title: Effects of beta-adrenergic agonists and antagonists on the growth hormone response to growth hormone-releasing hormone in anorexia nervosa.
abstract: BACKGROUND
  In anorexia nervosa (AN), growth hormone (GH) hypersecretion and low insulin-like growth factor I (IGF-I) levels are present. It is unclear whether this is due to a peripheral GH resistance and a reduced IGF-I negative feedback on GH secretion or to a primary hypothalamic dysfunction. In AN, in contrast to normal subjects, cholinergic antagonists and agonists, whose action is somatostatin (SS)-mediated, have reduced and absent effects on the GH response to growth hormone-releasing hormone (GHRH). Since arginine, another substance acting via inhibition of SS, maintains its potentiating effect on GH secretion in AN, it has been hypothesized that somewhat specific alteration of the SS-mediated cholinergic influence may be present in this condition. To further clarify the neural control of AH secretion in AN, we evaluated the effects of beta-adrenergic agonists and antagonists, which are known to inhibit and increase, respectively, the GHRH-induced GH secretion in normal subjects.
  
  
  METHODS
  We studied the effect of atenolol (ATE), a beta 1-adrenergic antagonist, and salbutamol (SALB), a beta 2-adrenergic agonist, on the GHRH-induced GH release in 10 patients with AN and in 10 normal age-matched women (NW).
  
  
  RESULTS
  Basal GH levels were higher, whereas IGF-I were lower in AN than in NW. The GHRH-induced GH rise in AN was higher than that in NW. ATE significantly enhanced the GH response to GHRH in NW, but not in AN. The GH responses to GHRH after ATE pretreatment were similar in NW and in AN. The GH response to GHRH was inhibited by SALB in both NW and AN. The GH responses to GHRH after SALB pretreatment were similar in NW and AN.
  
  
  CONCLUSIONS
  These data reveal an exaggerated somatotrope responsiveness to GHRH in AN that is not further increased by beta-adrenergic blockade, while is abolished by beta-adrenergic activation. This suggests that an impairment of beta-adrenergic influence on GH secretion is present in anorexia nervosa.
authors.affiliation: Department of Internal Medicine, University of Turin, Italy.
authors.forename: L
authors.initials: L
authors.lastname: Gianotti
authors.forename: E
authors.initials: E
authors.lastname: Arvat
authors.forename: M R
authors.initials: MR
authors.lastname: Valetto
authors.forename: J
authors.initials: J
authors.lastname: Ramunni
authors.forename: L
authors.initials: L
authors.lastname: Di Vito
authors.forename: B
authors.initials: B
authors.lastname: Maccagno
authors.forename: F
authors.initials: F
authors.lastname: Camanni
authors.forename: E
authors.initials: E
authors.lastname: Ghigo
mesh_terms: D000293:Adolescent; D000318:Adrenergic beta-Agonists / Q000009:adverse effects / Q000494:pharmacology*; D000319:Adrenergic beta-Antagonists / Q000009:adverse effects / Q000494:pharmacology*; D000328:Adult; D000420:Albuterol / Q000494:pharmacology; D000856:Anorexia Nervosa / Q000097:blood / Q000378:metabolism*; D019540:Area Under Curve; D001262:Atenolol / Q000494:pharmacology; D005260:Female; D013006:Growth Hormone / Q000097:blood*; D013007:Growth Hormone-Releasing Hormone / Q000009:adverse effects / Q000494:pharmacology*; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000378:metabolism
chemical_list: D000318:Adrenergic beta-Agonists; D000319:Adrenergic beta-Antagonists; D001262:Atenolol; D007334:Insulin-Like Growth Factor I; D013006:Growth Hormone; D013007:Growth Hormone-Releasing Hormone; D000420:Albuterol