Document Detail

Epithelial Na+ channel (ENaC), hormones, and hypertension.
MedLine Citation:
PMID:  20460373     Owner:  NLM     Status:  MEDLINE    
This minireview examines both the basic science and clinical observations over the past 20 years to show how and why overstimulation of the amiloride-sensitive epithelial Na(+) channel (ENaC) expressed by epithelial principal cells of the renal collecting duct may be responsible for a large portion of hypertension in modern society. This idea is based on the finding that, in Liddle syndrome, a mutation of the beta- and/or gamma-subunits of ENaC produces an activated ion channel, in turn resulting in severe hypertension that is resistant to most forms of conventional antihypertensive therapy. ENaC can also be stimulated to conduct sodium by two hormones: aldosterone and insulin. These hormones are both often elevated in obese individuals with therapy-resistant hypertension. Thus, overstimulation of ENaC by metabolic abnormalities in obese individuals may be a likely cause of the hypertension that accompanies obesity. The molecular mechanisms underlying both Liddle syndrome and obesity-related hypertension are different (i.e. genetic and hormonal, respectively), but both have the same end result, namely increased ENaC activity.
James K Bubien
Related Documents :
2180043 - Aldosterone-producing tumors (conn's syndrome).
8175163 - Diurnal blood pressure variation and hormonal correlates in fatal familial insomnia.
25005313 - Neonatal decompensation before surgery in hypoplastic left heart syndrome: a case contr...
Publication Detail:
Type:  Journal Article; Review     Date:  2010-05-11
Journal Detail:
Title:  The Journal of biological chemistry     Volume:  285     ISSN:  1083-351X     ISO Abbreviation:  J. Biol. Chem.     Publication Date:  2010 Jul 
Date Detail:
Created Date:  2010-07-26     Completed Date:  2010-09-14     Revised Date:  2013-05-29    
Medline Journal Info:
Nlm Unique ID:  2985121R     Medline TA:  J Biol Chem     Country:  United States    
Other Details:
Languages:  eng     Pagination:  23527-31     Citation Subset:  IM    
Department of Physiology and Biophysics, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Aldosterone / metabolism
Antihypertensive Agents / pharmacology
Epithelial Sodium Channels / chemistry*
Hormones / metabolism*
Hypertension / metabolism*
Insulin / metabolism
Kidney / metabolism
Models, Biological
Nitric Oxide / metabolism
Obesity / metabolism
Potassium Channels / metabolism
Reg. No./Substance:
0/Antihypertensive Agents; 0/Epithelial Sodium Channels; 0/Hormones; 0/Insulin; 0/Potassium Channels; 10102-43-9/Nitric Oxide; 52-39-1/Aldosterone

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Parallel in vivo and in vitro selection using phage display identifies protease dependent tumor targ...
Next Document:  Chronic alcohol exposure increases circulating bioactive oxidized phospholipids.