A nitrogén-monoxid-szintézis zavarai praeeclampsiában [Nitric oxide and preeclampsia]

Abstract

Preeclampsia is one of the leading causes of obstetric morbidity and mortality. The placenta has a crucial role in the development of preeclampsia. Despite intensive researches the cause of disorder is still unknown. Insufficient NO synthesis may have a key role in pathogenesis. Endothelial NO synthesis (eNOS) is the primary isoenzyme expressed in human placenta, its known disturbances are discussed. Deficiency of substrate (arginine), cofactor (tetrahydrobiopterin, BH4) and calcium can decrease the NO synthesis. Serum levels of free fatty acids (FFA), asymmetric dimethylarginine, reactive oxygen species and glucose may increase in preeclamptic pregnancy. These substances decrease NO production by different ways. The reduced affinity of eNOS to the cofactor BH4 may lead to insufficient NO, but increased superoxide production in preeclamptic placentas. Polymorphisms of eNOS gene (D298E,-786T→C) were associated with preeclamptic complications (not adequately documented). Data suggest that smoking has protective role against preeclampsia. The mechanism is not clear, even the actions of smoking on eNOS are ambivalent. The expression of eNOS is decreased, while the phosphorylation of the activator Ser1177 and also the deactivator Thr495 are increased by cigarette smoke. The oxidative stress directly decreases NO levels. Smoking lowers serum FFA levels, thus the activity of eNOS may be increased. CO produced during smoking mimics the effect of NO and can compensate its absence partially.