Vasoactive mediator release by fetal endothelial cells in intrauterine growth restriction and preeclampsia.
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.


METHODS
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.


CONCLUSIONS
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.
Harris Birthright Research Centre for Fetal Medicine, King's College Hospital, Denmark Hill, London, United Kingdom.
M C
MC
Parra
C
C
Lees
G E
GE
Mann
J D
JD
Pearson
K H
KH
Nicolaides
D015121:6-Ketoprostaglandin F1 alpha / Q000096:biosynthesis* / Q000502:physiology; D000293:Adolescent; D000328:Adult; D001120:Arginine / Q000378:metabolism / Q000493:pharmacokinetics / Q000502:physiology; D016022:Case-Control Studies; D002478:Cells, Cultured; D006152:Cyclic GMP / Q000096:biosynthesis / Q000378:metabolism; D004730:Endothelium, Vascular / Q000378:metabolism* / Q000473:pathology; D005260:Female; D005317:Fetal Growth Retardation / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D006801:Humans; D007700:Kinetics; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000096:biosynthesis / Q000502:physiology; D011225:Pre-Eclampsia / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D011247:Pregnancy; D012588:Scintillation Counting; D018709:Statistics, Nonparametric; D014316:Tritium; D014471:Umbilical Veins / Q000378:metabolism / Q000473:pathology
D014316:Tritium; D009569:Nitric Oxide; D015121:6-Ketoprostaglandin F1 alpha; D001120:Arginine; D006152:Cyclic GMP; D019331:NG-Nitroarginine Methyl Ester