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Vol. 50, No. 2, 1989
Issue release date: 1989
Section title: Original Paper
Neuroendocrinology 1989;50:117–123
(DOI:10.1159/000125210)

On the Role of Brain Mineralocorticoid (Type I) and Glucocorticoid (Type II) Receptors in Neuroendocrine Regulation

Ratka A. · Sutanto W. · Bloemers M. · de Kloet E.R.
Rudolf Magnus Institute for Pharmacology, Medical Faculty, University of Utrecht, The Netherlands

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: 8/22/1988
Accepted: 12/21/1988
Published online: 4/2/2008

Number of Print Pages: 7
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

Administrations of the glucocorticoid receptor antagonist (anti-glucocorticoid, RU38486) and the mineralocorticoid antagonist (anti-mineralocorticoid, RU28318) followed by frequent, sequential blood sampling were employed to investigate the possible role the brain mineralocorticoid receptor (MR, type I) and glucocorticoid receptor (GR, type II) have in the regulation of basal and stress-induced adrenocortical secretion in the rat. The anti-mineralocorticoid and anti-glucocorticoid were administered subcutaneously (s.c.) at doses of 2.5 mg and 1.0 mg/100 g body weight, respectively. Both antagonists were also given intracerebro-ventricularly (i.c.v.) at a dose of 100 ng/rat. Under basal non-stressed conditions (at the diurnal trough in the morning), injections of either saline, anti-glucocorticoid (s.c. or i.c.v.) or anti-mineralocorticoid (s.c.) did not have effect on the plasma corticosterone level. The anti-mineralocorticoid given intracerebroventricularly, however, caused an elevation of plasma corticosterone up to 60 min after the injection. Exposure of the rats to a novel environment resulted in a large increase in the plasma corticosterone level, which was slightly reduced in the rats treated with the anti-glucocorticoid. In vehicle-treated rats, the level returned to basal values at 90 min, while in the anti-glucocorticoid- and anti-mineralocorticoid-treated groups, it remained elevated for prolonged periods. The present study thus shows that (1) the anti-glucocorticoid RU38486 via the brain GR has no effect on the basal plasma corticosterone level in the morning but interferes with a glucocorticoid negative feedback following stress and (2) the anti-mineralocorticoid RU28318 via the brain MR elevates the basal plasma corticosterone level and enhances adrenocortical secretion following stress. Accordingly, both antagonists caused prolonged adrenocortical secretion following stress. Such an effect caused by the anti-mineralocorticoid is probably due to an enhanced stress responsiveness resulting from a blockade of the limbic MR and that caused by the anti-glucocorticoid resulting from a blockade of GR involved in the termination of the stress response.


  

Author Contacts

E. Ronald de Kloet, PhD, Rudolf Magnus Institute for Pharmacology, Medical Faculty, University of Utrecht, Vondellaan 6, NL-3521 GD Utrecht (The Netherlands)

  

Article Information

Received: August 22, 1988
Accepted after revision: December 21, 1988
Published online: April 02, 2008
Number of Print Pages : 7

  

Publication Details

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

Vol. 50, No. 2, 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: 8/22/1988
Accepted: 12/21/1988
Published online: 4/2/2008

Number of Print Pages: 7
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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Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in goverment regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
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