Abstract 13898: The Effect Of The Angiotensinogen Gene Variants On The Risk Of Arterial Hypertension And Vascular Function
Background: The renin-angiotensin system is associated with vascular damage potentially via activation of inflammatory process. In addition, the angiotensinogen (AGT) M235T polymorphism has been positively associated with essential hypertension, even though the results are inconsistent. In the present study we sought to investigate the impact of this polymorphism on vascular properties and inflammation as potential contributors in the risk of essential hypertension (EH).
Methods: The study population consisted of 302 untreated hypertensive patients, and 191 controls. The gene M235T polymorphism was determined by polymerase chain reaction (PCR) technique and appropriate restriction enzyme. Brachial artery flow-mediated dilation (FMD) was used to assess endothelial dysfunction. Aortic stiffness was evaluated, on the basis of carotid to femoral pulse wave velocity (c-f PWV). Interleukin-6 (IL-6) and high sensitivity C-reactive protein (hsCRP) levels were also measured.
Results: The risk for EH in TT was significantly increased compared with the other genotypes (OR: 2.830[1.461-5.480; p=0.002]). Interestingly, TT homozygotes had significantly lower FMD compared with M allele carriers in controls (4.70±0.7 vs 7.09±0.3, p=0.038). In addition, c-fPWV was higher in TT homozygotes compared with MM+MT genotypes in hypertensive patients (9.13±0.2 vs 8.55±0.1, p=0.025). Moreover, subjects with EH had significantly higher levels of IL-6 compared with controls (p=0.001). No significant effect was observed on IL-6 and hsCRP levels across the study genotypes in controls and hypertensives (p=NS for all).
Conclusions: The present study indicates that this polymorphism is associated with the risk of hypertension and increased arterial stiffness in hypertensives, without a significant impact on inflammatory process. These findings suggest that the angiotensinogen M235T polymorphism exerts an important effect on the vascular biology independently of inflammatory mechanisms.
- © 2011 by American Heart Association, Inc.