Document Detail


Lack of association between a polymorphism of the aldosterone synthase gene and left ventricular structure.
MedLine Citation:
PMID:  10226090     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Cardiac growth and function may be modulated in part by trophic effects of neurohormones. Specifically, aldosterone has been shown to stimulate the growth of cardiac myocytes and the accumulation of cardiac extracellular matrix proteins. Moreover, a variant of the aldosterone synthase gene (a cytosine/thymidine exchange at position -344 in the transcriptional regulatory region) has been associated with enlargement and disturbed filling of the left ventricle (LV) in a small sample of young white adults. The aim of the present study was to reinvestigate the implications of aldosterone synthase -344C/T allele status for serum aldosterone levels, blood pressure, and LV structure and function in large population-based samples. METHODS AND RESULTS: Individuals who participated in the echocardiographic substudy of the third MONICA (MONitoring trends and determinants in CArdiovascular disease) survey (n=1445) or in the second follow-up of the first MONICA survey (n=562) were studied by standardized anthropometric, echocardiographic, and biochemical measurements as well as genotyping for aldosterone synthase -344C/T allele status. In both surveys, the distribution of sex, age, arterial blood pressure, and body mass index was homogeneous in the aldosterone synthase genotype groups. Echocardiographic LV wall thicknesses, dimensions, and mass indexes were not significantly associated with a specific aldosterone synthase genotype. Likewise, no association was detectable with echocardiographic measures of LV systolic or diastolic function. Data were consistent in both samples and not materially different in subgroups defined by age, sex, or intake of antihypertensive medication. Finally, no significant association was observed for aldosterone synthase allele status and serum aldosterone levels in the group of 562 individuals. CONCLUSIONS: The data are not in favor of a significant contribution of the C/T exchange at position -344 in the aldosterone synthase transcriptional regulatory region to the variability of serum aldosterone levels, blood pressure, or cardiac size or function as found in 2 white population-based samples.
Authors:
H Schunkert; C Hengstenberg; S R Holmer; U Broeckel; A Luchner; M W Muscholl; S Kürzinger; A Döring; H W Hense; G A Riegger
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Circulation     Volume:  99     ISSN:  1524-4539     ISO Abbreviation:  Circulation     Publication Date:  1999 May 
Date Detail:
Created Date:  1999-05-20     Completed Date:  1999-05-20     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0147763     Medline TA:  Circulation     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  2255-60     Citation Subset:  AIM; IM    
Affiliation:
Klinik und Poliklinik für Innere Medizin II, University of Regensburg, Regensburg, Germany. heribert.schunkert@klinik.uni-regensburg.de
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MeSH Terms
Descriptor/Qualifier:
Adult
Aged
Aldosterone / blood
Aldosterone Synthase / genetics*
Echocardiography
Female
Genotype
Humans
Hypertrophy, Left Ventricular / etiology*
Male
Middle Aged
Polymorphism, Genetic*
Chemical
Reg. No./Substance:
52-39-1/Aldosterone; EC 1.14.15.4/Aldosterone Synthase

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


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