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A mouse model for Liddle's syndrome
A mouse model for Liddle's syndrome
- 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.
- Subjects :
- medicine.medical_specialty
Heterozygote
Metabolic alkalosis
Gene Expression
Biology
Kidney
chemistry.chemical_compound
Mice
Internal medicine
Renin
medicine
Animals
Humans
Liddle's syndrome
Genes, Dominant
Aldosterone
Reabsorption
Intercellular transport
Homozygote
Sodium, Dietary
General Medicine
Syndrome
medicine.disease
Hypokalemia
Mice, Mutant Strains
Mice, Inbred C57BL
Disease Models, Animal
medicine.anatomical_structure
Endocrinology
Phenotype
chemistry
Nephrology
Hypertension
medicine.symptom
Hypervolemia
Subjects
Details
- ISSN :
- 10466673
- Volume :
- 10
- Issue :
- 12
- Database :
- OpenAIRE
- Journal :
- Journal of the American Society of Nephrology : JASN
- Accession number :
- edsair.doi.dedup.....96f56c1bc9cbb1fe491acc1975419827