Dexamethasone (8 mg/day im) has been administered to rhesus monkeys (Macaca mulatto) from days 146–156 of pregnancy, until term. This treatment was ineffective in precipitating premature delivery, and the monkeys delivered spontaneously at the expected time (day 166–176). Maternal peripheral plasma progesterone concentrations were unaffected by the dexamethasone treatment. However, administration of the synthetic glucocorticoid resulted in a marked suppression of the maternal plasma estrone and estradiol-17β concentrations in all animals. In the 4 monkeys in which injections of dexamethasone were initiated earliest (days 146–150), the plasma unconjugated estrogen levels at term were 15–40% of those found prior to the start of treatment. At autopsy, the adrenal glands from the fetuses of dexamethasone-treated monkeys had markedly atrophied, and showed appreciable regression of the fetal zone. It is suggested that dexamethasone crosses the placenta and inhibits fetal ACTH release, resulting in regression of the fetal adrenal, and a reduction in its secretion of C19 steroids for placental aromatization. These results provide no support for the hypothesized role of the fetal adrenal in the initiation of normal parturition in primates.
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