Inhibitory effect of neurogenic and immune stressors on testosterone secretion in rats

We investigated the ability of foot shocks, endotoxemia and turpentine-induced tissue injury, to interfere with luteinizing hormone (LH) and testosterone (T) secretion, and the putative role of beta-adrenergic, opiate- and corticotropin-releasing factor (CRF) receptors in these responses.

Adult male rats were exposed to mild intermittent foot shocks for 1 h, administered endotoxin [lipopolysaccharide (LPS)] intravenously (i.v., 5 microg/kg), or injected with turpentine intradermally (i.m., 400 microl/kg), prior to injection with human chorionic gonadotropin (hCG, 1 U/kg i.v.). In some cases, antagonists to CRF, adrenergic or opiate receptors, or their vehicle were administered prior to the stressors. Levels of LH, T, tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), adrenocorticotropin (ACTH) and/or corticosterone were measured in serial blood samples.

All three challenges significantly lowered basal LH and T levels and blunted the T response to hCG, though the magnitude of this inhibition was significantly (p < 0.01) smaller in shocked rats (42%), compared to animals injected with LPS (92%) or turpentine (78%). Shocks, LPS and turpentine all significantly stimulated ACTH and corticosterone release, and the magnitude and time course of these responses were also stressor specific. While turpentine only increased circulating IL-6 concentrations, shocks and LPS both significantly increased circulating TNF-alpha and IL-6 levels, but the effect of shocks was markedly smaller. Pretreatment with propranolol did not restore T responses, while naloxone produced small and inconsistent effects. However, the CRF antagonist Astressin B, which significantly prevented stressor-induced increase in circulating levels of ACTH and corticosterone, partially reversed the inhibitory effect of LPS on hCG-induced T release.

(1) Both neurogenic and systemic stressors lower basal plasma LH and T levels and blunt the T response to hCG. (2) LPS, whose ability to release ACTH and corticosterone was similar to that of shocks, but caused increases in circulating TNF-alpha and IL-6 levels that were significantly larger than those due to the other stressors, was the most potent inhibitor of the T response to hCG. (3) Neither beta-adrenergic nor opiate receptors play a major role in the ability of the stressors we used to inhibit T release.