“…2 Systemic arteriolar vasodilatation, probably dependent on endothelial NO, 3,4 is responsible for the hemodynamics of the first half of the pregnancy (increased blood volume and cardiac output and decreased blood pressure). 5,6 Deficiencies in the vasodilatory, antithrombotic, and atheroprotective effects of NO 7,8 have been implicated in the pathogenesis of cardiovascular disease, for which preeclampsia is also a risk factor. 9,10 Therefore, the gene that encodes endothelial NO synthase (eNOS), the enzyme that regulates endothelial NO availability, is a candidate gene for preeclampsia.…”