Elevated levels of serum nitrate, a stable end product of nitric oxide, in women with pre-eclampsia.

Abstract

Nitric oxide released from vascular endothelial cells is a potent vasodilator and inhibits platelet adhesion. It has been suggested that decreased nitric oxide production from dysfunctional endothelial cells is implicated in the pathophysiology of pre-eclampsia. In this study evidence was sought for abnormal production of nitric oxide in pre-eclamptic women. Blood was collected from 20 women presenting with pre-eclampsia, from 20 matched healthy pregnant controls and from 12 nonpregnant women of childbearing age. Serum nitrate, the stable end metabolite of nitric oxide, was measured by vanadium III chloride reduction and chemiluminescence. Sera from women with pre-eclampsia had significantly higher nitrate concentrations (mean 47.4 mumol/L [SD 13.6]) compared with healthy pregnant (mean 31.2 mumol/L [SD 9.14]) and nonpregnant (mean 32.1 mumol/L [SD 10.0]) controls. These results do not support the hypothesis that decreased endothelial cell nitric oxide production may be important in the pathophysiology of pre-eclampsia. On the contrary, serum nitrate levels are increased which may reflect either increased production of nitric oxide from an unidentified source or decreased elimination through the kidneys.