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Effects of Adrenocorticotropin and Corticosterone on the Negative Feedback Action of Testosterone in the Adult Male Rat

Department of Endocrinology, Growth, and Reproduction, and Department of Internal Medicine HI and Clinical Endocrinology 3000 DR Rotterdam, The Netherlands
Faculty of Medicine, Erasmus University 3000 DR Rotterdam, The Netherlands

Address correspondence and requests for reprints to: J. T. M. Vreeburg, Department of Endocrinology, Growth, and Reproduction, P.O. Box 1738, 3000 DR Rotterdam, The Netherlands.

Abstract

Injections of ACTH (Synacthen depot) to intact male rats resulted in high serum levels of corticosterone and progesterone, and decreased levels of LH, FSH, and testosterone. In gonadectomized rats with low serum testosterone levels (1 ng/ml) induced by a small testosterone-filled silicone elastomer capsule, ACTH inhibited the postcastration rise in LH and FSH and reduced the wts of the prostate and seminal vesicles. After adrenalectomy the inhibitory effects of ACTH on serum gonadotropins and organ wts were almost totally absent. Administration of corticosterone acetate (10 mg/day) to gonadectomized and adrenalectomized male rats resulted in high serum levels of corticosterone (400 ng/ml) which were about 3 times higher than those measured in intact control animals. Nevertheless, in these rats the serum levels of LH and FSH were as high as those measured in gonadectomized and adrenalectomized oil-treated rats. However, when in addition to the injections of corticosterone acetate, a small testosterone-filled capsule was implanted, the postcastration rise in FSH was fully inhibited, whereas the serum levels of LH were below the level of detection. Significant inhibition of the postcastration rise in LH and FSH also occurred when smaller quantities of corticosterone acetate were given. Since in gonadectomized and adrenalectomized male rats similar testosterone-filled capsules did not prevent the postcastration rise in LH and FSH, it is concluded that a high serum level of corticosterone increases the sensitivity to the negative feedback effects of testosterone. (Endocrinology 115: 977–983, 1984)

Received September 9, 1983.

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