Concentrations of maternal plasma beta-endorphin (beta-EP) as measured by radioimmunoassay decline during pregnancy, reaching a nadir during the second trimester, rise during labor, remain elevated during the early postpartum period and are increased prior to elective cesarean section in the absence of labor. They decline in response to epidural anesthesia during labor and increase during induction of general but not regional anesthesia for cesarean section. Umbilical venous plasma beta-EP levels are not affected by the route or mode of delivery nor the presence or absence of labor, but rise in conjunction with fetal distress. In the presence of fetal distress, umbilical arterial plasma beta-EP levels appear to rise faster than umbilical venous beta-EP concentrations. Amniotic fluid beta-EP levels are higher during the second than third trimester. These data indicate that peripheral plasma beta-EP concentrations reflect stress in both mother and fetus. In the mother, pregnancy itself does not appear to be stressful, whereas pain associated with labor rather than uterine contractions as such increase plasma beta-EP levels. In the fetus, hypoxia and acidosis effectively raise plasma beta-EP concentrations. The origin and physiologic significance of amniotic fluid beta-EP, which appears to be unrelated to fetal maturity, remain to be established.