To determine the effects of suppressing fetal and maternal adrenal activity on parturition, we treated pregnant rhesus macaques with dexamethasone (0.25 to 4.0 mg, twice a day) from gestation day 130 until delivery (term = 167 days). Long-term dexamethasone treatment increased gestation length: 71% of fetuses were born postmaturely (after day 175 of gestation; X2 = 52.6; P less than 0.001). The dexamethasone decreased basal levels of maternal estradiol and cortisol, but not progesterone, and abolished the prepartum estrogen and prolactin surges; doses greater than 0.16 mg/kg per day resulted in fetal death but not premature delivery. That vaginal delivery was induced by estradiol benzoate in monkeys with prolonged pregnancy and dead fetuses, but not in those with live fetuses, suggests active fetal inhibition of prostaglandin synthesis. The dexamethasone retarded fetal growth (410 +/- 16 gm versus 501 +/- 5 gm for controls; P less than 0.001) and decreased thymus, spleen, and adrenal weights (P less than 0.01). A less significant decrease in brain weight was noted (P less than 0.1), as were decreases in biparietal diameter, occipitofrontal diameter, and head circumference (P less than 0.05). These results indicate that corticosteroids do not induce premature labor in primates. On the contrary, long-term dexamethasone administration is associated with prolonged pregnancy and suppression of estrogen biosynthesis.