Genetic Variants in the Epithelial Sodium Channel in Relation to Aldosterone and Potassium Excretion and Risk for Hypertension

• Published in: Hypertension (Dallas, Tex. 1979) Tex. 1979), 1999-10, Vol.34 (4, Part 1), p.631-637
• Main Authors: Ambrosius, Walter T, Bloem, Laura J, Zhou, Lifen, Rebhun, John F, Snyder, Peter M, Wagner, Mary Anne, Guo, Chunlu, Pratt, J Howard
• Format: Article
• Language: English
• Subjects: Adolescent; African Continental Ancestry Group - genetics; Aldosterone - blood; Aldosterone - metabolism; Aldosterone - urine; Arterial hypertension. Arterial hypotension; Biological and medical sciences; Blood and lymphatic vessels; Blood Pressure - genetics; Cardiology. Vascular system; Clinical manifestations. Epidemiology. Investigative techniques. Etiology; Cohort Studies; Epithelial Cells - metabolism; European Continental Ancestry Group - genetics; Exons; Female; Humans; Hypertension - genetics; Male; Medical sciences; Potassium - blood; Potassium - metabolism; Potassium - urine; Renin - metabolism; Risk Factors; Sodium Channels - genetics; Sodium Channels - metabolism
• ISSN: 0194-911X; 1524-4563
• DOI: 10.1161/01.hyp.34.4.631

Renin and aldosterone secretion is often lower in blacks than in whites, characteristics that resemble a milder form of Liddle syndrome in which a mutation in the amiloride-sensitive epithelial sodium channel (ENaC) of the kidney results in enhanced resorption of sodium. In the present study, we looked for evidence that the intrinsic level of ENaC activity is indeed higher in blacks than in whites. In overnight urine samples collected from young people (249 white and 181 black subjects, mean age 13.4 years), the urinary aldosterone/potassium ratio, which is typically very low in Liddle syndrome, was lower in blacks than in whites0.421±0.024 (mean±SE) versus 0.582±0.016 nmol/mmol (P