Problem: Pre-eclampsia involves endothelial vascular dysfunction. The aim of this study was to test the hypothesis that (i) endothelial nitric oxide (NO) synthase Glu298Asp gene polymorphism limits constitutive NO production causing endothelial dysfunction and (ii) inflammatory cytokines impairs endothelium dependent relaxation in pre-eclampsia.
Method of study: This cross-sectional study included 50 women with pre-eclampsia and 50 healthy pregnant women. Their blood samples were analyzed for NO, inflammatory cytokines and endothelial NO synthase (eNOS) gene polymorphism.
Result: Decreased NO levels whereas increased tumor necrosis factor-alpha, interleukin (IL)-6 and interleukin-2 were found in pre-eclampsia (P < 0.001). No significant differences were found in genotype/allele distribution between two groups. Significant negative correlation was observed between NO and IL-6 in pre-eclamptic group (P = 0.001).
Conclusion: An IL-6-mediated endothelium dependent NO-cyclic guanine monophosphate-mediated relaxation pathway may be inhibited in systemic vessels in pre-eclampsia. As observed in this study Glu298Asp eNOS gene polymorphism did not showed significant association with pre-eclampsia.