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

S. Watson et al., Effect of hydrocortisone on the pituitary response to growth hormone releasing hormone, PSYCHOPHAR, 152(1), 2000, pp. 40-46
Citations number
Categorie Soggetti
Neurosciences & Behavoir
Journal title
Year of publication
40 - 46
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Rationale: In depression, the growth hormone (GH) response to clonidine and L-tryptophan (L-TRP) is reduced, suggesting reduced alpha(2)-adrenergic an d serotonin (5-HT)(1A) receptor function. Pretreatment with hydrocortisone (100 mg, orally II h before) also blunts the GH response to L-TRP. This eff ect may be mediated at the hypothalamic level via reduced 5-HT1A receptor f unction or at the pituitary level, either by a direct effect on somatotrope cells or via enhanced insulin-like growth Factor-1 (IGF-I) or somatostatin (SS) release. Objectives: To examine the effects of acute and chronic expo sure to hydrocortisone on baseline and stimulated GH release from the pitui tary. Methods: Twelve healthy male volunteers received pretreatment with ac ute hydrocortisone (100 mg, 11 h before), chronic hydrocortisone (20 mg twi ce a day for 1 week) and placebo in a double blind, balanced order, crossov er design. Serial measurements of plasma GH, IGF-I and thyroid stimulating hormone (TSH) levels were made at baseline and following intravenous admini stration of 1 mcg/kg GHRH. Results: The GH response to growth hormone relea sing hormone (GHRH) was significantly blunted by pretreatment with both acu te and chronic hydrocortisone. Baseline IGF-1 levels were significantly low er at baseline after chronic hydrocortisone compared with placebo. Baseline TSH levels were significantly lower after acute hydrocortisone compared wi th placebo, suggesting an increase in somatostatin levels. Conclusions: The se data suggest that hydrocortisone acts at the pituitary level to reduce G H release. The TSH and IGF-1 data support the hypothesis that hydrocortison e reduces GH release by enhancing somatostatin and IGF-1 release.