Endothelial nitric oxide synthase in placental villous tissue from normal, pre-eclamptic and intrauterine growth restricted pregnancies

Nitric oxide (NO) regulates blood flow in the human placenta. As increasedresistance to blood flow is seen in the fetal-placental vasculature inpregnancies complicated by pre-eclampsia and/or intrauterine growthrestriction (IUGR), we examined expression of endothelial nitric oxidesynthase (eNOS) in these placentas. Placental villous tissue sections wereobtained from normotensive control (n = 5), IUGR alone (n = 5) orpre-eclamptic (with or without IUGR (n = 9) patients, immunostained foreNOS and scored for localization, type (punctate or diffuse) and intensityof eNOS staining in syncytiotrophoblast and placental vessels. Thesignificance of differences was calculated using the Mann-Whitney U-test.No differences in intensity or type of immunostaining insyncytiotrophoblast were seen. Placentas from patients with pre- eclampsiawith or without IUGR had a significantly more basal distribution of eNOS insyncytiotrophoblast. eNOS immunostaining was absent in terminal villouscapillary and faint in stem villous vessel endothelium of normal placentas,but was intense in the endothelium of both of these types of vessels in theIUGR and pre-eclampsia groups, with significantly greater staining seen instem vessels of patients with IUGR alone. This increased eNOS expressionand hence increased NO production in the fetal-placental vasculature may bean adaptive response to the increased resistance and poor perfusion inthese pathological pregnancies.