In Liddle Syndrome, Epithelial Sodium Channel Is Hyperactive Mainly in the Early Part of the Aldosterone-Sensitive Distal Nephron-Reference-Cited by-同舟云学术

In Liddle Syndrome, Epithelial Sodium Channel Is Hyperactive Mainly in the Early Part of the Aldosterone-Sensitive Distal Nephron

Published:2016-06 Issue:6 Volume:67 Page:1256-1262
ISSN:0194-911X
Container-title:Hypertension
language:en
Short-container-title:Hypertension

Author:

Nesterov Viatcheslav¹,Krueger Bettina¹,Bertog Marko¹,Dahlmann Anke¹,Palmisano Ralf¹,Korbmacher Christoph¹

Affiliation:

1. From the Institut für Zelluläre und Molekulare Physiologie (V.N., B.K., M.B., C.K.), Universitätsklinikum Erlangen, Medizinische Klinik 4–Nephrologie und Hypertensiologie (A.D.), and Optical Imaging Center Erlangen (OICE) (R.P.), Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), Erlangen, Germany.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Internal Medicine

Reference37 articles.

1. A familial renal disorder simulating primary aldosteronism but with negligible aldosterone secretion.;Liddle GW;Trans Assoc Am Physicians,1963

2. A mutation in the epithelial sodium channel causing Liddle disease increases channel activity in the Xenopus laevis oocyte expression system.

3. Epithelial sodium channel (ENaC) and the control of blood pressure

4. Liddle syndrome: An autosomal dominant form of human hypertension

5. Aldosterone responsiveness of the epithelial sodium channel (ENaC) in colon is increased in a mouse model for Liddle's syndrome

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