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Vol. 50, No. 4, 1989
Issue release date: 1989
Section title: Original Paper
Neuroendocrinology 1989;50:427–432
(DOI:10.1159/000125259)

Single-Dose Ethanol Administration Activates the Hypothalamic-Pituitary-Adrenal Axis: Exploration of the Mechanism of Action

Thiagarajan A.B. · Mefford I.N. · Eskay R.L.
aLaboratory of Clinical Studies, National Institute on Alcohol Abuse and Alcoholism and bLaboratory of Clinical Science, National Institute of Mental Health, Bethesda, Md., USA

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: 10/11/1988
Accepted: 2/16/1989
Published online: 4/2/2008

Number of Print Pages: 6
Number of Figures: 0
Number of Tables: 0

ISSN: 0028-3835 (Print)
eISSN: 1423-0194 (Online)

For additional information: http://www.karger.com/NEN

Abstract

Activation of the hypothalamic-pituitary-adrenal axis (HPAA) by single-dose ethanol administration, which achieved moderately high blood ethanol levels, was explored in naive rats in order to determine the mechanism of ethanoΓs activation of the stress axis. Adult male rats received a single dose (3.2 g/kg body weight–1 of a 12% solution of ethanol in physiological saline. The plasma concentration of immunoreactive (ir) adrenocorticotropic hormone (ACTH), beta-endorphin (BE) and corticosterone (CS) was determined by radioimmunoassay, whereas, plasma concentrations of epinephrine (E) and norepinephrine (NE) were quantified following reverse-phase liquid chromatographic separation and amperometric detection. Ethanol induced maximal plasma ACTH levels within minutes, which declined toward basal levels by 60 min, whereas, plasma concentration of CS rose rapidly and remained elevated at 60 min. Plasma ACTH and CS levels in saline-treated control animals did not vary significantly at any time point. Consistent with co-release of ACTH from corticotrophs, the plasma concentration of ir-BE increased 5-fold at 15 min and declined towards basal levels at 60 min after-ethanol challenge. Plasma E increased 10- to 20-fold as compared to saline controls or preinjection levels and returned to preinjection levels by 90 min, in a manner similar to ethanol-induced changes in proopiomela-nocortin-derived peptides and CS. Removal of the adrenal medulla and thus the source of E prior to ethanol administration, did not attenuate activation of the HPAA. Passive immunoneutralization of arginine vasopressin (AVP), using a high-titer AVP anti-serum and a protocol which was found to block ether-induced ACTH secretion by 40% in adult male rats, failed to even partially block ethanol-induced ACTH or CS secretion. The results of this study indicate that neither adrenal medulla-derived E nor AVP are significant regulators or coregulators of corticotroph secretions following a moderately high, single-dose, intragastric administration of ethanol.


  

Author Contacts

Robert L. Eskay, PhD, Laboratory of Clinical Studies, NIAAA, NIH, Building 10, Rm 3C-216, 9000 Rockville Pike, Bethesda, MD 20892 (USA)

  

Article Information

Received: October 11, 1988
Accepted after revision: February 16, 1989
Published online: April 02, 2008
Number of Print Pages : 6

  

Publication Details

Neuroendocrinology (International Journal for Basic and Clinical Studies on Neuroendocrine Relationships)

Vol. 50, No. 4, Year 1989 (Cover Date: 1989)

Journal Editor: Millar R.P. (Edinburgh)
ISSN: 0028–3835 (Print), eISSN: 1423–0194 (Online)

For additional information: http://www.karger.com/NEN


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: 10/11/1988
Accepted: 2/16/1989
Published online: 4/2/2008

Number of Print Pages: 6
Number of Figures: 0
Number of Tables: 0

ISSN: 0028-3835 (Print)
eISSN: 1423-0194 (Online)

For additional information: http://www.karger.com/NEN


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