title: Lack of association between renin-angiotensin system, gene polymorphisms, and wall thickness of the radial and carotid arteries.
abstract: To investigate the relationship between polymorphisms of the angiotensin-converting enzyme (ACE) and the angiotensin II type 1 receptor (AT1R) genes and structural phenotypes of arteries, we studied a cohort of 340 subjects (aged 49+/-12 years) without evidence of cardiovascular disease and who had never been treated previously with any cardiovascular treatments. Structural phenotypes (wall thickness and internal diameter) were evaluated for the common carotid and the radial arteries using high-resolution echo-tracking devices (NIUS-02 and Wall Track System). The influence of ACE insertion/deletion (I/D) and AT1R A/C1166 polymorphism genotypes on structural parameters was tested by ANOVA and logistic regression analysis. For the radial artery, mean wall thickness among subjects according to the ACE I/D or AT1R A/C1166 genotypes was not different. This lack of association persisted in a logistic regression analysis or when the comparison was restricted to a subgroup of subjects potentially at high genetic risk (DD and CC or AC) compared with subjects at low genetic risk (AA and II or ID). Also, no association was observed between the carotid artery intima-media thickness and the 2 polymorphisms. In conclusion, the ACE I/D and the AT1R A/C1166 gene polymorphisms are not markers of vascular hypertrophy in subjects with no evidence of cardiovascular disease. These results suggest that these gene polymorphisms have an undetectable role in the geometry of the radial and carotid arteries compared with usual determinants such as blood pressure and age.
authors.affiliation: From the Department of Internal Medicine and INSERM U337, the Department of Pharmacology and INSERM U337 and the Laboratory of Molecular Biology, Broussais Hospital, Paris, France. girerd@hbroussais.fr
authors.forename: X
authors.initials: X
authors.lastname: Girerd
authors.forename: O
authors.initials: O
authors.lastname: Hanon
authors.forename: J J
authors.initials: JJ
authors.lastname: Mourad
authors.forename: P
authors.initials: P
authors.lastname: Boutouyrie
authors.forename: S
authors.initials: S
authors.lastname: Laurent
authors.forename: X
authors.initials: X
authors.lastname: Jeunemaitre
mesh_terms: D000328:Adult; D000704:Analysis of Variance; D001794:Blood Pressure; D002339:Carotid Arteries / Q000000981:diagnostic imaging / Q000473:pathology*; D015331:Cohort Studies; D005260:Female; D005838:Genotype; D006801:Humans; D006984:Hypertrophy; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D010641:Phenotype; D011110:Polymorphism, Genetic; D017534:Radial Artery / Q000000981:diagnostic imaging / Q000473:pathology*; D044140:Receptor, Angiotensin, Type 1; D011945:Receptors, Angiotensin / Q000235:genetics*; D012084:Renin-Angiotensin System / Q000235:genetics*; D012307:Risk Factors; D014463:Ultrasonography
chemical_list: D044140:Receptor, Angiotensin, Type 1; D011945:Receptors, Angiotensin; D007703:Peptidyl-Dipeptidase A