Document Detail


Impaired endothelium-dependent flow-mediated vasodilation in hypertensive subjects with hyperaldosteronism.
MedLine Citation:
PMID:  15173035     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Recent studies suggest that aldosterone may impair endothelium-dependent vascular function through suppression of nitric oxide formation. Assessments of forearm blood flow or arterial compliance suggest a similar effect in humans. The present study was designed to determine whether chronic aldosterone excess in subjects with resistant hypertension impairs endothelium-dependent vascular reactivity as indexed by direct assessment of brachial artery flow-mediated dilation (FMD). METHODS AND RESULTS: Consecutive subjects (n=80) with resistant hypertension were prospectively evaluated with an early-morning ratio of plasma aldosterone to plasma renin activity and 24-hour urinary aldosterone and sodium. Changes in brachial artery diameter during reactive hyperemia were measured by high-resolution ultrasound. Hyperaldosteronism was diagnosed on the basis of a renin activity <1.0 ng x mL(-1) x h(-1), urinary aldosterone >12 microg/24 h, and urinary sodium >200 mEq/24 h. FMD was significantly lower in 36 subjects with hyperaldosteronism (1.8+/-1.3% versus 3.9+/-1.9% from baseline; P<0.0001) compared with the 44 subjects without hyperaldosteronism. FMD was negatively and significantly correlated with plasma aldosterone (r=-0.38, P=0.0006), 24-hour urinary aldosterone (r=-0.49, P<0.0001), and ratio of plasma aldosterone to plasma renin activity (r=-0.43, P<0.0001) but was independent of blood pressure, age, and body mass index. In 30 subjects, 3 months of treatment with spironolactone significantly increased FMD (2.5+/-1.7 versus 6.0+/-2.0%; P<0.0001) independently of blood pressure change. CONCLUSIONS: These data demonstrate a strong association between aldosterone excess and impaired endothelial function in human subjects as indexed by flow-mediated arterial vasodilation. These results suggest that chronic aldosteronism may have a blood pressure-independent effect on cardiovascular disease progression in subjects with resistant hypertension.
Authors:
Mari K Nishizaka; M Amin Zaman; Sharon A Green; Kerry Y Renfroe; David A Calhoun
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.     Date:  2004-06-01
Journal Detail:
Title:  Circulation     Volume:  109     ISSN:  1524-4539     ISO Abbreviation:  Circulation     Publication Date:  2004 Jun 
Date Detail:
Created Date:  2004-06-15     Completed Date:  2004-12-03     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0147763     Medline TA:  Circulation     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2857-61     Citation Subset:  AIM; IM    
Affiliation:
Vascular Biology and Hypertension Program, University of Alabama at Birmingham, Birmingham, USA. marikn@uab.edu
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MeSH Terms
Descriptor/Qualifier:
Adult
Aldosterone / urine
Brachial Artery / physiopathology,  ultrasonography
Endothelium, Vascular / physiopathology*
Female
Hemorheology*
Humans
Hyperaldosteronism / complications,  physiopathology*
Hyperemia / physiopathology
Hypertension / complications,  physiopathology*
Male
Middle Aged
Prospective Studies
Renin / blood
Sodium / urine
Vasodilation / physiology*
Grant Support
ID/Acronym/Agency:
HL-07457/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
52-39-1/Aldosterone; 7440-23-5/Sodium; EC 3.4.23.15/Renin

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


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