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Biomedical subjects

M D Calderón

Publications and source records attributed to M D Calderón.

4 recordsLinked to original sources
PubMed1991

Stress induced changes in testis function.

The mechanism through which chronic stress inhibits the hypothalamic-pituitary-testicular axis has been investigated. Chronic restraint stress decreases testosterone secretion, an effect that is associated with a decrease in plasma gonadotropin levels. In chronically stressed rats there was a decrease in hypothalamic luteinizing hormone-releasing hormone (LHRH) content and the response on plasma gonadotropins to LHRH administration was enhanced. Thus the inhibitory effect of chronic stress on plasma LH and FSH levels seems not to be due to a reduction in pituitary responsiveness to LHRH, but rather to a modification in LHRH secretion. It has been suggested that beta-endorphin might interfere with hypothalamic LHRH secretion during stress. Chronic immobilization did not modify hypothalamic beta-endorphin, while an increase in pituitary beta-endorphin secretion was observed. Since we cannot exclude that changes in beta-endorphin secreted by the pituitary or other opioids may play some role in the stress-induced decrease in LHRH secretion, the effect of naltrexone administration on plasma gonadotropin was studied in chronically stressed rats. Naltrexone treatment did not modify the decrease in plasma concentrations of LH or FSH. These findings suggest that the inhibitory effect of restraint on the testicular axis is exerted at hypothalamic level by some mechanism other than opioids.

Adrenal Glands↗
PubMed1989

Role of the adrenal cortex in chronic stress-induced inhibition of prolactin secretion in male rats.

The response of prolactin to chronic stress in intact, adrenalectomized and adrenomedullectomized male rats was studied. Immobilization stress in intact animals induced a significant increase in plasma concentrations of prolactin after 20 and 45 min and a significant decrease when the rats were submitted to chronic restraint (6 h daily for 4 days). Five weeks after adrenomedullectomy, plasma prolactin and corticosterone responses to chronic stress were not modified. In contrast, the inhibitory effect of chronic stress on prolactin secretion was totally suppressed by adrenalectomy. When treated with dexamethasone during the 4 days of restraint, adrenalectomized stressed rats showed similar plasma concentrations of prolactin to the intact stressed rats. These data indicate that the adrenal cortex is able to play an inhibitory role on prolactin secretion during stress only through a prolonged release of glucocorticoids.

Adrenal Cortex↗
PubMed1989

Effect of adrenomedullectomy and propranolol treatment on the response of gonadotrophins to chronic stress in male rats.

In order to study the involvement of the adrenal medulla in stress-induced inhibition of gonadotrophin secretion, we measured plasma concentrations of LH, FSH and corticosterone in adult male rats subjected to chronic restraint after surgical ablation of the adrenal medulla. In intact animals, chronic restraint (6 h daily over 4 days) induced a significant (P less than 0.05) decrease in plasma concentrations of LH, whereas plasma concentrations of corticosterone showed the expected significant (P less than 0.01) increase. Adrenomedullectomy did not significantly modify basal plasma concentrations of LH or corticosterone. In these rats, there was no significant decrease of LH after stress, while the increase in corticosterone was as significant as in sham-operated animals (P less than 0.01). In order to confirm the role of adrenomedullary catecholamines in stress-induced gonadotrophin inhibition another group of rats was treated s.c. with the beta-adrenergic blocker propranolol (2 mg/kg twice daily). These rats showed an attenuated inhibition of LH during stress similar to that observed in adrenomedullectomized rats. Levels of FSH were significantly reduced after stress in the saline-treated group, while there were no differences between stressed or unstressed rats in the propranolol-treated group. These results may be considered as evidence that medullary catecholamines, acting through beta-receptors, are factors involved in gonadotrophin inhibition during chronic stress.

Adrenal Medulla↗