Associations between human aldosterone synthase (CYP11B2) gene polymorphisms and left ventricular size, mass, and function

Aldosterone has direct and indirect effects on the heart, and genetic variations in aldosterone synthesis could therefore influence cardiac structure and function. Such variations might be associated with polymorphisms in the gene encoding aldosterone synthase (CYP11B2), the enzyme catalyzing the la...

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Bibliographic Details
Published in:Circulation (New York, N.Y.) N.Y.), 1998-02, Vol.97 (6), p.569-575
Main Authors: KUPARI, M, HAUTANEN, A, LANKINEN, L, KOSKINEN, P, VIROLAINEN, J, NIKKILA, H, WHITE, P. C
Format: Article
Language:English
Subjects:
Adult
Biological and medical sciences
Cytochrome P-450 CYP11B2 - genetics
Echocardiography
Echocardiography, Doppler
Female
Fundamental and applied biological sciences. Psychology
Genotype
Heart
Heart Ventricles - anatomy & histology
Heart Ventricles - drug effects
Humans
Male
Polymorphism, Genetic
Regression Analysis
Sodium, Dietary - pharmacology
Statistics as Topic
Ventricular Function, Left - physiology
Vertebrates: cardiovascular system
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Summary:Aldosterone has direct and indirect effects on the heart, and genetic variations in aldosterone synthesis could therefore influence cardiac structure and function. Such variations might be associated with polymorphisms in the gene encoding aldosterone synthase (CYP11B2), the enzyme catalyzing the last steps of aldosterone biosynthesis. A Finnish population sample of 84 persons (44 women) aged 36 to 37 years was studied by M-mode and Doppler echocardiography to assess left ventricular size, mass, and function. Subjects were genotyped through the use of the polymerase chain reaction for two diallelic polymorphisms in CYP11B2: one in the transcriptional regulatory region (promoter) and the other in the second intron. In multiple regression analyses, the CYP11B2 promoter genotype predicted statistically significant variations in left ventricular end-diastolic diameter (beta=.40, P
ISSN:0009-7322
1524-4539
DOI:10.1161/01.cir.97.6.569