Document Detail

Aldosterone-related genetic effects in hypertension.
MedLine Citation:
PMID:  10981163     Owner:  NLM     Status:  MEDLINE    
Our basic understanding of Na(+) transport mechanisms provides unique insights into epithelial transport processes. Unusual clinical syndromes can arise from mutations of these ion transporters. These genetic disorders affect Na(+) balance, resulting in both N(a+) retaining and Na(+) wasting conditions. A major focus has been the epithelial sodium channel (ENaC), which can be activated by mutations (eg, Liddle's syndrome), changes in the response to mineralocorticoids (apparent mineralocorticoid excess syndrome), or production of mineralocorticoids (glucocorticoid-remediable aldosteronism). As a result, we now have clearly defined Mendelian syndromes in which ENaC activity is "dysregulated." This dysregulation leads to systemic hypertension associated with suppressed plasma renin activity, which can be attributed to a primary renal mechanism. Applying these insights to the far more common disorder of low-renin hypertension may shed new light on the underlying pathophysiology of this common form of human hypertension.
D G Warnock
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.; Review    
Journal Detail:
Title:  Current hypertension reports     Volume:  2     ISSN:  1522-6417     ISO Abbreviation:  Curr. Hypertens. Rep.     Publication Date:  2000 Jun 
Date Detail:
Created Date:  2000-10-13     Completed Date:  2000-10-13     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  100888982     Medline TA:  Curr Hypertens Rep     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  295-301     Citation Subset:  IM    
Division of Nephrology, University of Alabama at Birmingham, 1530 3rd Avenue South, THT 647, Birmingham, AL 35294-0007, USA.
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MeSH Terms
Aldosterone / genetics*
Aldosterone Synthase / genetics
Epithelium / metabolism
Hyperaldosteronism / genetics
Hypertension / blood,  genetics*,  metabolism,  physiopathology
Ion Transport / genetics
Kidney / metabolism
Mineralocorticoids / genetics
Mutation / genetics
Renin / blood,  physiology
Sodium / metabolism
Sodium Channels / genetics
Grant Support
Reg. No./Substance:
0/Mineralocorticoids; 0/Sodium Channels; 52-39-1/Aldosterone; 7440-23-5/Sodium; EC Synthase; EC

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