The role of stress in female reproduction: animal and human considerations.

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.

Inhibin from cultures of rat seminiferous tubules.

Medium from cultures of mature rat seminiferous tubules contained a substance which suppressed, in a dose-related manner, the luteinizing hormone releasing hormone (LH-RH)-stimulated secretion of FSH by cultured rat pituitary cells. The secretion of LH was suppressed to a lesser extent and the basal secretion of both LH and FSH was inconsistently affected. Gel filtration on Sephadex G-100 did not fractionate the activity. The active material did not inhibit the secretion of TSH or destroy LH-RH and the activity was not due to testosterone or oestradiol in the medium. Control media from liver cultures were inactive. It is concluded that inhibin is present in media from cultures of rat seminiferous tubules.