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INHIBITION OF SEROTONIN‐INDUCED ACTH RELEASE IN MAN BY CLONIDINE
Author(s) -
Jackson R. V.,
Grice J. E.,
Jackson A. J.,
Vella R. D.,
Armour M. B.
Publication year - 1988
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1988.tb01076.x
Subject(s) - clonidine , fenfluramine , endocrinology , medicine , agonist , placebo , adrenocorticotropic hormone , serotonin , chemistry , hormone , receptor , alternative medicine , pathology
SUMMARY 1. Clonidine, an α 2 ‐adrenergic agonist, is thought to inhibit noradrenergic neuronal activity (NNA) in the central nervous system (CNS) by a presynaptic α 2 ‐receptor mechanism. Central NNA is thought to be the primary monoaminergic stimulus to pituitary ACTH release. Fenfluramine, a serotonin releasing agent and uptake inhibitor, causes ACTH release in normal man. 2. The present study investigated the effect of clonidine on fenfluramine‐induced ACTH release in six normal volunteers. Four protocols were used: 1.5 mg/kg body weight oral fenfluramine; 4.3 μg/kg body weight oral clonidine; oral clonidine + oral fenfluramine 1 h later; placebo clonidine. Plasma ACTH and cortisol were measured at intervals for 5 h after clonidine and for 4 h after fenfluramine. 3. The mean plasma ACTH and cortisol levels and the mean maximal changes in these levels were significantly lower during the clonidine + fenfluramine test than during fenfluramine alone. Plasma ACTH and cortisol levels were not lowered significantly more by clonidine than by placebo. 4. In conclusion, clonidine blocked the ACTH‐releasing activity of fenfluramine in normal humans. This inhibition of active ACTH release may result from clonidine blockade of fenfluramine‐induced activation of central NNA. Clonidine alone was no more effective than placebo in lowering plasma ACTH and cortisol.