Epithelial sodium channel stiffens the vascular endothelium in vitro and in Liddle mice
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چکیده
Titre Epithelial sodium channel stiffens the vascular endothelium in vitro and in Liddle mice Type de publication Article de revue Auteur Jeggle, P. [1], Callies, C. [2], Tarjus, A. [3], Fassot, Céline [4], Fels, J. [5], Oberleithner, H. [6], Jaisser, F. [7], Kusche-Vihrog, K. [8] Editeur American Heart Association Type Article scientifique dans une revue à comité de lecture Année 2013 Langue Anglais Date 2013 Numéro 5 Pagination 1053 9 Volume 61 Titre de la revue Hypertension ISSN 1524-4563
منابع مشابه
Epithelial sodium channel stiffens the vascular endothelium in vitro and in Liddle mice.
Liddle syndrome, an inherited form of hypertension, is caused by gain-of-function mutations in the epithelial Na(+) channel (ENaC), the principal mediator of Na(+) reabsorption in the kidney. Accordingly, the disease pathology was ascribed to a primary renal mechanism. Whether this is the sole responsible mechanism, however, remains uncertain as dysregulation of ENaC in other tissues may also b...
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The epithelial sodium channel (ENaC) is rate limiting for Na(+) absorption in the aldosterone-sensitive distal nephron comprising the late distal convoluted tubule (DCT2), the connecting tubule (CNT), and the entire collecting duct. Liddle syndrome (pseudohyperaldosteronism), a severe form of salt-sensitive hypertension, is caused by gain-of-function mutations of ENaC, but the precise tubular s...
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Dietary salt plays a major role in the regulation of blood pressure, and the mineralocorticoid hormone aldosterone controls salt homeostasis and extracellular volume. Recent observations suggest that a small increase in plasma sodium concentration may contribute to the pressor response of dietary salt. Because endothelial cells are (i) sensitive to aldosterone, (ii) in physical contact with pla...
متن کاملMutations causing Liddle syndrome reduce sodium-dependent downregulation of the epithelial sodium channel in the Xenopus oocyte expression system.
Liddle syndrome is an autosomal dominant form of hypertension resulting from deletion or missense mutations of a PPPxY motif in the cytoplasmic COOH terminus of either the beta or gamma subunit of the epithelial Na channel (ENaC). These mutations lead to increased channel activity. In this study we show that wild-type ENaC is downregulated by intracellular Na+, and that Liddle mutants decrease ...
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