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

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Serval ID
serval:BIB_0A05A99AD637
Type
Article: article from journal or magazin.
Publication sub-type
Review (review): journal as complete as possible of one specific subject, written based on exhaustive analyses from published work.
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Publications
Institution
Title
Regulation of blood pressure and renal function by NCC and ENaC: lessons from genetically engineered mice.
Journal
Current Opinion in Pharmacology
Author(s)
Verouti S.N., Boscardin E., Hummler E., Frateschi S.
ISSN
1471-4973 (Electronic)
ISSN-L
1471-4892
Publication state
Published
Issued date
2015
Peer-reviewed
Oui
Volume
21C
Pages
60-72
Language
english
Abstract
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.
Pubmed
Web of science
Create date
29/01/2015 17:26
Last modification date
20/08/2019 13:32
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