Preeclampsia (PE) is a multi-system disorder of widespread vascular endothelial malfunction and vasospasm, characterized by new onset of hypertension and either proteinuria or endorgan dysfunction or both after 20 weeks of gestation in a formerly normotensive woman. Albeit most influenced pregnancies convey at term or close term with adverse maternal and fetal outcome, these pregnancies are at expanded danger for maternal and fetal mortality or morbidity worldwide (Hutcheon et al. 2011). Preeclampsia is further sub classified into, mild and severe, early onset and late-onset syndrome (American College of Obstetricians and Gynecologists; Hypertension in Pregnancy Preeclampsia has a complex pathophysiology; the essential etiopathogenesis being played by the placenta (Roberts and Cooper 2001), as defective invasion of the spiral arteries by cytotrophoblast cells is detected during preeclampsia (Fisher et al. 2009). This might be because of the nitric oxide pathway that controls the vascular tone. Increased uterine arterial resistance triggers higher sensitivity to vasoconstriction and subsequently chronic placental ischemia and oxidative stress, which cause intrauterine fetal growth retardation (FGR) and death. In addition, oxidative stress actuates release of substances into the maternal circulation such as free radicals, cytokines, and vascular endothelial growth factor 1. These abnormalities are in charge of endothelial dysfunction (Roberts 1998), with vascular hyperpermeability, and hypertension.