Progesterone and estradiol production by normal and preeclamptic placentas

Placentas obtained from women with preeclampsia produce more thromboxane, a potent vasoconstrictor, and less prostacyclin, a potent vasodilator, than normal. Although the factors responsible for this are not known, steroids are known to affect eicosanoid production, and the placenta is a rich source of progesterone and estradiol. If placental steroids contribute to the imbalance of increased thromboxane/decreased prostacyclin in preeclamptic placentas, then their placental production might also be abnormal. The following study was performed to see whether the placentas of preeclamptic women produce progesterone or estradiol abnormally. Fresh human term placentas were obtained immediately after delivery from normal and mild preeclamptic pregnancies. Whole placental tissues (350 mg) were incubated for three hours. Samples were collected and analyzed for progesterone and estradiol-17 beta by radioimmunoassay. Progesterone production was significantly higher in preeclamptic than in normal placentas without the addition of a precursor and with the addition of pregnenolone sulfate as a precursor, but not with the addition of pregnenolone alone. Both normal and preeclamptic placentas converted pregnenolone sulfate into progesterone as efficiently as they converted pregnenolone into progesterone. Estradiol production rates were similar in both preeclamptic and normal placentas, regardless of whether dehydroepiandrosterone sulfate was added as a precursor. These data indicate that placentas of women with mild preeclampsia produce more progesterone than normal, probably because they contain more pregnenolone sulfatase and larger stores of endogenous cholesterol. Higher concentrations of progesterone in the preeclamptic placenta could contribute to lower prostacyclin production because progesterone inhibits placental prostacyclin production.