| Impaired endothelium-dependent flow-mediated vasodilation in hypertensive subjects with hyperaldosteronism. | |
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MedLine Citation:
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PMID: 15173035 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Mari K Nishizaka; M Amin Zaman; Sharon A Green; Kerry Y Renfroe; David A Calhoun |
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Publication Detail:
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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:
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Title: Circulation Volume: 109 ISSN: 1524-4539 ISO Abbreviation: Circulation Publication Date: 2004 Jun |
Date Detail:
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Created Date: 2004-06-15 Completed Date: 2004-12-03 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 0147763 Medline TA: Circulation Country: United States |
Other Details:
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Languages: eng Pagination: 2857-61 Citation Subset: AIM; IM |
Affiliation:
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Vascular Biology and Hypertension Program, University of Alabama at Birmingham, Birmingham, USA. marikn@uab.edu |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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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:
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HL-07457/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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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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