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Effect of hydrocortisone on the pituitary response to growth hormone releasing hormone

Lookup NU author(s): Dr Stuart Watson, Dr Richard Porter, Professor Allan Young

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Abstract

Rationale: In depression, the growth hormone (GH) response to clonidine and L-tryptophan (L-TRP) is reduced, suggesting reduced alpha2-adrenergic and serotonin (5-HT)(1A) receptor function. Pretreatment with hydrocortisone (100 mg, orally 11 h before) also blunts the GH response to L-TRP. This effect may be mediated at the hypothalamic level via reduced 5-HT(1A) receptor function or at the pituitary level, either by a direct effect on somatotrope cells or via enhanced insulin-like growth factor-1 (IGF-1) or somatostatin (SS) release. Objectives: To examine the effects of acute and chronic exposure to hydrocortisone on baseline and stimulated GH release from the pituitary. Methods: Twelve healthy male volunteers received pretreatment with acute hydrocortisone (100 mg, 11 h before), chronic hydrocortisone (20 mg twice a day for 1 week) and placebo in a double blind, balanced order, crossover design. Serial measurements of plasma GH, IGF-1 and thyroid stimulating hormone (TSH) levels were made at baseline and following intravenous administration of 1 mcg/kg GHRH. Results: The GH response to growth hormone releasing hormone (GHRH) was significantly blunted by pretreatment with both acute and chronic hydrocortisone. Baseline IGF-1 levels were significantly lower at baseline after chronic hydrocortisone compared with placebo. Baseline TSH levels were significantly lower after acute hydrocortisone compared with placebo, suggesting an increase in somatostatin levels. Conclusions: These data suggest that hydrocortisone acts at the pituitary level to reduce GH release. The TSH and IGF-1 data support the hypothesis that hydrocortisone reduces GH release by enhancing somatostatin and IGF-1 release.

Publication metadata

Author(s): Watson S; Young AH; Porter RJ

Publication type: Article

Publication status: Published

Journal: Psychopharmacology

Year: 2000

Volume: 152

Issue: 1

Pages: 40-46

Print publication date: 01/01/2000

ISSN (print): 0033-3158

ISSN (electronic): 1432-2072

Publisher: Springer

URL: http://dx.doi.org/10.1007/s002130000491

DOI: 10.1007/s002130000491

PubMed id: 11041314

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