This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Baker, E. H. Articles by MacGregor, G. A. Search for Related Content PubMed PubMed Citation Articles by Baker, E. H. Articles by MacGregor, G. A. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Medline Plus Health Information High Blood Pressure Related Collections Other hypertension Other etiology

(Hypertension. 1999;33:1031-1035.)
© 1999 American Heart Association, Inc.

Scientific Contributions

Epithelial Sodium Channel Activity Is Not Increased in Hypertension in Whites

Emma H. Baker; A. James Portal; Teresa A. McElvaney; Alison M. Blackwood; Michelle A. Miller; Nirmala D. Markandu; Graham A. MacGregor

From the Blood Pressure Unit (E.H.B., A.J.P., T.A.M., A.M.B., M.A.M., N.D.M., G.A.M.) and Department of Pharmacology (E.H.B.), St George's Hospital Medical School, London, UK.

Correspondence and reprint requests to Dr Emma Baker, Department of Pharmacology and Clinical Pharmacology, St George's Hospital and Medical School, Cranmer Terrace, London, SW17 0RE, UK. E-mail ebaker{at}sghms.ac.uk

Abstract—Abnormal renal sodium transport causing excess reabsorption of sodium may be one mechanism that causes high blood pressure. For example, increased activity of epithelial sodium channels in the distal tubule is the cause of high blood pressure in Liddle's syndrome, a rare familial form of hypertension. We have shown that the increase in sodium channel activity can be detected in the nose using transepithelial potential difference measurements in 1 family with Liddle's syndrome. We therefore used nasal potential difference measurements to look for increased sodium channel activity in white patients with essential hypertension. Transnasal potential difference was measured in 42 white hypertensive (HT) subjects and 38 white normotensive (NT) subjects before and after topical application of 10^-4 mol/L of amiloride. There was no difference in maximum potential between HT and NT subjects (HT, -18.8±0.9 mV; NT, -18.2±1.0 mV) (values mean±SEM; lumen-negative with respect to the submucosa). However, the postamiloride potential was significantly higher (HT, -12.6±0.7 mV; NT, -10.5±0.7 mV; P=0.015) and the change in potential in response to amiloride significantly lower (HT, 6.2±0.5 mV, 33.1±2.0%; NT, 7.7±0.6 mV, 41.9±2.0%; P=0.046 and 0.003, respectively) in HT than in NT subjects. These results suggest that sodium channel activity is not increased in whites with essential hypertension and indicate that sodium channel overactivity similar to that seen in Liddle's syndrome is unlikely to be the cause of high blood pressure in this group. Increased postamiloride potential may reflect increased activity of chloride channels or amiloride-insensitive sodium channels.

Key Words: hypertension, essential • whites • sodium channels • amiloride • nasal mucosa • membrane potentials