1980EndocrinologyRequires access

The Interaction of Castration and Adrenalectomy on Pituitary Responses to Loss of Target Gland Negative Feedback in the Male Rat*

JANICE R. LORENZEN, CINDY SCHLEPPHORST, Neena B. Schwartz

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Abstract

Simultaneous adrenalectomy and castration causes a delay in the gonadotropin rise which normally occurs by 12 h post castration. It was postulated that this delay could be due to 1) the absence of progesterone release from the adrenals which, if present, could cause acute LH/FSH secretion in the absence of the testes, 2) the absence of a corticosterone background necessary for acute release of LH/FSH in response to castration, or 3) a competition at the level of the pituitary or central nervous system between secretion of ACTH in response to adrenalectomy and LH/FSH in response to castration. These experiments were designed to assess these possibilities by separating the time of adrenalectomy from the time of castration. Adrenalectomy either 12 h before or 12 h after castration still delayed the gonadotropin castration response for 24 h. Sham adrenalectomy 12 h after castration also delayed the LH/FSH rise. Thus, the delaying effect could not be due simply to the absence of either progesterone or corticosterone. Measurement of PRL, ACTH, and the gonadotropins suggested that PRL inhibition of gonadotropin release may be a factor in the stalled gonadotropin response seen 12 h post surgery when adrenalectomy is performed with or after castration, since PRL is high 12 h post adrenalectomy or sham surgery. Since ACTH was secreted maximally after either adrenalectomy (for at least 1 h) or sham surgery (for at least 10 min), a competition at some level between simultaneous ACTH secretion and LH/FSH secretion or a direct inhibitory influence of ACTH on gonadotropin release may still be a factor in the delay. Furthermore, a secondary finding in the study is that the responses of ACTH and PRL to surgical stress are not identical in the male rat, since while both are elevated at 10 min post operative stress, at 1 h post surgery, regardless of whether the animal had previously been castrated, sham castrated, or unoperated, PRL falls to baseline assay levels while ACTH continues to rise. (Endocrinology106: 592, 1980)

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Simultaneous adrenalectomy and castration causes a delay in the gonadotropin rise which normally occurs by 12 h post castration. It was postulated that this delay could be due to 1) the absence of progesterone release from the adrenals which, if present, could cause acute LH/FSH secretion in the absence of the testes, 2) the absence of a corticosterone background necessary for acute release of LH/FSH in response to castration, or 3) a competition at the level of the pituitary or central nervous system between secretion of ACTH in response to adrenalectomy and LH/FSH in response to castration. These experiments were designed to assess these possibilities by separating the time of adrenalectomy from the time of castration. Adrenalectomy either 12 h before or 12 h after castration still delayed the gonadotropin castration response for 24 h. Sham adrenalectomy 12 h after castration also delayed the LH/FSH rise. Thus, the delaying effect could not be due simply to the absence of either progesterone or corticosterone. Measurement of PRL, ACTH, and the gonadotropins suggested that PRL inhibition of gonadotropin release may be a factor in the stalled gonadotropin response seen 12 h post surgery when adrenalectomy is performed with or after castration, since PRL is high 12 h post adrenalectomy or sham surgery. Since ACTH was secreted maximally after either adrenalectomy (for at least 1 h) or sham surgery (for at least 10 min), a competition at some level between simultaneous ACTH secretion and LH/FSH secretion or a direct inhibitory influence of ACTH on gonadotropin release may still be a factor in the delay. Furthermore, a secondary finding in the study is that the responses of ACTH and PRL to surgical stress are not identical in the male rat, since while both are elevated at 10 min post operative stress, at 1 h post surgery, regardless of whether the animal had previously been castrated, sham castrated, or unoperated, PRL falls to baseline assay levels while ACTH continues to rise. (Endocrinology106: 592, 1980)

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Available abstract

Simultaneous adrenalectomy and castration causes a delay in the gonadotropin rise which normally occurs by 12 h post castration. It was postulated that this delay could be due to 1) the absence of progesterone release from the adrenals which, if present, could cause acute LH/FSH secretion in the absence of the testes, 2) the absence of a corticosterone background necessary for acute release of LH/FSH in response to castration, or 3) a competition at the level of the pituitary or central nervous system between secretion of ACTH in response to adrenalectomy and LH/FSH in response to castration. These experiments were designed to assess these possibilities by separating the time of adrenalectomy from the time of castration. Adrenalectomy either 12 h before or 12 h after castration still delayed the gonadotropin castration response for 24 h. Sham adrenalectomy 12 h after castration also delayed the LH/FSH rise. Thus, the delaying effect could not be due simply to the absence of either progesterone or corticosterone. Measurement of PRL, ACTH, and the gonadotropins suggested that PRL inhibition of gonadotropin release may be a factor in the stalled gonadotropin response seen 12 h post surgery when adrenalectomy is performed with or after castration, since PRL is high 12 h post adrenalectomy or sham surgery. Since ACTH was secreted maximally after either adrenalectomy (for at least 1 h) or sham surgery (for at least 10 min), a competition at some level between simultaneous ACTH secretion and LH/FSH secretion or a direct inhibitory influence of ACTH on gonadotropin release may still be a factor in the delay. Furthermore, a secondary finding in the study is that the responses of ACTH and PRL to surgical stress are not identical in the male rat, since while both are elevated at 10 min post operative stress, at 1 h post surgery, regardless of whether the animal had previously been castrated, sham castrated, or unoperated, PRL falls to baseline assay levels while ACTH continues to rise. (Endocrinology106: 592, 1980)

Key concepts: Castration, Adrenalectomy, Internal medicine, Endocrinology, Corticosterone, Gonadotropin, Orchiectomy, Medicine

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The Interaction of Castration and Adrenalectomy on Pituitary Responses to Loss of Target Gland Negative Feedback in the Male Rat* — Research Paper | ScholarLens