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• W2007189891 abstract "The increased fetal-placental vascular resistance seen in preeclampsia and/or IUGR has been empirically ascribed to deficiencies in synthesis of vasodilator autocoids in this vascular bed. However, abnormal development of the vascular tree and thus increased resistance to flow could lead to alterations in production of autocoids as a compensatory response, particularly as physical factors such as flow/shear stress over endothelial cells are potent stimuli to autocoid synthesis. The nitric oxide radical (NO) is a potent vasodilator of the human fetal-placental vasculature. Alterations in NO synthesis have been reported in the placenta in preeclampsia. The bioactivity of NO is regulated by its interaction with and inactivation by the superoxide anion. However, the product of this interaction, the strong-lived oxidant peroxynitrite, while acting acutely as a vasodilator, acts in a chronic manner to exert deleterious cytotoxic effects and causes vascular dysfunction. Production and action of peroxynitrite can be identified by the presence of nitrotyrosine residues. We have determined the immunohistochemical localization and quantification of the endothelial nitric oxide synthase isoform (eNOS) and of nitrotyrosine residues (NT) in placental villous tissue from normotensive pregnancies in comparison with those complicated by preeclampsia and/or IUGR. Whereas, there was no difference in quantity of eNOS immunostaining in syncytiotrophoblast between the four groups of tissues, more intense eNOS staining was seen in the villous vascular endothelium of preeclamptic and/or IUGR placentae. This parallels our previous observation of increased concentrations of nitrite, a breakdown product of NO, in the umbilical circulation of these pregnancies. No NT immunostaining was seen in trophoblast cells of any placentae or in the vascular endothelium of normotensive placentae. However, significantly more intense NT immunostaining was apparent in the villous vascular endothelium of the pathologic placentae and diffusing into vascular smooth muscle and stroma. Therefore, the increased vascular resistance and abnormal umbilical blood flow velocity waveforms seen in preeclampsia and/or IUGR cannot simply be ascribed to reduced synthesis and action of vasodilator autocoids in fetal placental vasculature. Rather, increased synthesis of some of these vasodilator autocoids e.g., NO may be occurring in the first instance as an adaptive or compensatory response to increased resistance or to a primary anatomic defect found in this vasculature. The effect of this increased autocoid expression will be to try to vasodilate this vasculature to increase blood flow to the placenta and increase oxygen and nutrient extraction. However, in common with many other conditions of oxidative stress where endothelial dysfunction is seen, concomitant increased synthesis of nitric oxide and superoxide may lead to the formation of the deleterious compound peroxynitrite, which results in vascular damage. The relative rates and sites of synthesis and the opportunity for interaction between these radicals may be key to determining whether potentially beneficial or deleterious effects are seen." @default.
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• W2007189891 date "1998-01-01" @default.
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• W2007189891 title "Autocoid synthesis and action in abnormal placental flows reviewed: Causative vs. compensatory roles" @default.
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• W2007189891 doi "https://doi.org/10.1016/s0143-4004(98)80022-2" @default.
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