Publication | Closed Access
Effect of Orchiectomy on Pituitary Secretion of ACTH
47
Citations
0
References
1971
Year
SpermatogenesisNeuroendocrinologyFemale Reproductive FunctionReproductive BiologyPituitary SecretionReproductive EndocrinologyAdrenal GlandPituitary GlandReproductive MedicinePituitary DiseasePublic HealthPituitary Acth ReleaseAnimal PhysiologyEndocrine MechanismEndocrinologyPhysiologyAdrenal HealthTestosterone ReplacementMedicineEndocrine ResearchReproductive HormoneAnesthesiology
The effects of prepuberal gonadectomy on pituitary secretion of ACTH were studied in adult male rats. Plasma concentration of ACTH in unstressed adrenalectomized rats was increased following orchiectomy to 197% (95% confidence limits 134-289%) of the control level. Higher plasma ACTH concentrations were also observed in castrated animals with adrenals intact after the acute stress of ether anesthesia when compared to similarly stressed controls (159%; 121-215%). In both experiments, replacement with testosterone reversed the response to orchiectomy. Unstimulated release of ACTH in vitro by whole pituitary glands from orchiectomized donors, without or with testosterone replacement in vivo, did not differ from that of control glands. Addition of stalk-median eminence extract to the incubating glands, however, resulted in a greater release of ACTH by pituitary glands from the orchiectomized group (162% of control; 124 – 211%) and partial restoration toward the control level with testosterone replacement (130% of control; 110-153%). Parallel studies with pituitary glands from adrenalectomized animals yielded similar results. Direct addition of testosterone in vitro did not affect pituitary ACTH release. Hypothalamic content of corticotropin releasing activity was not altered by castration or testosterone replacement. The data indicate that orchiectomy results in elevated pituitary ACTH release independently of concomitant changes in adrenal function or conditions related to steroid feed-back. The increase seems related, at least in part, to pituitary hyperresponsiveness to corticotropin releasing factor. (Endocrinology89: 1024, 1971)