: 2015 Jan 20.
DOI: 10.1016/j.coph.2014.12.012
Abstrakt: The activity of the thiazide-sensitive Na(+)/Cl(-) cotransporter (NCC) and of the amiloride-sensitive epithelial Na(+) channel (ENaC) is pivotal for blood pressure regulation. NCC is responsible for Na(+) reabsorption in the distal convoluted tubule (DCT) of the nephron, while ENaC reabsorbs the filtered Na(+) in the late DCT and in the cortical collecting ducts (CCD) providing the final renal adjustment to Na(+) balance. Here, we aim to highlight the recent advances made using transgenic mouse models towards the understanding of the regulation of NCC and ENaC function relevant to the control of sodium balance and blood pressure. We thus like to pave the way for common mechanisms regulating these two sodium-transporting proteins and their potential implication in structural remodeling of the nephron segments and Na(+) and Cl(-) reabsorption.
(Copyright © 2015 Elsevier Ltd. All rights reserved.)
Databáze: MEDLINE
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