EFFECTS OF BETA-ADRENERGIC AGONISTS AND ANTAGONISTS ON THE GROWTH-HORMONE RESPONSE TO GROWTH HORMONE-RELEASING HORMONE IN ANOREXIA-NERVOSA

Background: In anorexia nervosa (AN), growth hormone (GH) hypersecreti on 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 re duced IGF-I negative feedback on GH secretion or to a primary hypothal amic dysfunction. In AN, in contrast to normal subjects, cholinergic a ntagonists and agonists, whose action is somatostatin (SS)-mediated, h ave reduced and absent effects on the GH response to growth hormone-re leasing hormone (GHRH). Since arginine, another substance acting via i nhibition 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 evaluate d the effects of beta-adrenergic agonists and antagonists, which are k nown to inhibit and increase, respectively, the GHRH-induced GH secret ion in normal subjects. Methods: We studied the effect of atenolol (AT E), a beta 1-adrenergic antagonist, and salbutamol (SALB), a beta 2-ad renergic agonist, on the GHRH-induced GH release in 10 patients with A N and in 20 normal age-matched women (NW). Results: Basal GH levels we re 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 G HRH after SALB pretreatment were similar in NW and AN. Conclusions: Th ese data reveal an exaggerated somatotrope responsiveness to GHRH in A N that is not further increased by beta-adrenergic blockade, while is abolished by beta-adrenergic activation. This suggests that an impairm ent of beta-adrenergic influence on GH secretion is present in anorexi a nervosa. (C) 1998 Society of Biological Psychiatry.