title: Aldosterone synthase (CYP11B2) -344 C/T polymorphism is associated with left ventricular structure in human arterial hypertension.
abstract: OBJECTIVE
  This study examined the association between the -344 C/T polymorphism of the human aldosterone synthase promoter and left ventricular structure in arterial hypertension.
  
  
  BACKGROUND
  Because of conflicting results from different studies, the mechanism of such an association, if any, has not been determined.
  
  
  METHODS
  We examined the aldosterone synthase promoter genotype in 120 young (age: 26 +/- 3 years) male, white subjects with normal or mildly elevated blood pressure. Left ventricular structural parameters and urinary sodium excretion over 24 h before and after additional oral sodium load (6 g/day over 1 week) were determined.
  
  
  RESULTS
  Hypertensive subjects with the CC genotype had a greater left ventricular end-diastolic diameter but smaller relative wall thickness than those with the TT genotype (54 +/- 2 vs. 50 +/- 4 mm, and 0.37 +/- 0.07 vs. 0.44 +/- 0.06 mm, respectively; p < 0.05). Hypertensive subjects with the TT genotype (n = 15) had a greater increase in urinary sodium excretion after oral sodium load than those with the CC genotype (n = 11) (135 +/- 95 vs. 24 +/- 133 mmol/liter/day; p < 0.05). Serum aldosterone levels were found to be decreased after oral sodium load in hypertensive subjects with the TT and CT genotypes only (-37 +/- 45 and -38 +/- 51 pg/ml, respectively; all p < 0.01) but not in those with the CC genotype (-12 +/- 30 pg/ml, n.s.). Such differences were not found in normotensive subjects.
  
  
  CONCLUSIONS
  Hypertensive subjects with the -344 CC genotype of the aldosterone synthase promoter are characterized by a pattern of early eccentric left ventricular hypertrophy. Differences in renal sodium handling across the genotypes might contribute to this finding.
authors.affiliation: Department of Medicine/Nephrology, University of Erlangen, Nürnberg, Germany.
authors.forename: C
authors.initials: C
authors.lastname: Delles
authors.forename: J
authors.initials: J
authors.lastname: Erdmann
authors.forename: J
authors.initials: J
authors.lastname: Jacobi
authors.forename: K F
authors.initials: KF
authors.lastname: Hilgers
authors.forename: E
authors.initials: E
authors.lastname: Fleck
authors.forename: V
authors.initials: V
authors.lastname: Regitz-Zagrosek
authors.forename: R E
authors.initials: RE
authors.lastname: Schmieder
mesh_terms: D000328:Adult; D019405:Cytochrome P-450 CYP11B2 / Q000235:genetics*; D005838:Genotype; D006801:Humans; D006973:Hypertension / Q000000981:diagnostic imaging / Q000201:enzymology* / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000201:enzymology* / Q000503:physiopathology; D007668:Kidney / Q000503:physiopathology; D008297:Male; D011110:Polymorphism, Genetic; D012084:Renin-Angiotensin System / Q000502:physiology; D012964:Sodium / Q000652:urine; D014463:Ultrasonography
chemical_list: D012964:Sodium; D019405:Cytochrome P-450 CYP11B2