title: A common polymorphism in the renin angiotensin system is associated with differential outcome of antihypertensive pharmacotherapy prescribed to Brazilian older women.
abstract: BACKGROUND
  Since variations on the renin angiotensin (RA) system tend to exert effects on blood pressure, we investigated the association of the common ACE and AT1R polymorphisms with response to a multivariate pharmacotherapy.
  
  
  METHODS
  This prospective study involved 169 hypertensive, community-dwelling older women. Genotypes were obtained by length analysis or direct sequencing of PCR products. Blood pressure-lowering pharmacotherapy was conducted according to current Brazilian Guidelines on Hypertension.
  
  
  RESULTS
  Genotype frequencies were in agreement to the Hardy-Weinberg equilibrium. Interventions were found to represent actual hypertension-management practices in Brazil, and accounted for a significant reduction in both systolic (P<0.001) and diastolic (P<0.001) blood pressure. Concerning the effect of polymorphisms, no influence of the ACE and AT1R genotypes were found on the magnitude of the treatment-induced blood pressure reduction (P>0.05). Nonetheless, the clinical result varied according to the ACE alleles since mean systolic pressure was roughly 10 mm Hg higher in insertion (I) homozygotes than in the deletion (D) counterparts either in baseline (P=0.001) and endpoint (P=0.010).
  
  
  CONCLUSIONS
  The outcome of the antihypertensive pharmacotherapy advocated by national guidelines was significantly influenced by the ACE I/D polymorphism but not by the AT1R 1166 A/C polymorphism among postmenopausal women.
authors.affiliation: Postgraduation Program Stricto Sensu in Gerontology, Catholic University of Brasília (UCB), Geriatrics Service, Hospital of the Catholic University of Brasília, Brasília-DF, Brazil.
authors.forename: Clayton F
authors.initials: CF
authors.lastname: Moraes
authors.forename: Elias R
authors.initials: ER
authors.lastname: Souza
authors.forename: Vinícius C
authors.initials: VC
authors.lastname: Souza
authors.forename: Eloá F F
authors.initials: EF
authors.lastname: Medeiros
authors.forename: Thiago F
authors.initials: TF
authors.lastname: Gonçalves
authors.forename: Juliana O
authors.initials: JO
authors.lastname: Toledo
authors.forename: Mauro
authors.initials: M
authors.lastname: Karnikowski
authors.forename: Lucy
authors.initials: L
authors.lastname: Gomes
authors.forename: Margô G O
authors.initials: MG
authors.lastname: Karnikowski
authors.forename: Cláudio
authors.initials: C
authors.lastname: Córdova
authors.forename: Otávio T
authors.initials: OT
authors.lastname: Nóbrega
mesh_terms: D000368:Aged; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D001794:Blood Pressure / Q000187:drug effects; D001938:Brazil / Q000453:epidemiology; D005260:Female; D005838:Genotype; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000453:epidemiology / Q000503:physiopathology; D007703:Peptidyl-Dipeptidase A / Q000235:genetics / Q000378:metabolism; D011110:Polymorphism, Genetic / Q000235:genetics*; D044140:Receptor, Angiotensin, Type 1 / Q000235:genetics; D012084:Renin-Angiotensin System / Q000187:drug effects* / Q000235:genetics*; D016896:Treatment Outcome
chemical_list: D000959:Antihypertensive Agents; D044140:Receptor, Angiotensin, Type 1; C488034:ACE protein, human; D007703:Peptidyl-Dipeptidase A