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Am J Physiol Endocrinol Metab. 2007 Apr;292(4):E1173-82. Epub 2006 Dec 19.

Estrogen potentiates adrenocortical responses to stress in female rats.

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Department of Psychiatry, University of Cincinnati, Genome Research Institute, Psychiatry North, ML 0506, Bldg. 43, 2nd Floor, 2170 East Galbraith Road, Reading, OH 45237-0506, USA.


It is well established that estrogens markedly enhance the glucocorticoid response to acute stress in females. However, the precise mechanism responsible for this regulation is poorly understood. Here, we tested whether estrogens enhance the activation of the paraventricular nucleus (PVN) of the hypothalamus by measuring stress-induced c-fos mRNA expression in the PVN of restraint-stressed ovariectomized (OVX) rats treated with physiologically relevant doses of estradiol (E(2)), the major female estrogen. As expected, E(2) enhanced plasma corticosterone responses to restraint in OVX females. However, E(2) markedly attenuated the stress-induced c-fos gene expression in the PVN and inhibited plasma ACTH responses in these animals. Furthermore, E(2)-inhibitory effects were mimicked by progesterone (P) alone or in combination with E(2). Interestingly, the suppressive central effects of both E(2) and P were apparently independent of basal paraventricular corticotropin-releasing hormone (CRH) transcription, since these ovarian steroids did not significantly affect PVN CRH mRNA expression in unstressed rats. These unexpected findings suggested that E(2) promotes glucocorticoid hypersecretion in females by additional peripheral (i.e., adrenal) mechanisms. Indeed, E(2) markedly enhanced plasma corticosterone responses and adrenal corticosterone content in dexamethasone-blocked OVX rats challenged with varying doses of exogenous ACTH. These results suggest that enhanced adrenal sensitive to ACTH is an important physiological mechanism mediating E(2)-related glucocorticoid hypersecretion in stressed females.

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