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The epithelial Na+ channel: cell surface insertion and retrieval in Na+ homeostasis and hypertension
Journal article   Open access   Peer reviewed

The epithelial Na+ channel: cell surface insertion and retrieval in Na+ homeostasis and hypertension

Peter M Snyder
Endocrine reviews, Vol.23(2), pp.258-275
04/2002
DOI: 10.1210/edrv.23.2.0458
PMID: 11943747
url
https://doi.org/10.1210/edrv.23.2.0458View
Published (Version of record) Open Access

Abstract

The epithelial Na+ channel (ENaC) forms the pathway for Na+ absorption in the kidney collecting duct and other epithelia. Dominant gain-of-function mutations cause Liddle's syndrome, an inherited form of hypertension resulting from excessive renal Na+ absorption. Conversely, loss-of-function mutations cause pseudohypoaldosteronism type I, a disorder of salt wasting and hypotension. Thus, ENaC has a critical role in the maintenance of Na+ homeostasis and blood pressure control. Altered Na+ absorption in the lung may also contribute to the pathogenesis of cystic fibrosis. Epithelial Na+ absorption is regulated in large part by mechanisms that control the expression of ENaC at the cell surface. Nedd4, a ubiquitin protein ligase, binds to ENaC and targets the channel for endocytosis and degradation. Liddle's syndrome mutations disrupt the interaction between ENaC and Nedd4, resulting in an increase in the number of ENaC channels at the cell surface. Aldosterone and vasopressin also regulate Na+ absorption to defend against hypotension and hypovolemia. Both hormones increase the expression of ENaC at the cell surface. The goal of this review is to summarize recent data on the regulation of ENaC expression at the cell surface.
 Animals Epithelium - metabolism Homeostasis - physiology Humans Sodium Channels - metabolism Hypertension - genetics Sodium - metabolism Hypertension - metabolism

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