Abstract
In many species, including human beings, pregnancy results in an activation of the hypothalamus-pituitary-adrenal (HPA) axis, resulting in increased maternal cortisol secretion. This increase is important for maintaining an environment to support fetal growth and development, because adrenal excess or insufficiency results in disturbances in maternal and fetal homeostasis. The mechanism of the HPA axis activation is not completely understood, and in the human, may involve placental secretion of corticotropin releasing hormone. However, a common mechanism is likely to be the interaction of progesterone with mineralocorticoid receptors in the brain, resulting in an increase in set-point for cortisol. In the human, maternal cortisol can cross the placenta and affect fetal physiology before the fetal adrenal maturation. As the fetus matures, transplacental passage of cortisol decreases, and the fetal adrenal cortisol and androgen secretion increases. The maturing fetal HPA axis ultimately controls the timing of parturition by determining the rate of estrogen secretion from the placenta, thereby stimulating increased myometrial activity during labor. At term, interactions between the HPA and placental hormones may result in positive feedback cycles, which amplify and coordinate the increases in HPA secretion, myometrial activity, and fetal organ maturation.
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