title: The ACE-DD genotype is associated with endothelial dysfunction in postmenopausal women.
abstract: OBJECTIVE
  To evaluate the effects of the angiotensin-converting enzyme (ACE) insertion/deletion (I/D), the angiotensinogen M235T and the angiotensin II type 1 receptor A1166C polymorphisms, and hormone therapy used on endothelial function in postmenopausal women without manifestation of coronary artery disease.
  
  
  METHODS
  Sixty-four postmenopausal women (42 hormone therapy users and 22 hormone therapy nonusers) without clinical manifestation of coronary artery disease were evaluated using external vascular ultrasonography to measure endothelium-dependent (hyperemic response, flow-mediated dilatation) and -independent (nitroglycerin) dilatation. Genotypes were determined by polymerase chain reaction amplification.
  
  
  RESULTS
  Women with the ACE-DD genotype displayed a lower flow-mediated dilatation compared to those with the ACE-II genotype (8.4% +/- 3.9% vs 12.6% +/- 5.4%, P = 0.04). Endothelial function was not associated with the angiotensinogen M235T and anglotensin II type 1 receptor A1166C polymorphisms. ACE polymorphism seems to modulate endothelial function among postmenopausal women without hormone therapy (8.2% +/- 5.1% vs 18.4% +/- 5.9% for the DD and the II genotype, respectively, P = 0.02). However, in hormone therapy users, flow-mediated dilatation was similar according to the ACE genotypes.
  
  
  CONCLUSIONS
  Our findings suggest that ACE-I/D polymorphism is related to endothelial dysfunction in postmenopausal women. Furthermore, a potential interaction between estrogen users and ACE polymorphism on endothelial function may be present.
authors.affiliation: Quebec Heart Institute/Laval Hospital, Laval University, Ste-Foy, Quebec, Canada.
authors.forename: Julie
authors.initials: J
authors.lastname: Méthot
authors.forename: Bettina A
authors.initials: BA
authors.lastname: Hamelin
authors.forename: Marie
authors.initials: M
authors.lastname: Arsenault
authors.forename: Peter
authors.initials: P
authors.lastname: Bogaty
authors.forename: Sylvain
authors.initials: S
authors.lastname: Plante
authors.forename: Paul
authors.initials: P
authors.lastname: Poirier
mesh_terms: D000483:Alleles; D000808:Angiotensinogen / Q000235:genetics*; D001916:Brachial Artery / Q000000981:diagnostic imaging; D004730:Endothelium, Vascular / Q000502:physiology*; D005260:Female; D017353:Gene Deletion; D005838:Genotype; D020249:Hormone Replacement Therapy; D006801:Humans; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic; D017698:Postmenopause / Q000235:genetics* / Q000502:physiology; D044140:Receptor, Angiotensin, Type 1 / Q000235:genetics*; D012084:Renin-Angiotensin System; D014463:Ultrasonography
chemical_list: D044140:Receptor, Angiotensin, Type 1; D000808:Angiotensinogen; D007703:Peptidyl-Dipeptidase A