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OBJECTIVES: 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. PARTICIPANTS: Blood was collected from 20 women presenting with pre-eclampsia, from 20 matched healthy pregnant controls and from 12 nonpregnant women of childbearing age. METHODS: Serum nitrate, the stable end metabolite of nitric oxide, was measured by vanadium III chloride reduction and chemiluminescence. RESULTS: 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. CONCLUSIONS: 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.


Journal article


Br J Obstet Gynaecol

Publication Date





538 - 543


Adult, Diet, Female, Humans, Nitrates, Nitric Oxide, Pre-Eclampsia, Pregnancy