title: Growth hormone releasing hormone 1-44 NH2 and 1-40 OH levels in normal subjects during growth hormone stimulation tests.
abstract: OBJECTIVE
  Little is known about the relative circulating concentrations of growth hormone releasing hormone (GHRH) 1-44 NH2 and 1-40 OH in response to dynamic GH stimulation. We therefore studied the concentrations of growth hormone-releasing hormone (GHRH) 1-44 NH2 and 1-40 OH in the peripheral plasma of normal male subjects during GH stimulation tests.
  
  
  METHODS
  Tests were performed at 0900 h after an overnight fast. Stimulation tests, commenced at 0 minutes, included alpha-adrenergic activation with adrenaline (10 micrograms/min from 0 to 30 minutes) following beta-blockade with propranolol (1.5 mg/min from -10 to 0 minutes), alpha 2-adrenergic activation with clonidine 150 micrograms i.v., insulin hypoglycaemia (0.15 U/kg soluble insulin), L-arginine infusion (30 g from 0 to 30 minutes), L-dopa (500 mg orally) and oral glucose (100 g).
  
  
  METHODS
  Groups of healthy male volunteers aged 20-42 years, all within 10% of ideal body weight.
  
  
  METHODS
  Serum GH and plasma GHRH 1-44 NH2 and 1-40 OH were measured at intervals for between 60 and 390 minutes, depending on the stimulation test.
  
  
  RESULTS
  There were no significant changes in either GHRH 1-44 or 1-40 following alpha-adrenergic activation with propranolol/adrenaline infusion, alpha 2-adrenergic activation with i.v. clonidine, insulin-induced hypoglycaemia or arginine infusion despite the expected rise in GH levels. After oral glucose, GH was initially suppressed with a late rise. There were no changes in GHRH 1-44 or 1-40 levels during either phase of this response. After L-dopa GH levels peaked at 90 minutes, 24.5 +/- 11.0 mU/l (mean +/- SEM). At 0 minutes GHRH 1-44 and 1-40 levels were 3.25 +/- 0.89 and 4.93 +/- 1.28 pmol/l respectively and rose in both cases, peaking at 60 minutes at 4.23 +/- 1.01 and 7.55 +/- 1.80 pmol/l (P < 0.05). At no time was there any evidence of differential secretion of GHRH 1-44 or 1-40.
  
  
  CONCLUSIONS
  We have confirmed previous studies demonstrating a small rise in GHRH before the GH response to L-dopa. However, in all other situations of pharmacological stimulation of GH release we were unable to detect any significant changes in GHRH 1-44 or 1-40 levels. It seems most likely that peripheral GHRH does not reflect hypothalamic secretion. As yet there is no evidence for differential release of GHRH 1-44 and 1-40.
authors.affiliation: Department of Medicine, University of Wales, College of Medicine, Heath Park, Cardiff, UK.
authors.forename: M D
authors.initials: MD
authors.lastname: Page
authors.forename: C
authors.initials: C
authors.lastname: Dieguez
authors.forename: R
authors.initials: R
authors.lastname: Valcavi
authors.forename: H P
authors.initials: HP
authors.lastname: Koppeschaar
authors.forename: M F
authors.initials: MF
authors.lastname: Scanlon
mesh_terms: D000328:Adult; D004837:Epinephrine; D013006:Growth Hormone / Q000097:blood*; D013007:Growth Hormone-Releasing Hormone / Q000031:analogs & derivatives* / Q000097:blood*; D006801:Humans; D007980:Levodopa; D008297:Male; D010446:Peptide Fragments / Q000097:blood*; D010901:Pituitary Function Tests; D010902:Pituitary Gland / Q000187:drug effects; D013268:Stimulation, Chemical
chemical_list: D010446:Peptide Fragments; C036893:somatotropin releasing factor 40; C040786:somatotropin releasing hormone (1-44)amide; D007980:Levodopa; D013006:Growth Hormone; D013007:Growth Hormone-Releasing Hormone; D004837:Epinephrine