title: Angiotensin converting enzyme gene polymorphism predicts blood pressure response to angiotensin II receptor type 1 antagonist treatment in hypertensive patients.
abstract: OBJECTIVE
  To determine whether polymorphisms in the renin-angiotensin system can predict blood pressure-lowering response to antihypertensive treatment; more specifically, in response to treatment with irbesartan or atenolol.
  
  
  METHODS
  Eighty-six patients with hypertension were randomized to double-blind treatment with either the angiotensin II type 1 receptor antagonist irbesartan or the beta1 adrenergic receptor blocker atenolol and followed for 3 months. We analysed angiotensinogen T174M and M235T, angiotensin converting enzyme (ACE) I/D and angiotensin II type 1 receptor A1166C polymorphisms and related them to blood pressure reduction.
  
  
  RESULTS
  The mean reductions in blood pressure were similar for both treatments. In the irbesartan group, individuals homozygous for the ACE gene I allele showed a greater reduction in diastolic blood pressure, exceeding those with the D allele (-18 +/- 11 SD versus -7 +/- 10 mmHg, P = 0.0096). This was not the case during treatment with atenolol, and the interaction term between type of treatment and ACE II genotype was significant (P = 0.0176). The angiotensinogen and angiotensin II type 1 receptor polymorhisms were not related to the response to treatment.
  
  
  CONCLUSIONS
  ACE genotyping predicted the blood pressure-lowering response to antihypertensive treatment with irbesartan but not atenolol. Thus, specific genotypes might predict the response to specific antihypertensive treatment.
authors.affiliation: Department of Internal Medicine, Uppsala University Hospital, Uppsala, Sweden. lisa.kurland@medsci.uu.se
authors.forename: L
authors.initials: L
authors.lastname: Kurland
authors.forename: H
authors.initials: H
authors.lastname: Melhus
authors.forename: J
authors.initials: J
authors.lastname: Karlsson
authors.forename: T
authors.initials: T
authors.lastname: Kahan
authors.forename: K
authors.initials: K
authors.lastname: Malmqvist
authors.forename: K P
authors.initials: KP
authors.lastname: Ohman
authors.forename: F
authors.initials: F
authors.lastname: Nyström
authors.forename: A
authors.initials: A
authors.lastname: Hägg
authors.forename: L
authors.initials: L
authors.lastname: Lind
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D057911:Angiotensin Receptor Antagonists; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D001262:Atenolol / Q000627:therapeutic use; D001713:Biphenyl Compounds / Q000627:therapeutic use*; D001794:Blood Pressure / Q000187:drug effects*; D004311:Double-Blind Method; D005260:Female; D005544:Forecasting; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000235:genetics*; D000077405:Irbesartan; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic / Q000502:physiology*; D044140:Receptor, Angiotensin, Type 1; D013777:Tetrazoles / Q000627:therapeutic use*; 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; D001262:Atenolol; D007703:Peptidyl-Dipeptidase A; D000077405:Irbesartan