Stress, of both physical and emotional origin, has effects on the reproductive system. Although both ACTH and glucocorticoids are elevated in stress, there is little evidence that these hormones directly affect gonadotropin secretion or ovulation. Corticotropin-releasing factor (CRF) does interact with gonadotropin-releasing hormone (GnRH)-producing neurons, probably through an opioidergic pathway, suppressing gonadotropin secretion. Opioids, primarily beta-endorphin, originating through CRF-independent mechanisms in the brain or even the pituitary may also inhibit GnRH production. Tonic, pulsatile gonadotropin secretion is inhibited by stress and by administered morphine, but morphine does not block the estrogen-induced preovulatory surge in primates. Accordingly, impaired follicular development appears to be the most common cause of reproductive dysfunction attributable to stress in the human female. New developments in the understanding of the role of stress in reproduction must take into consideration the many differences between the hormonal responses to stress in the human and laboratory animals.