Angiotensin II type 1 receptor−153A/G and 1166A/C gene polymorphisms and increase in aortic stiffness with age in hypertensive subjects


    loading  Checking for direct PDF access through Ovid

Abstract

ObjectivesArterial stiffness is associated with excess morbidity and mortality, independently of other cardiovascular risk factors. Age is the main determinant responsible for arterial wall changes leading to arterial stiffening. Environmental and genetic factors may however influence the magnitude of the effects of age on large artery stiffness.Design and methodsThe present study assessed whether or not the relationship between age and aortic stiffness was influenced by genetic variants of angiotensinogen (AGT 174T/M, 235M/T), angiotensin converting enzyme (ACE I/D), angiotensin II type 1 receptor (AT11166A/C, −153A/G) and aldosterone synthase (CYP11B2−344T/C). This study was realized in 441 untreated hypertensive subjects of European origin (aged 18–74 years). Aortic stiffness was assessed by carotid–femoral pulse wave velocity (PWV).ResultsCarriers of the angiotensin II type 1 receptor −153G allele showed a steeper age/PWV relationship than the AT1−153AA subjects. The effect of the AT1−153A/G polymorphism on aortic stiffness became apparent after the age of 55 years. In subjects with the AT11166C allele, the relationship age/PWV is shifted upward, indicating higher values of aortic stiffness at any age compared to the AT11166AA patients. Carriers of both the AT11166C and −153G alleles presented the additive effects of these 2 genotypes on aortic stiffness. Angiotensinogen, ACE and CYP11B2 genotypes did not influence the effects of age on PWV.ConclusionsAT1 receptor genotypes could influence arterial ageing in hypertensive subjects. These results also show that the association between genotypes and arterial stiffness may manifest itself later in life.

    loading  Loading Related Articles