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

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Télécharger: 5_25613995_Postprint.pdf (2436.52 [Ko])
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ID Serval
serval:BIB_0A05A99AD637
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Titre
Regulation of blood pressure and renal function by NCC and ENaC: lessons from genetically engineered mice.
Périodique
Current Opinion in Pharmacology
Auteur(s)
Verouti S.N., Boscardin E., Hummler E., Frateschi S.
ISSN
1471-4973 (Electronic)
ISSN-L
1471-4892
Statut éditorial
Publié
Date de publication
2015
Peer-reviewed
Oui
Volume
21C
Pages
60-72
Langue
anglais
Résumé
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
Création de la notice
29/01/2015 16:26
Dernière modification de la notice
20/08/2019 12:32
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