title: Angiotensinogen M235T polymorphism is associated with plasma angiotensinogen and cardiovascular disease.
abstract: BACKGROUND
  Genes encoding components of the renin-angiotensin system have been associated with elevated blood pressure (BP) and an increased risk of coronary artery disease. To explore the role of the angiotensinogen (AGT) gene in coronary atherosclerosis and thrombosis, we studied the effect of the AGT M235T gene variant on plasma AGT levels and BP in patients with coronary artery disease and in the subgroup of survivors of myocardial infarction as compared with angiographically defined control subjects.
  
  
  RESULTS
  This was a case-control study of 301 white male subjects examined at Frankfurt University medical center. Plasma AGT levels increased stepwise according to the number of T235 alleles present (no T235 allele, 14.8 +/- 3.9 nmol/L; 1 allele, 15.7 +/- 5.1 nmol/L; 2 alleles, 17.3 +/- 4.7 nmol/L; P =.006). In a multivariate model, circulating AGT emerged as the most important predictor of diastolic pressure (P =.001). In addition, AGT M235T gene polymorphism remained a significant predictor of diastolic BP in a multivariate model adjusted for age, body mass index, fasting glucose, apolipoprotein B, presence of coronary artery disease, and treatment with antihypertensive agents ( P <.05). Finally, homozygosity for T235 was associated with increased univariate risk of coronary artery disease and myocardial infarction (odds ratio estimates 1.5; 95% confidence intervals 1.1 to 2.1, P =.03, and 1.0 to 2.1, P =.05, respectively).
  
  
  CONCLUSIONS
  The significant relations observed between the AGT M235T variant, its protein product, and the cardiovascular disease phenotypes provide evidence for a possible role of elevated circulating AGT in the pathogenesis of coronary artery disease.
authors: Department of Cardiology, Ludwigshafen Heart Center, Frankfurt, Germany.
authors: B R
authors: BR
authors: Winkelmann
authors: A P
authors: AP
authors: Russ
authors: M
authors: M
authors: Nauck
authors: B
authors: B
authors: Klein
authors: B O
authors: BO
authors: Böhm
authors: V
authors: V
authors: Maier
authors: R
authors: R
authors: Zotz
authors: G
authors: G
authors: Matheis
authors: A
authors: A
authors: Wolf
authors: H
authors: H
authors: Wieland
authors: W
authors: W
authors: Gross
authors: D J
authors: DJ
authors: Galton
authors: W
authors: W
authors: März
mesh_terms: D000483:Alleles; D000808:Angiotensinogen / Q000097:blood* / Q000235:genetics*; D001794:Blood Pressure / Q000235:genetics; D002318:Cardiovascular Diseases / Q000235:genetics*; D016022:Case-Control Studies; D003324:Coronary Artery Disease / Q000235:genetics; D003328:Coronary Thrombosis / Q000235:genetics; D005787:Gene Frequency; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D009203:Myocardial Infarction / Q000235:genetics; D016017:Odds Ratio; D007703:Peptidyl-Dipeptidase A / Q000097:blood; D011110:Polymorphism, Genetic; D012084:Renin-Angiotensin System / Q000235:genetics*; D012307:Risk Factors
chemical_list: D000808:Angiotensinogen; D007703:Peptidyl-Dipeptidase A