| Abstract: | In order to determine the mechanism by which stress may affect the secretion and function of luteinizing hormone (LH) in primates, the response of the adrenal and gonadal axes was followed in male rhesus monkeys during brief restraint in primate chairs and during various hormone treatments. To further assess the responsiveness of the gonadal axis, gonadotropin releasing hormone (GnRH) was administered during the experiments. Corticosteroid levels were elevated throughout the first restraint trial as compared to those in subsequent trials. LH was elevated in the first sample of the first trial as compared to that in the following trials. The responses of LH to GnRH were equivalent in all trials, while the testosterone response to GnRH was attenuated in the first trial. A single injection of adrenocorti-cotropin (ACTH, 40 IU), while increasing circulating corticosteroids similarly to that observed during the first restraint trial, failed to cause an acute initial release of LH. However, ACTH did lower the testosterone response to GnRH. Following 5 days of ACTH treatment (40 IU twice daily), basal LH was suppressed, and the testosterone response to GnRH was decreased. Following 5 days of cortisol injections (100 mg twice daily), basal LH and testosterone were suppressed, but again only the testosterone response to GnRH was attenuated. Acute restraint stress, acting by some mechanism other than the activation of adrenal axis, stimulates a transient release of LH. While the stress-stimulated release of corticosteroids failed to affect the LH response following GnRH administration, it did act directly on the testes to prevent the normal release of testosterone. Finally, chronic elevation of corticosteroids, produced by ACTH or cortisol administration, suppressed basal serum LH and attenuated the response of testosterone to GnRH. |
