STUDIES ON THE MECHANISM OF ACTION OF OESTROGENS ON THE PITUITARY-ADRENAL FUNCTION IN THE MALE RAT

• Published in: Acta endocrinologica (Copenhagen) Vol. 68; no. 4; pp. 737 - 748
• Main Author: Perklev, T
• Format: Journal Article
• Language: English
• Published: Denmark 01.12.1971
• Subjects: Adrenal Glands - analysis; Adrenal Glands - drug effects; Animals; Corticosterone - blood; Diethylstilbestrol - pharmacology; Follicle Stimulating Hormone - pharmacology; Gonads - physiology; Hydroxysteroid Dehydrogenases - analysis; Hydroxysteroid Dehydrogenases - metabolism; Luteinizing Hormone - pharmacology; Male; Organ Size; Prostate - analysis; Rats; Sodium Chloride - pharmacology; Testosterone - pharmacology
• ISSN: 0804-4643; 0001-5598; 1479-683X
• DOI: 10.1530/acta.0.0680737

ABSTRACT A single injection of a long-acting oestrogen, polydiethylstilboestrol phosphate (PSP; 200 μg/100 g body weight), into adult male rats caused an enlargement of the adrenal glands and an approximate doubling of total adrenal 3β-hydroxysteroid dehydrogenase (3β-OHD) activity and plasma corticosterone concentration in animals sacrificed 11 to 14 days following injection. The administration of interstitial cell stimulating hormone (ICSH) of human origin or a long-acting testosterone ester (Andradurin®) into the PSP-treated animals partially or completely counteracted the effects of the PSP treatment on adrenal weight and 3β-OHD activity. Daily injections of corticotrophin (ACTH) into intact male rats for 7 days caused a significant rise in the adrenal 3β-OHD activity. Gonadectomy of male rats resulted in increased adrenal weights and elevated adrenal 3β-OHD activity. The plasma corticosterone concentration was unaffected. PSP treatment significantly augmented the effects of the gonadectomy on the adrenal weight and 3β-OHD activity and caused an elevated plasma corticosteroid concentration. The adrenal enlargement following gonadectomy was completely reversed by testosterone replacement but was not influenced by daily injections of ICSH. The data are interpreted as suggesting that the oestrogen-induced hyper-secretion of ACTH in the male rat may be mediated through an elevated activity of the corticosteroid-binding globulin, caused by a reduced plasma testosterone level and a stimulated thyroid activity.