Another potential mechanism responsible for pathogenesis of pre-eclampsia is placental hypoperfusion which in turn releases various factors that trigger endothelial activation / dysfunction. Nitric oxide, disordered endothelin metabolism, thromboxane/prostaglandin imbalance, cellular fibronectin, inflammatory cytokines (TNF-α, IL-6, IL-1α, and IL-1β) and other factors such as lipid peroxides and reactive oxygen intermediateshave all been implicated in mediating the endothelial cell injury12. This is well-supported by the fact that pre-eclampsia commonly occurs in pre-existing metabolic (diabetes, hypercholesterolemia), renal, vascular disorders (hypertension) and connective tissue disorders that result in poor placental circulation. In cases of multiple gestation or increased placental mass, it is not surprising for the placenta to become under perfused. However, majority of the pre-eclamptic women do not suffer from any underlying medical conditions. In these women, lack of placental cytotrophoblast invasion of uterine spiral arterioles and arrest of arteriolar remodeling results from failure of pseudo-vascularization of the invasive cytotrophoblasts13. Deregulation of angiogenesis-related gene products such as vascular endothelial growth factor (VEGF), angiopoietin and ephrin family proteins, placental growth factor (PlGF) and their receptors have been implicated in this process14.Shallow placentation leads to reduced placental perfusion and subsequent ischemia.