Effect of Ovariectomy on Pituitary Secretion of ACTH

Coyne, Mary D.; Kitay, Julian I.

doi:10.1210/endo-85-6-1097

Cited by 118 publications

(53 citation statements)

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“…On the other hand, acute estrogen deficit caused a central reduction in DA which could lead to a reduction in CRH receptors on corticotropic cells. Similar observations were made by other researchers (25) who used hypothalamic extracts to stimulate pituitary release of ACTH and found a reduction in pituitary sensitivity after ovariectomy; this sensitivity was partially restored by administration of estrogens.…”

Section: Discussionsupporting

confidence: 86%

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Hypothalamo-pituitary-adrenal axis and adrenal function before and after ovariectomy in premenopausal women

Leo

Marca²,

Talluri³

et al. 1998

European Journal of Endocrinology

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The hypothalamo-pituitary-adrenal (HPA) axis is modulated by sex hormones. Few data exist on the relation between acute estrogen deficit and HPA axis response to corticotropin-releasing hormone (CRH).The effects of a sudden drop in estradiol levels on basal and CRH-stimulated levels of ACTH, cortisol, testosterone, androstenedione and 17-hydroxyprogesterone (17-OHP) were assessed in nine premenopausal women (44-48 years of age), before and after ovariectomy. The CRH test was performed before and 8 days after ovariectomy.A significant reduction in ACTH and adrenal steroids but not in cortisol response to CRH was observed after ovariectomy.The ratio of Dmax androstenedione/17-OHP after CRH stimulation was substantially the same before and after ovariectomy, whereas Dmax 17-OHP/cortisol was significantly lower in ovariectomized women showing increased 21-and 11b-hydroxylase activity. The results show that the acute estrogen deficit induces changes in the HPA axis characterized by reduced stimulated secretion of ACTH and steroids but normal stimulated cortisol production.

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Section: Discussionsupporting

confidence: 86%

“…These and other studies (5,23,24) provide evidence of the facilitatory effect of estrogens on the HPA axis, not only in animal models but also in humans. A reduction in the synthesis and release of pituitary ACTH after ovariectomy, restored by estradiol administration, has also been observed (25,26).…”

Section: Discussionmentioning

confidence: 87%

Hypothalamo-pituitary-adrenal axis and adrenal function before and after ovariectomy in premenopausal women

Leo

Marca²,

Talluri³

et al. 1998

European Journal of Endocrinology

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“…The restriction of the effects of testosterone in the current results to (ACTH) stimulated rather than basal conditions (Nowak et al, 1995) suggests that testosterone may interfere with ACTH signaling at the adrenal. While testosterone-related decreases in ACTH bioactivity have been observed in vitro (Coyne and Kitay, 1969), the Figure 2 Ratio of CRH-stimulated cortisol and ACTH values (mean7SE) during induced hypogonadal (leuprolide plus placebo) and testosterone replaced (leuprolide plus testosterone) conditions. A trend is seen for lower cortisol : ACTH ratios during the testosterone replacement condition.…”

Section: Discussionmentioning

confidence: 96%

Testosterone Suppression of CRH-Stimulated Cortisol in Men

Rubinow

Roca

Schmidt

et al. 2005

Neuropsychopharmacol

135

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Despite observations of age-dependent sexual dimorphisms in hypothalamic-pituitary-adrenal (HPA) axis activity, the role of androgens in the regulation of HPA axis activity in men has not been examined. We assessed this role by performing CRH stimulation tests in 10 men (ages 18-45 years) during gonadal suppression with leuprolide acetate and during testosterone addition to leuprolide. CRHstimulated cortisol levels as well as peak cortisol and greatest cortisol excursion were significantly lower (po0.05, 0.005, and 0.01, respectively) during testosterone replacement compared with the induced hypogonadal condition (leuprolide plus placebo); cortisol area under the curve was lower at a trend level (po0.1). Paradoxically, CRH-stimulated corticotropin (ACTH) was increased significantly during testosterone replacement (po0.05). The cortisol : ACTH ratio, a measure of adrenal sensitivity, was lower during testosterone replacement (po0.1). A mixed effects regression model showed that testosterone but not estradiol or CBG significantly contributed to the variance of cortisol. These data demonstrate that testosterone regulates CRH-stimulated HPA axis activity in men, with the divergent effects on ACTH and cortisol suggesting a peripheral (adrenal) locus for the suppressive effects on cortisol. Our results further demonstrate that the enhanced stimulated HPA axis activity previously described in young men compared with young women cannot be ascribed to an activational upregulation of the axis by testosterone.

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“…Whereas estradiol treatment appears to enhance, and testosterone treatment inhibits HPA reactivity, the mechanisms by which testosterone and estradiol act to influence HPA function have not been completely resolved. Evidence of estradiol and testosterone acting at the adrenal gland (Kitay 1965), anterior pituitary (Coyne and Kitay, 1969, 1971, Viau and Meaney, 2004 and hypothalamus (Viau and Meaney, 1996;Viau et al, 2003 has been reported. Although contributions of each level of the axis likely mediate the sex differences in HPA function, in this review we will focus our attention on the hypothalamic effects of the androgenic component of this regulation.…”

Section: Sex Differences Are Found In the Hpa Axis Response To Stressmentioning

confidence: 99%

An alternate pathway for androgen regulation of brain function: Activation of estrogen receptor beta by the metabolite of dihydrotestosterone, 5α-androstane-3β,17β-diol

Handa

Pak

Kudwa

et al. 2008

Hormones and Behavior

184

122

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The complexity of gonadal steroid hormone actions is reflected in their broad and diverse effects on a host of integrated systems including reproductive physiology, sexual behavior, stress responses, immune function, cognition, and neural protection. Understanding the specific contributions of androgens and estrogens in neurons that mediate these important biological processes is central to the study of neuroendocrinology. Of particular interest in recent years has been the biological role of androgen metabolites. The goal of this review is to highlight recent data delineating the specific brain targets for the dihydrotestosterone metabolite, 5α-androstane, 3β, 17β-diol (3β-Diol). Studies using both in vitro and in vivo approaches provide compelling evidence that 3β-Diol is an important modulator of the stress response mediated by the hypothalmo-pituitary-adrenal axis. Further, the actions of 3β-Diol are mediated by estrogen receptors, and not androgen receptors, often through a canonical estrogen response element in the promoter of a given target gene. These novel findings compel us to re-evaluate the interpretation of past studies and the design of future experiments aimed at elucidating the specific effects of androgen receptor signaling pathways.

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Effect of Ovariectomy on Pituitary Secretion of ACTH

Cited by 118 publications

References 0 publications

Hypothalamo-pituitary-adrenal axis and adrenal function before and after ovariectomy in premenopausal women

Hypothalamo-pituitary-adrenal axis and adrenal function before and after ovariectomy in premenopausal women

Testosterone Suppression of CRH-Stimulated Cortisol in Men

An alternate pathway for androgen regulation of brain function: Activation of estrogen receptor beta by the metabolite of dihydrotestosterone, 5α-androstane-3β,17β-diol

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