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The stresses of electrical shock or laparotomy were repeated at various intervals up to 24 hr after the initial stress in an attempt to demonstrate inhibition of the second response as a consequence of corticosterone secreted after the first stress. In all cases the second response was equal to or greater in magnitude than the first. When the stress of prolonged (60-90 min) restraint was paired with the minor stress of injection several hr later, no inhibition of the corticosterone response to injection was observed. However, if the plasma corticosterone levels provoked by restraint stress were mimicked by injections of corticosterone or of ACTH, the subsequent response to injection stress was inhibited. We conclude from these, and previous studies in the adrenalectomized rat, that corticosterone does act to inhibit ACTH secretion, but that stress causes a prolonged period of hyper—responsiveness in either CNS or anterior pituitary components of the adrenocortical system. (Endocrinology92: 1367, 1973) This content is only available as a PDF. Author notes 1 This investigation was supported by USPHS Grants AM-06704, AM-0S613, and NS-09528. 2 Traveling scholar of the Wellcome Trust. Present address: Senior Lecturer, Sherrington School of Physiology, St. Thomas’s Hospital Medical School, London, Great Britain. Copyright © 1973 by The Endocrine Society
Endocrinology – Oxford University Press
Published: May 1, 1973
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