Hormonal Mechanisms Controlling Parturition

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Abstract
In summarizing these data regarding the hormonal control of parturition we are presenting the following hypothetical model: A stimulus to the fetal hypothalamus invokes the fetal pituitary-adrenal axis to increase glucocorticoid secretion. This may result from maturation of the appropriate hypothalamic centers permitting a response to stimuli already present; from the occurrences of new stresses in the maturing fetus which we do not presently recognize; or this may be due to maturation or changes in other organs of the body such as the lung, liver or kidney. This area clearly requires much more study. This increase in fetal adrenal glucocorticoid production is a constant occurrence in all mammals prior to parturition. The increased fetal adrenal activity provides additional precursors for an increased estrogen synthesis by the placenta. Increased prostaglandin production by the uterus follows the rise in fetal glucocorticoid production and can be produced by administration of exogenous glucocorticoids, Prostaglandins may exert an effect on myometrial activity, cause a decrease in progesterone production, effect an oxytocin release and stimulate estrogen production by the placenta. All of these effects have been documented in one or more species and the relative importance of these responses may vary between species. A decrease in maternal plasma progesterone and progesterone concentration in the myometrium occurs. This may result from the action of prostaglandins on the corpus luteum but is difficult to associate with prostaglandins in species such as the sheep or human which have a placental source of progesterone. It is also true that a progesterone decline is not an absolute requirement for parturition in all mammals. The decrease in myometrial progesterone may result from a decrease in myometrial cell protein receptor, increased degradation of progesterone to less active metabolites or both. An increase in estrogens occurs in all malmals in late pregnancy. Although there is a gradual increase throughout pregnancy we are most concerned with the sharp increase which occurs from 1 to 7 days prepartum in the various species. This increase is associated with the increased prostaglandin production by the uterus and it has been suggested that prostaglandin and estrogen production form a self-reinforcing cycle since administration of either one will stimulate an increase in the other. As mentioned above, the availability of an increased supply of precursors from the fetal adrenal is also important in this estrogen increase. The change to estrogen dominance prepares the uterus for a stronger and more rhythmic response to the process of fetal expulsion. This altered ratio also increases the release of oxytocin from the neurohypophysis in response to neural stimuli from the reproductive tract. Increased estrogen levels are also important in a general relaxation of the birth canal and dilatation of the cervix and vagina. These latter effects may also be due to the action of relaxin produced by the placenta, uterus and/or the ovary. Finally the fetus is expelled from the uterus. In this process, myometrial contractions resulting from the stimulatory effects of prostaglandins and oxytocin and the abdominal press exerted by the musculature of the abdominal wall combine to bring about the delivery of the fetus or fetuses.

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