Depletion of pituitary corticotrophin by various stresses and by neurohypophysial preparations
The Journal of PhysiologyPublished 23 April 1959Open access
G. J. Rochefort, John Rosenberger, Murray Saffran
Citations46
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MedicineBiochemistry, Genetics and Molecular Biology
Journal of Biological ChemistryPROTEIN MEASUREMENT WITH THE FOLIN PHENOL REAGENT
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The rapidity with which the pituitary can release adrenocorticotropic hormone (ACTH) in response to various stimuli suggests that the nervous system must play a role in regulatingpituitary function.
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A great deal of evidence indicates that the release of pituitary adrenocorticotrophin resulting from stress is under neural control, and it appears likely that the hypothalamus constitutes a major pathway for excitation of ACTH release.
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Exposure of rats to intense sound or light was shown to elicit a rapid and intense discharge of ACTH, as evidenced by the depletion of the adrenal ascorbic acid content.
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The development of a technic for the analysis of blood ACTH has overcome difficulties and more nearly reflects pituitary activity at any instant and it is entirely possible that stress acting in combination with ACTH will produce an alteration in the concentrations of adrenal metabolites of greater magnitude than that produced by ACTH alone.
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Although results have varied somewhat, destructive lesions in different sites of the hypothalamus have been reported by several investigators to inhibit the release of ACTH by using pituitary transplants in the rat and rabbit.
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The results are interpreted to mean that vasopressin can evoke ACTH release in rats with those hypothalamic lesions which prevent the adrenal response to certain non-specific stimuli and that the ACTH-releasing activity of neurohypophyseal extracts, when tested in vivo, is accounted for by their content of vasoppressin.
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A fairly exhaustive classification of mechanisms regardless of available experimental support is set out, which justifies the popularity of acceptance of the thesis that the portal venous system carries a neurohumor from the median eminence to the adenohypophysis.
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It is concluded that at least one mechanism whereby high levels of the adrenal cortical hormones inhibit the release of ACTH following stress is by blocking the secretion from a cerebral structure, presumably the hypothalamus, of a pituitary stimulating substance (s).
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On the basis of the results reported by McDermott et al. (1950) one of the mechanisms controlling the release of adrenocorticotropin (ACTH) from the pituitary is due to an activation of the sympathetic nervous system.
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The small saphenous vein on the foot of the rat is far more satisfactory than the more commonly used tail vein for intravenous injection, according to Dr. Everett and Sawyer1.
