title: Effect of hydrocortisone on the pituitary response to growth hormone releasing hormone.
abstract: BACKGROUND
  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-HT1A 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.
  
  
  OBJECTIVE
  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.
authors.affiliation: Department of Neuroscience and Psychiatry, University of Newcastle, Royal Victoria Infirmary, Newcastle upon Tyne, UK.
authors.forename: S
authors.initials: S
authors.lastname: Watson
authors.forename: R J
authors.initials: RJ
authors.lastname: Porter
authors.forename: A H
authors.initials: AH
authors.lastname: Young
mesh_terms: D000328:Adult; D019540:Area Under Curve; D015306:Biogenic Monoamines / Q000378:metabolism; D018592:Cross-Over Studies; D004311:Double-Blind Method; D013007:Growth Hormone-Releasing Hormone / Q000097:blood*; D019382:Human Growth Hormone / Q000097:blood; D006801:Humans; D006854:Hydrocortisone / Q000494:pharmacology*; D007031:Hypothalamus / Q000187:drug effects / Q000378:metabolism; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D008297:Male; D010902:Pituitary Gland / Q000187:drug effects / Q000378:metabolism*; D011388:Prolactin / Q000097:blood
chemical_list: D015306:Biogenic Monoamines; D019382:Human Growth Hormone; D007334:Insulin-Like Growth Factor I; D011388:Prolactin; D013007:Growth Hormone-Releasing Hormone; D006854:Hydrocortisone