Implication of ENaC in salt-sensitive hypertension

Détails

ID Serval
serval:BIB_56FE4D372F63
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
Implication of ENaC in salt-sensitive hypertension
Périodique
Journal of Steroid Biochemistry and Molecular Biology
Auteur(s)
Hummler  E.
ISSN
0960-0760 (Print)
Statut éditorial
Publié
Date de publication
06/1999
Volume
69
Numéro
1-6
Pages
385-90
Notes
Journal Article
Research Support, Non-U.S. Gov't
Review --- Old month value: Apr-Jun
Résumé
Arterial blood pressure is critically dependent on sodium balance. The kidney is the key player in maintaining sodium homeostasis. Aldosterone-dependent epithelial sodium transport in the distal nephron is mediated by the highly selective, amiloride-sensitive epithelial sodium channel (ENaC). Direct evidence that dysfunction of ENaC participates in blood pressure regulation has come from the molecular analysis of two human genetic diseases, Liddle's syndrome and pseudohypoaldosteronism type 1 (PHA-1). Both, increased sodium reabsorption despite low aldosterone levels in Liddle's patients and decreased sodium reabsorption despite high aldosterone levels in PHA-1 patients, demonstrated that ENaC is an effector for aldosterone action. Gene-targeting and classical transgenic technology enable the generation of mouse models for these diseases and the analysis of the involvement of the epithelial sodium channel (ENaC) in the progress of these diseases. A first mouse model using alphaENaC transgenic knockout mice [alphaENaC(-/-)Tg] mimicked several clinical features of PHA-1, like salt-wasting, metabolic acidosis, high aldosterone levels, growth retardation and increased early mortality. Such mouse models will be necessary in testing the involvement of genetic and/or environmental factors like salt-intake in hypertension.
Mots-clé
Aldosterone/physiology Animals Biological Transport Disease Models, Animal Epithelial Sodium Channel Humans Hypertension/*physiopathology Pseudohypoaldosteronism/physiopathology Renin-Angiotensin System Sodium Channels/*physiology
Pubmed
Web of science
Création de la notice
24/01/2008 13:42
Dernière modification de la notice
20/08/2019 15:11
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