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

Abstract

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

Polymorphisms in the endothelial nitric oxide synthase gene associated with recurrent miscarriage

“…Furthermore, the placental production of human chorionic gonadotropin, an important angiogenic factor for neoangiogenic interaction and trophoblast migration (Zygmunt et al, 2002), is modulated by eNOS during gestation (Sanyal et al, 2000). Abnormal levels of NO have been reported in the placentae from preeclamptic pregnancies as well as from term pregnancies with fetal growth retardation (Myatt et al, 1997). In mice, placental NO production mediates abortion induced by lipopolysaccharide (Haddad et al, 1995), whereas pharmacological inhibition of NO release with aminoguanidine successfully rescues lipopolysaccharide-induced abortion (Athanassakis et al, 1999).…”

Gene expression of nitric oxide synthase by human umbilical vein endothelial cells: the effect of fetal plasma from pregnancy with umbilical placental vascular disease

“…In contrast, in pre-eclampsia with no umbilical artery Doppler flow velocity waveform evidence of vascular disease, we showed no alteration of mRNA expression of nitric oxide synthase. Immunostaining of endothelial cell nitric oxide synthases, which are found in the endothelium of the terminal villous capillary and stem villous vessels, was greater in both IUGR and pre-eclampsia cases 24 . These findings are consistent with our results.…”

Selected physicochemical properties of amniotic fluid according to week of pregnancy

“…In patients with preterm premature rupture of membranes and in patients with preterm labour and subsequent premature delivery these were signifi cantly higher than the concentrations in patients who delivered at term. There is evidence that NO is also released by the foetoplacental tissues (23), and there are a few studies oriented on the determination of nitrites in amniotic fl uid and its possible applications. The concentration of NOx increases during pregnancy and is not related to foetal haemolysis (24).…”