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Vasoactive mediator release by fetal endothelial cells in intrauterine growth restriction and preeclampsia
1Harris Birthright Research Centre for Fetal Medicine, King's College Hospital, Denmark Hill, London, United Kingdom.
Insights
Preeclampsia increases cyclic guanosine monophosphate in fetal cells, potentially aiding placental blood flow. Fetal growth restriction shows a reduced response, possibly causing vasoconstriction.
Area of Science:
- Obstetrics and Gynecology
- Fetal Medicine
- Vascular Biology
Background:
- Preeclampsia and fetal growth restriction are linked to impaired placental perfusion.
- These conditions may involve altered vasoactive substance release in the fetoplacental circulation.
Purpose of the Study:
- To investigate the impact of preeclampsia and fetal growth restriction on nitric oxide and prostacyclin signaling pathways.
- To analyze cyclic guanosine monophosphate (cGMP) and 6-keto-prostaglandin F1alpha production in fetal endothelial cells.
Main Methods:
- Human umbilical vein endothelial cells were cultured from control, preeclampsia, and intrauterine growth restriction pregnancies.
- Measurements included intracellular cGMP accumulation and 6-keto-prostaglandin F1alpha production.
Main Results:
- cGMP accumulation was significantly higher in preeclampsia and lower in growth restriction compared to controls.
- No significant difference in 6-keto-prostaglandin F1alpha production was observed across the groups.
Conclusions:
- Preeclampsia may induce increased cGMP production to maintain fetoplacental vasodilation and blood flow.
- Fetal growth restriction might involve an impaired endothelial cell response to hypoxia, leading to vasoconstriction.
Objective:
Preeclampsia and fetal growth restriction are associated with poor placental perfusion, which may be accompanied by a compensatory release of vasoactive substances in the fetoplacental circuit. This study examines the effects of preeclampsia and fetal growth restriction on nitric oxide and prostacyclin signaling pathways in fetal endothelial cells.
Study Design:
Human umbilical vein endothelial cells from 30 control pregnancies, 18 pregnancies with preeclampsia, and 9 pregnancies with intrauterine growth restriction were cultured. Intracellular cyclic guanosine monophosphate accumulation and 6-keto-prostaglandin F1alpha production were determined.
Results:
Intracellular accumulation of cyclic guanosine monophosphate was significantly higher in the preeclampsia group and lower in the growth restriction group than in the control group (9.8, 1.8, and 3.9 pmol/microg protein for 5 minutes, respectively), whereas 6-keto-prostaglandin F1alpha production was not significantly different in the 3 groups.
Conclusion:
The data suggest that the fetoplacental vascular response to preeclampsia is to increase production of cyclic guanosine monophosphate, perhaps to maintain vessel dilatation and maximum flow through placental villi. In fetal growth restriction the umbilical vein endothelial cells do not or cannot respond to chronic hypoxia by increasing cyclic guanosine monophosphate, which may lead to fetoplacental vasoconstriction.
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