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A mouse model for Liddle's syndrome

A mouse model for Liddle's syndrome

Authors :
Bernard C. Rossier
Sylvain Pradervand
Jean Daniel Horisberger
Edith Hummler
Friedrich Beermann
Michel Burnier
Qing Wang
Source :
Journal of the American Society of Nephrology : JASN. 10(12)
Publication Year :
1999

Abstract

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.

Details

ISSN :
10466673
Volume :
10
Issue :
12
Database :
OpenAIRE
Journal :
Journal of the American Society of Nephrology : JASN
Accession number :
edsair.doi.dedup.....96f56c1bc9cbb1fe491acc1975419827