Document Detail


Increased levels of oxidative stress, subclinical inflammation, and myocardial fibrosis markers in primary aldosteronism patients.
MedLine Citation:
PMID:  20683341     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Patients with primary aldosteronism experience greater left ventricular hypertrophy and a higher frequency of cardiovascular events than do essential hypertensive patients with comparable blood pressure levels. Aldosterone has been correlated with increased oxidative stress, endothelial inflammation, and fibrosis, particularly in patients with heart disease.
AIM: To evaluate oxidative stress, subclinical endothelial inflammation, and myocardial fibrosis markers in patients with primary aldosteronism and essential hypertension. DESIGN AND INDIVIDUALS: We studied 30 primary aldosteronism patients and 70 control essential hypertensive patients, matched by age, sex and median blood pressure. For all patients, we measured the serum levels of aldosterone, plasma renin activity, malondialdehyde (MDA), xanthine oxidase, metalloproteinase-9, ultrasensitive C-reactive protein and amino terminal propeptides of type I (PINP), and type III procollagen. We also evaluated the effect of PA treatment in 19 PA individuals.
RESULTS: PA patients showed elevated levels of MDA (1.70 ± 0.53 versus 0.94 ± 0.65 μmol/l, P <0.001) and PINP (81.7 ± 50.6 versus 49.7 ± 27 mg/l, P = 0.002) compared with essential hypertensive controls. We found a positive correlation between MDA, PINP, and the serum aldosterone/plasma renin activity ratio in primary aldosteronism patients. Clinically, treating primary aldosteronism patients decreased MDA and PINP levels.
CONCLUSION: We detected higher levels of MDA and PINP in primary aldosteronism patients, suggesting increased oxidative stress and myocardial fibrosis in these individuals. Treating primary aldosteronism patients reduced MDA and PINP levels, which may reflect the direct effect of aldosterone greater than endothelial oxidative stress and myocardial fibrosis, possibly mediated by a mineralocorticoid receptor.
Authors:
Carlos B Stehr; Rosemarie Mellado; Maria P Ocaranza; Cristian A Carvajal; Lorena Mosso; Elia Becerra; Margarita Solis; Lorena García; Sergio Lavandero; Jorge Jalil; Carlos E Fardella
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of hypertension     Volume:  28     ISSN:  1473-5598     ISO Abbreviation:  J. Hypertens.     Publication Date:  2010 Oct 
Date Detail:
Created Date:  2010-09-16     Completed Date:  2011-01-18     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8306882     Medline TA:  J Hypertens     Country:  England    
Other Details:
Languages:  eng     Pagination:  2120-6     Citation Subset:  IM    
Affiliation:
Department of Endocrinology, Faculty of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile.
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MeSH Terms
Descriptor/Qualifier:
Adult
Aldosterone / blood
Biological Markers / blood
Blood Pressure / physiology
C-Reactive Protein / metabolism
Cardiomyopathies / blood*,  physiopathology
Case-Control Studies
Female
Fibrosis / blood,  physiopathology
Humans
Hyperaldosteronism / blood*,  physiopathology*
Hypertension / blood*,  physiopathology*
Inflammation / blood*,  physiopathology
Male
Malondialdehyde / blood
Middle Aged
Oxidative Stress / physiology*
Peptide Fragments / blood
Procollagen / blood
Renin / blood
Chemical
Reg. No./Substance:
0/Biological Markers; 0/Peptide Fragments; 0/Procollagen; 0/procollagen Type I N-terminal peptide; 52-39-1/Aldosterone; 542-78-9/Malondialdehyde; 9007-41-4/C-Reactive Protein; EC 3.4.23.15/Renin

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


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