title: Association of -344/T/C aldosterone synthase polymorphism (CYP11B2) with left ventricular structure and humoral parameters in young normotensive men.
abstract: BACKGROUND
  Aldosterone plays an important role in development of left ventricular (LV) hypertrophy and myocardial fibrosis. We assessed the influence of the T-344C polymorphism of aldosterone synthase - the rate-limiting enzyme in aldosterone biosynthesis - on the structure of the left ventricle in young normotensive men.
  
  
  METHODS
  The population included 113 normotensive mid-European Caucasian men aged 18-40 years (mean 27 +/- 5 years). The genotype was assessed using polymerase chain reaction with subsequent cleavage with restriction enzyme HAEIII (restriction fragment length polymorphism method) and visualization with ethidium bromide. Plasma renin activity (PRA) and plasma aldosterone were measured. All subjects were examined by echocardiography and LV mass was assessed by using M-mode based ASE formula.
  
  
  RESULTS
  The distribution of the genotypes was TT 23%:TC 55%:CC 22%. There were no differences in blood pressure among the groups. Men with the TT genotype had significantly higher levels of PRA (2.7 +/- 1.7 vs 1.8 +/- 1.0 vs 1.8 +/- 1.1 ng/ml/h, p < 0.01) and slightly higher plasma levels of aldosterone (113 +/- 64 vs 93 +/- 43 vs 87 +/- 39 pg/ml, p = 0,12). In the whole population, LV mass index (LVMI) did not differ significantly among the genotypes (92 +/- 16 vs 86 +/- 18 vs 84 +/- 16 g/m, p=0.20). In the population divided according to PRA, subjects with high renin had significantly higher LVMI in presence of the TT genotype (95 +/- 17 vs 84 +/- 16 vs 81 +/- 15 g/m, p < 0.05).
  
  
  CONCLUSIONS
  In agreement with previous studies, we found that the TT genotype of T-344C polymorphism of aldosterone synthase gene was associated with significantly higher levels of PRA in normotensive men. In subjects with high PRA, the TT genotype was associated with higher values of the LVMI.
authors.affiliation: 2nd Department of Internal Medicine, 1st School of Medicine, Charles University, Prague, Czech Republic. shel@lf1.cuni.cz
authors.forename: Samuel
authors.initials: S
authors.lastname: Heller
authors.forename: Ales
authors.initials: A
authors.lastname: Linhart
authors.forename: Antonín
authors.initials: A
authors.lastname: Jindra
authors.forename: Marie
authors.initials: M
authors.lastname: Jáchymová
authors.forename: Karel
authors.initials: K
authors.lastname: Horký
authors.forename: Jan
authors.initials: J
authors.lastname: Peleska
authors.forename: Zuzana
authors.initials: Z
authors.lastname: Hlubocká
authors.forename: Vera
authors.initials: V
authors.lastname: Umnerová
authors.forename: Michael
authors.initials: M
authors.lastname: Aschermann
mesh_terms: D000293:Adolescent; D000328:Adult; D000450:Aldosterone / Q000097:blood; D000483:Alleles; D001483:Base Sequence; D001794:Blood Pressure; D003430:Cross-Sectional Studies; D019405:Cytochrome P-450 CYP11B2 / Q000235:genetics*; D004247:DNA / Q000235:genetics; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000201:enzymology* / Q000235:genetics* / Q000503:physiopathology; D008297:Male; D020641:Polymorphism, Single Nucleotide; D012083:Renin / Q000097:blood
chemical_list: D000450:Aldosterone; D004247:DNA; D019405:Cytochrome P-450 CYP11B2; D012083:Renin