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

• Published in: Acta endocrinologica (Copenhagen) Vol. 44; no. 1; pp. 36 - 46
• Main Author: SMELIK, P G
• Format: Journal Article
• Language: English
• 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
• DOI: 10.1530/acta.0.0440036
• ISSN: 0804-4643; 0001-5598

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.