A mouse model for Liddle's syndrome

Détails

ID Serval
serval:BIB_27A74C9C2D1D
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
A mouse model for Liddle's syndrome
Périodique
Journal of the American Society of Nephrology
Auteur(s)
Pradervand  S., Wang  Q., Burnier  M., Beermann  F., Horisberger  J. D., Hummler  E., Rossier  B. C.
ISSN
1046-6673 (Print)
Statut éditorial
Publié
Date de publication
12/1999
Volume
10
Numéro
12
Pages
2527-33
Notes
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Dec
Résumé
Liddle's syndrome (or pseudoaldosteronism) is an autosomal dominant form of salt-sensitive hypertension, due to abnormal sodium transport by the renal tubule. To study the pathophysiology of salt sensitivity, a mouse model for Liddle's syndrome has been generated by Cre/loxP-mediated recombination. Under normal salt diet, mice heterozygous (L/+) and homozygous (L/L) for Liddle mutation (L) develop normally during the first 3 mo of life. In these mice, BP is not different from wild type despite evidence for increased sodium reabsorption in distal colon and low plasma aldosterone, suggesting chronic hypervolemia. Under high salt intake, the Liddle mice develop high BP, metabolic alkalosis, and hypokalemia accompanied by cardiac and renal hypertrophy. This animal model reproduces to a large extent a human form of salt-sensitive hypertension and establishes a causal relationship between dietary salt, a gene expressed in kidney and hypertension.
Mots-clé
Animals Disease Models, Animal Gene Expression Genes, Dominant Heterozygote Homozygote Humans Hypertension/etiology/*genetics/physiopathology Kidney/physiopathology Mice Mice, Inbred C57BL Mice, Mutant Strains Phenotype Renin/genetics Sodium, Dietary/administration & dosage Syndrome
Pubmed
Web of science
Création de la notice
24/01/2008 13:38
Dernière modification de la notice
20/08/2019 14:06
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