LACK OF ASSOCIATION BETWEEN RENIN-ANGIOTENSIN SYSTEM, GENE POLYMORPHISMS, AND WALL THICKNESS OF THE RADIAL AND CAROTID ARTERIES

To investigate the relationship between polymorphisms of the angiotens in-converting enzyme (ACE) and the angiotensin II type 1 receptor (AT( 1)R) genes and structural phenotypes of arteries, we studied a cohort of 340 subjects (aged 49+/-12 years) without evidence of cardiovascula r disease and who had never been treated previously with any cardiovas cular treatments. Structural phenotypes (wall thickness and internal d iameter) were evaluated for the common carotid and the radial arteries using high-resolution echo-tracking devices (NIUS-02 and Wall Track S ystem). The influence of ACE insertion/deletion (I/D) and AT(1)R A/C-1 166 polymorphism genotypes on structural parameters was tested by ANOV A and logistic regression analysis. For the radial artery, mean wall t hickness among subjects according to the ACE I/D or AT(1)R A/C-1166 ge notypes was not different. This lack of association persisted in a log istic regression analysis or when the comparison was restricted to a s ubgroup 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, n o association was observed between the carotid artery intima-media thi ckness and the 2 polymorphisms. In conclusion, the ACE I/D and the AT( 1)R A/C-1166 gene polymorphisms are not markers of vascular hypertroph y in subjects with no evidence of cardiovascular disease. These result s suggest that these gene polymorphisms have an undetectable role in t he geometry of the radial and carotid arteries compared with usual det erminants such as blood pressure and age.