title: [The effect of the angiotensinogen M235T and the angiotensin-converting enzyme I/D polymorphisms on arterial hypertension and other cardiovascular risk factors].
abstract: BACKGROUND
  It has been reported the association between M235T angiotensinogen (AGT) and I/D angiotensin converting enzyme (ACE) gene polymorphisms and hypertension and other cardiovascular risk factors. However there are few data about Spanish population. So that we have studied the relationship among the aforementioned polymorphisms and hypertension and the possibility of association between any polymorphism and a worse cardiovascular risk profile.
  
  
  METHODS
  251 hypertensive and 245 control normotensive subjects were studied. The M235T AGT and the I/D ACE gene polymorphisms were determined by polymerase chain reaction (PCR). Family and personal history of cardiovascular disease, lipoprotein profile, microalbuminuria and left ventricular hypertrophy (LVH) by Sokolow index were analyzed in hypertensive patients.
  
  
  RESULTS
  The distribution of the different polymorphisms was similar among hypertensive and normotensive subjects. There was not any relationship among AGT nor ACE genotypes and target organ damage. The II ACE genotype was associated with higher lipoprotein (a) (Lp[a]) levels and greater cerebrovascular disease family history and the MT AGT genotype with lower total cholesterol (TC) and triglycerides (TG) levels.
  
  
  CONCLUSIONS
  In our study there was not any relationship between arterial hypertension and M235T AGT or I/D ACE gene polymorphisms. None specific genotype was associated with worse cardiovascular risk profile. The II ACE genotype was a predictor of cerebrovascular disease risk through higher levels of Lp(a) and the MT AGT genotype was associated with a better lipid profile.
authors.affiliation: Departamento de Medicina Interna, Hospital Universitario Virgen del Rocío, Sevilla.
authors.forename: E
authors.initials: E
authors.lastname: Pamies Andreu
authors.forename: C
authors.initials: C
authors.lastname: Palmero Palmero
authors.forename: R
authors.initials: R
authors.lastname: García Lozano
authors.forename: P
authors.initials: P
authors.lastname: Stiefel García-Junco
authors.forename: M L
authors.initials: ML
authors.lastname: Miranda Guisado
authors.forename: V
authors.initials: V
authors.lastname: Martín Sanz
authors.forename: J
authors.initials: J
authors.lastname: Villar Ortiz
authors.forename: A
authors.initials: A
authors.lastname: Núñez Roldán
authors.forename: J
authors.initials: J
authors.lastname: Carneado de la Fuente
mesh_terms: D000328:Adult; D000808:Angiotensinogen / Q000235:genetics*; D002318:Cardiovascular Diseases / Q000235:genetics*; D015342:DNA Probes; D005260:Female; D005838:Genotype; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000235:genetics*; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D008969:Molecular Sequence Data; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D016133:Polymerase Chain Reaction / Q000379:methods; D011110:Polymorphism, Genetic / Q000235:genetics*; D012307:Risk Factors
chemical_list: D015342:DNA Probes; D008055:Lipids; D000808:Angiotensinogen; D007703:Peptidyl-Dipeptidase A