Document Detail

Renin-angiotensin-aldosterone system in cirrhosis.
MedLine Citation:
PMID:  7000629     Owner:  NLM     Status:  MEDLINE    
According to traditional concepts, ascites formation and portal hypertension in cirrhosis lead to a deficit in the 'effective' extracellular fluid (ECF) and blood volumes respectively. The renin-angiotensin-aldosterone (RAA) system is thus stimulated and the kidneys retain fluid as a homeostatic mechanism to restore the ECF and blood volumes. Recent studies, however, show that approximately two-thirds of patients with ascites do not have a stimulated RAA system and in those without clinical evidence of fluid retention the RAA system is actually suppressed. These findings are incompatible with the concepts of reduced effective ECF and blood volumes. Despite the fact that most patients retaining sodim and accumulating ascites have a normal plasma aldosterone concentration, other evidence strongly suggests a dominant role for aldosterone in the regulation of renal sodium excretion. There might therefore be an increased renal tubular sensitivity to aldosterone in cirrhosis. For the one-third of patients with ascites who do have a stimulated RAA system this may well be a response to reduced effective ECF and/or blood volumes in accord with traditional concepts.
S P Wilkinson; R Williams
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Gut     Volume:  21     ISSN:  0017-5749     ISO Abbreviation:  Gut     Publication Date:  1980 Jun 
Date Detail:
Created Date:  1981-01-16     Completed Date:  1981-01-16     Revised Date:  2010-09-13    
Medline Journal Info:
Nlm Unique ID:  2985108R     Medline TA:  Gut     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  545-54     Citation Subset:  AIM; IM    
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MeSH Terms
Aldosterone / metabolism*
Angiotensin II / metabolism*
Ascites / etiology
Blood Volume
Edema / etiology
Extracellular Space / metabolism
Kidney Failure, Acute / etiology
Liver Cirrhosis / complications,  metabolism*
Renin / metabolism*
Sodium / metabolism
Reg. No./Substance:
11128-99-7/Angiotensin II; 52-39-1/Aldosterone; 7440-23-5/Sodium; EC

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

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