title: Aldosterone synthase (CYP11B2) -344 C/T polymorphism is related to antihypertensive response: result from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA) trial.
abstract: BACKGROUND
  Our aim was to determine whether the aldosterone synthase (CYP11B2) -344 C/T polymorphism was associated with the blood pressure (BP)-lowering response to antihypertensive treatment.
  
  
  METHODS
  Patients with mild-to-moderate primary hypertension and left ventricular hypertrophy were randomized in a double-blind study to receive treatment with either the angiotensin II type 1 (AT1) receptor antagonist irbesartan (n = 43), or the beta1-adrenergic receptor blocker atenolol (n = 43). The aldosterone synthase (CYP11B2) -344 C/T polymorphism was analyzed using solid-phase minisequencing and related to BP reduction after 3 months treatment. Serum aldosterone levels were measured.
  
  
  RESULTS
  After 3 months treatment the mean reductions in BP were similar for both treatment groups. When assessing the systolic BP reduction in the irbesartan group, patients with the TT variant had a more pronounced reduction (-21 +/- 19 SD mm Hg, n = 17) than both the TC (-14 +/- 18 mm Hg, n= 18) and CC (0 +/- 17 mm Hg, n = 8) genotypes (P = .04). There was no association between this polymorphism and the diastolic BP response. The -344 C/T polymorphism was not associated with the BP response to atenolol. Nor was it related to the baseline serum aldosterone level.
  
  
  CONCLUSIONS
  The aldosterone synthase -344 C/T polymorphism was related to the BP-lowering response in hypertensive patients treated with the AT1-receptor antagonist irbesartan.
authors.affiliation: Department of Internal Medicine, Uppsala University Hospital, Sweden. lisa.kurland@medsci.uu.se
authors.forename: Lisa
authors.initials: L
authors.lastname: Kurland
authors.forename: Håkan
authors.initials: H
authors.lastname: Melhus
authors.forename: Julia
authors.initials: J
authors.lastname: Karlsson
authors.forename: Thomas
authors.initials: T
authors.lastname: Kahan
authors.forename: Karin
authors.initials: K
authors.lastname: Malmqvist
authors.forename: Peter
authors.initials: P
authors.lastname: Ohman
authors.forename: Fredrik
authors.initials: F
authors.lastname: Nyström
authors.forename: Anders
authors.initials: A
authors.lastname: Hägg
authors.forename: Lars
authors.initials: L
authors.lastname: Lind
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use*; D000450:Aldosterone / Q000097:blood; D057911:Angiotensin Receptor Antagonists; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D001262:Atenolol / Q000627:therapeutic use*; D001483:Base Sequence / Q000235:genetics; D001713:Biphenyl Compounds / Q000627:therapeutic use*; D001794:Blood Pressure; D019405:Cytochrome P-450 CYP11B2 / Q000235:genetics*; D003596:Cytosine; D004311:Double-Blind Method; D005260:Female; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000188:drug therapy* / Q000235:genetics* / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000188:drug therapy; D000077405:Irbesartan; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic; D044140:Receptor, Angiotensin, Type 1; D013777:Tetrazoles / Q000627:therapeutic use*; D013941:Thymine; D016896:Treatment Outcome
chemical_list: D000319:Adrenergic beta-Antagonists; D057911:Angiotensin Receptor Antagonists; D000959:Antihypertensive Agents; D001713:Biphenyl Compounds; D044140:Receptor, Angiotensin, Type 1; D013777:Tetrazoles; D000450:Aldosterone; D001262:Atenolol; D003596:Cytosine; D019405:Cytochrome P-450 CYP11B2; D000077405:Irbesartan; D013941:Thymine