The epithelial sodium channel: from molecule to disease

Détails

ID Serval
serval:BIB_3FE6BEE7FF53
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
The epithelial sodium channel: from molecule to disease
Périodique
Reviews of Physiology, Biochemistry and Pharmacology
Auteur(s)
Schild  L.
ISSN
0303-4240 (Print)
Statut éditorial
Publié
Date de publication
2004
Volume
151
Pages
93-107
Notes
Journal Article
Review
Résumé
Genetic analysis has demonstrated that Na absorption in the aldosterone-sensitive distal nephron (ASDN) critically determines extracellular blood volume and blood pressure variations. The epithelial sodium channel (ENaC) represents the main transport pathway for Na+ absorption in the ASDN, in particular in the connecting tubule (CNT), which shows the highest capacity for ENaC-mediated Na+ absorption. Gain-of-function mutations of ENaC causing hypertension target an intracellular proline-rich sequence involved in the control of ENaC activity at the cell surface. In animal models, these ENaC mutations exacerbate Na+ transport in response to aldosterone, an effect that likely plays an important role in the development of volume expansion and hypertension. Recent studies of the functional consequences of mutations in genes controlling Na+ absorption in the ASDN provide a new understanding of the molecular and cellular mechanisms underlying the pathogenesis of salt-sensitive hypertension.
Mots-clé
Aldosterone/metabolism Amino Acid Motifs Animals Biological Transport Epithelial Sodium Channel Humans Kidney/metabolism Mutation Proline/chemistry Salts/pharmacology Sodium/metabolism Sodium Channels/*metabolism/*physiology
Pubmed
Web of science
Création de la notice
24/01/2008 13:55
Dernière modification de la notice
20/08/2019 14:37
Données d'usage