We have examined factors concerned with the maintenance of uterine quiescence during pregnancy and the onset of uterine activity at term in an animal model, the sheep, and in primate species. We suggest that in both species the fetus exerts a critical role in the processes leading to birth, and that activation of the fetal hypothalamic-pituitary-adrenal axis is a central mechanism by which the fetal influence on gestation length is exerted. Increased cortisol output from the fetal adrenal gland is a common characteristic across animal species. In primates, there is, in addition, increased output of estrogen precursor from the adrenal in late gestation. The end result, however, in primates and in sheep is similar: an increase in estrogen production from the placenta and intrauterine tissues. We have revised the pathway by which endocrine events associated with parturition in the sheep come about and suggest that fetal cortisol directly affects placental PGHS expression. In human pregnancy we suggest that cortisol increases PGHS expression, activity, and PG output in human fetal membranes in a similar manner. Simultaneously, cortisol contributes to decreases in PG metabolism and to a feed-forward loop involving elevation of CRH production from intrauterine tissues. In human pregnancy, there is no systemic withdrawal of progesterone in late gestation. We have argued that high circulating progesterone concentrations are required to effect regionalization of uterine activity, with predominantly relaxation in the lower uterine segment, allowing contractions in the fundal region to precipitate delivery. This new information, arising from basic and clinical studies, should further the development of new methods of diagnosing the patient at risk of preterm labor, and the use of scientifically based strategies specifically for the management of this condition, which will improve the health of the newborn.

/pdf/endocrine-and-paracrine-regulation-of-birth-at-term-and-4igz1kdkru.pdf

Endocrine and paracrine regulation of birth at term and preterm

The effects of oral administration of progesterone for premature labor

Saliva oestriol, oestradiol, oestrone and progesterone levels in pregnancy: spontaneous labour at term is preceded by a rise in the saliva oestriol:progesterone ratio.

The intent of this review was a selective consideration of recent advances in understanding placental steroidogenesis in humans. While we have omitted material, both intentionally and unintentionally, we hope this discourse presents a flavour of the current molecular endocrinology of placental steroidogenesis. In particular, advances in knowledge as it relates to the enzymes involved in progesterone and oestrogen metabolism have been addressed and correlated with placental development. Finally, because relatively less is known about regulation of steroidogenesis in the human placenta beyond the aspects of growth and differentiation, we have discussed regulation in general terms using recent data obtained in animal species.

4 Placental steroid hormones

Treatment of pregnant rats with the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME), has been shown to produce symptoms similar to pre-eclampsia (i.e. elevated blood pressure, proteinuria and fetal growth retardation). After L-NAME infusion is initiated on day 17 or 18 of gestation, the blood pressure proceeds in a biphasic pattern (immediate rise, followed by a decline, then increasing again in the post-partum period). The blood pressure actually begins to rise prior to delivery on days 21-22, i.e. after progesterone withdrawal occurs, suggesting that these responses may be regulated by changes in steroid hormone concentrations during pregnancy. Therefore, we evaluated the effects of the different steroid hormones: progestins (progesterone, promegestone, levonorgestrel), antiprogestins (mifepristone), 17 beta-oestradiol or androgens (testosterone, dihydrotestosterone) on systolic blood pressure in pregnant, non-pregnant female and normal male rats with and without L-NAME treatment and spontaneously hypertensive male rats. The animals received continuous infusions of L-NAME (150 mg/kg/day) or vehicle through osmotic mini-pumps and daily s.c. injections of steroid hormones. In pregnant rats the pump was inserted on day 17 or 18 of gestation and steroid hormone injections were started on the first day following delivery at term and continued daily until post-partum day 10. In non-pregnant female or male rats steroid hormone injections were initiated 5 days after the L-NAME pump was inserted. Systolic blood pressure was measured daily from the tail with a pneumatic tail-cuff device. R5020 (1.5 mg/kg/day) significantly attenuated the blood pressure elevation induced by L-NAME during the post-partum period. Similarly, it lowered blood pressure in L-NAME treated non-pregnant female rats or male rats. R5020 also lowered blood pressure in spontaneously hypertensive male rats. Progesterone (6 mg/kg/day) had similar effects on blood pressure in the post-partum period, although it also lowered the blood pressure in control animals. Interestingly, administration of two different doses of levonorgestrel (0.3 and 1.5 mg/kg/day) did not decrease the blood pressure in either L-NAME-infused rats or controls. Mifepristone (RU486, 30 mg/kg/day) further increased blood pressure in L-NAME-treated rats post-partum. 17 beta-oestradiol (30 micrograms/kg/day) had no effect on blood pressure in either L-NAME infused rats in the post-partum period or controls, whereas both testosterone (0.3 mg/kg/day) and dihydrotestosterone (0.3 mg/kg/day) significantly attenuated the blood pressure increase after L-NAME, while raising the blood pressure in vehicle-infused animals. These results suggest that the control of systemic blood pressure during pregnancy may be modulated by steroid hormones. Progesterone may be the steroid hormone with the major action on vascular tension during pregnancy.

Regulation of vascular adaptation during pregnancy and post-partum: effects of nitric oxide inhibition and steroid hormones

Steroid modulation of pregnenolone to progesterone conversion by human placental cells in vitro

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Steroid modulation of pregnenolone to progesterone conversion by human placental cells in vitro