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  • Title: Potentiation of adrenocortical response upon intermittent stimulation with corticotropin in normal subjects.
    Author: Kolanowski J, Pizarro MA, Crabbé.
    Journal: J Clin Endocrinol Metab; 1975 Sep; 41(3):453-65. PubMed ID: 169285.
    Abstract:
    Modifications of adrenocortical steroidogenic response to ACTH as a consequence of acute prior exposure to this hormone, were studied in 106 normal subjects divided in 15 experimental groups. Adrenocortical response was assessed by the changes in plasma cortisol level and in urinary excretion of cortisol, 17-ketogenic and 17-ketosteroids; in some experiments plasma 11-deoxycortisol, corticosterone, progesterone and 17-hydroxyprogesterone were determined as well, together with urinary excretion of the unconjugated form of 11-deoxycortisol and corticosterone. Slow (8-h) intravenous administration of ACTH in amounts producing maximal response, leaves the adrenal cortex in a hyperresponsive state in case of further stimulation for up to 3 days, while the adrenocortical secretion comes back to baseline in the meantime. This potentiation phenomenon seems to concern essentially cortisol secretion since, among the compounds measured only cortisol and 11-deoxycortisol secretions increased progressively in amplitude when ACTH was administered repeatedly. Futhermore the degree of ACTH-induced adrenocortical hyperresponsiveness was found to depend on the amount of ACTH injected and on the time during which the adrenal cells are exposed to high peptide hormone concentrations. Increased adrenocortical responsiveness to ACTH persists when endogenous corticotropin secretion was suppressed for a few days by dexamethasone in normal subjects. Thus the potentiation phenomenon is not critically dependent on continued exposure of adrenal cells to endogenous corticotropin.
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