A mouse model for Liddle's syndrome

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 fo r Liddle's syndrome has been generated by Cre/loxP-mediated recombination. Under normal salt diet, mice heterozygous (L/+) and homozygous (L/L) for Li ddle 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 sod ium reabsorption in distal colon and low plasma aldosterone, suggesting chr onic hypervolemia. Under high salt intake, the Liddle mice develop high BP, metabolic alkalosis, and hypokalemia accompanied by cardiac and renal hype rtrophy. This animal model reproduces to a large extent a human form of sal t-sensitive hypertension and establishes a causal relationship between diet ary salt, a gene expressed in kidney and hypertension.