FAILURE TO INHIBIT CORTICOTROPHIN SECRETION BY EXPERIMENTALLY INDUCED INCREASES IN CORTICOID LEVELS

ABSTRACT The present experiments were designed in order to investigate whether physiological elevations in corticoid blood levels would inhibit the pituitary-adrenal response to stress. Plasma corticosterone (11β,21-dihydroxypregn-4-ene-3,20-dione) levels and the in vitro corticoid production by exc...

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Bibliographic Details
Published inActa endocrinologica (Copenhagen) Vol. 44; no. 1; pp. 36 - 46
Main Author SMELIK, P G
Format Journal Article
LanguageEnglish
Published Denmark 01.09.1963
Subjects
Adrenal Cortex Hormones
Adrenocorticotropic Hormone
Blood Chemical Analysis
Corticosterone
Heart Arrest
Histamine
Pharmacology
Rats
Stress, Physiological
CORTICOSTERONE
BLOOD CHEMICAL ANALYSIS
PHARMACOLOGY
EXPERIMENTAL LAB STUDY
RATS
HISTAMINE
STRESS
CORTICOTROPIN
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Summary:ABSTRACT The present experiments were designed in order to investigate whether physiological elevations in corticoid blood levels would inhibit the pituitary-adrenal response to stress. Plasma corticosterone (11β,21-dihydroxypregn-4-ene-3,20-dione) levels and the in vitro corticoid production by excised adrenals were determined in anaesthetized rats, pretreated with corticosterone solutions injected intravenously or intramuscularly. Intravenous administration of small amounts of corticosterone induced a very high but transient peak in plasma corticosterone concentrations. Corticosterone infusion caused a constant increase in plasma corticosterone levels. Increases exceeding maximal physiological values did not prevent the adrenocortical activation produced by histamine or corticotrophin. The summation of exogenous (infused) and endogenous (produced) corticosterone in the plasma became incomplete with increasing levels. This summation was not due to an increasing inhibition of the endogenous production, but to a higher rate of disappearance from the blood. It is concluded that these data are not in agreement with the »variable set point control theory[00AP], and demonstrate that physiological variations in plasma corticoid concentration do not affect the acute stress-induced corticotrophin release.
ISSN:0804-4643
0001-5598
1479-683X
DOI:10.1530/acta.0.0440036