ABSTRACT
Nitric oxide [NO] is a vasorelaxant agent, while endothelin-1 [Et-1] is a potent vasoconstrictor peptide. In this study, maternal venous plasma nitrite [N02] + nitrate [N03], stable metabolites of NO and ET-1 were measured in 20 non-pregnant cases, 20 normal pregnancy and 20 preeclamptic pregnancy. There was a significant increase in N02 + N03 and a significant decrease in ET-1 in normal pregnancy. In preeclampsia, N02 + N03 was significantly lower, while ET-1 was significantly higher than in normal pregnancy. There was a significant negative correlation between N02 + N03 and ET-1 in preeclamptic cases. Neither NO nor ET-1 correlated with mean arterial pressure. These data indicated that preeclampsia may reflect a state of impaired NO syntheses and increased ET-1 production. The pathophysiologic mechanism is a failure of vasodilatation and decreased vascular reactivity characteristic of normal pregnancy together with enhancement of vasoconstriction. Although the changes in NO and ET-1 are related to hypertension in preeclampsia, other mechanisms are probably activated