Nitric oxide dysfunction in the pathophysiology of preeclampsia

Researchers disagree as to the importance of nitric oxide (NO) in preeclampsia. Many researchers have alluded to NO's possible primary or secondary role in the development of preeclampsia, but few have correlated the dysfunction of nitric oxide production with the other metabolic derangements seen in this condition. This paper will review the evidence that the primary dysfunction in preeclampsia is a relative deficiency of available NO (secondary to oxidative degradation) and an excess of peroxynitrite (ONOO(-)). The combination of a deficiency of NO and an increase in ONOO(-) can directly or indirectly initiate the vast majority of physiological and serological changes associated with preeclampsia, such as blood pressure, increased glomerular filtration rate, proteinuria, platelet dysfunction, increased thromboxane and endothelin, and a decrease in prostacyclin. Understanding the complex role of nitric oxide in this condition may explain why previous interventions have been unsuccessful and suggest possible strategies for prevention and treatment in the future.