Renin–angiotensin system genetic polymorphisms: Lack of association with CRP levels in patients with coronary artery disease

Abstract

Angiotensin (Ang) II is believed to be a potential pro-inflammatory factor. The capability of Ang II to stimulate C-reactive protein (CRP) production has recently been described. Genetic polymorphisms of renin angiotensin system (RAS) components have been described to be associated with the development of coronary artery disease (CAD). This study investigated the association between six different genetic polymorphisms of RAS and serum CRP levels in a sample of CAD patients. Genotyping of RAS genes polymorphisms in 176 patients with documented CAD was performed by a modified polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. Measurement of high-sensitivity (hs)-CRP was performed using standard immunoturbidimetric methods. Results show no significant differences in serum CRP regarding different variants of the six polymorphisms studied (p = 0.41, 0.24, 0.25, 0.19, 0.29, and 0.05 for Ang-converting enzyme (ACE) insertion/deletion (I/D), A-240T and A2350G, angiotensinogen M235T, AT1 receptor A1166C, and AT2 receptor C3123A polymorphisms, respectively). In conclusion, genetic polymorphisms of RAS are not associated with increased serum CRP in CAD. Compensation of an increased activity of ACE through counter-regulation and the secretion of CRP under the influence of Ang II in the vessel being local could explain the lack of association between the studied polymorphisms and CRP levels in CAD patients.