Abstract

Preeclampsia occurs in the umbilical artery with proteinuria and edema accompanying pregnancy-induced hypertension. Vasoconstriction results in severe complications such as intrauterine growth restriction, preterm birth, fetal death due to decreased uteroplacental blood flow. Preeclampsia may cause perinatal mortality and morbidity and it is one of the most important causes of maternal mortality. The etiology and pathogenesis of preeclampsia, which is present in 7,18% of all pregnancies, has not yet been elucidated. However, it is thought that one of the causes of pathogenesis may be caused by possible changes in the synthesis of endothelial nitric oxide synthase (eNOS) mediated nitric oxide (NO). DNA sequencing studies revealed many single nucleotide polymorphisms (SNPs) in the promoter region, exons and introns of this gene. T-786C SNP is found in the promoter region of the eNOS gene. There are several agents affecting eNOS activity in preeclampsia.

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