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Hemorrhage‐Induced Activations of Adrenocorticotropin Release and Catecholamine Metabolism in the Ventrolateral Medulla are Differently Affected by Glucocorticoid Feedback
Author(s) -
Ponec J.,
Lachuer J.,
SuaudChagny M. F.,
Tappaz M.
Publication year - 1992
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1111/j.1365-2826.1992.tb00187.x
Subject(s) - endocrinology , medicine , stimulation , prazosin , catecholamine , propranolol , chemistry , catecholaminergic , antagonist , glucocorticoid , adrenal medulla , dexamethasone , metabolism , receptor
We have compared the effects of increasing doses of dexamethasone on the hemorrhage‐induced stimulation of the corticotropic axis and the metabolism of the catecholamines of the A1 group in the ventrolateral medulla. Adrenocorticotropin was measured in sequential samples of plasma while the metabolism of the catecholamines was recorded by in vivo electrochemistry in urethane‐anesthetized rats. Combined intracerebroventricular injection of specific adrenergic blockers (α 1 ‐antagonist, prazosin and ß‐antagonist, propranolol) prevented the stimulation of the adrenocorticotropin release by hemorrhage. Pretreatment with dexamethasone (1 mg/kg sc) fully blocked the hemorrhage‐induced adrenocorticotropin release but did not affect the concomitant stimulation of the catecholamine metabolism in A1 cells. The latter was partially decreased only with the highest dose (10 mg/kg sc). While a central catecholaminergic input appears to be necessary for the hemorrhage‐induced stimulation of the corticotropic axis, it does not seem to play a significant role in the feedback regulation by glucocorticoids.