Therapeutical doses of salbutamol inhibit the somatotropic responsiveness to growth hormone-releasing hormone in asthmatic children.

In humans beta-adrenergic receptors mediate an inhibitory effect on somatotropic function, likely via stimulation of hypothalamic somatostatin release. Accordingly, salbutamol (SAL), a beta 2-agonist, given iv abolishes the GH response to GH-releasing hormone (GHRH) in adults. Taking into account that in bronchial asthma an alteration in the beta-adrenergic neural control of airways has been hypothesized, we aimed to verify whether, in asthmatic children, beta-adrenergic activation inhibits or not GH secretion. To this goal, we studied the effect of therapeutical doses of SAL on GH response to GHRH in 15 asthmatic children (12 M and 3 F, 5.9-11.1 yr, pubertal stage I-II). All children underwent a GHRH test (1 microgram/kg iv). Moreover, in 7 children (group A), SAL was administered orally (0.125 mg/kg) 1 h before GHRH, while in 8 (group B) by inhaled aerosol (2 mg) 30 min before GHRH. Oral SAL (group A) abolished the GHRH-induced GH rise (AUC, mean +/- SE 165.1 +/- 33.3 vs 959.9 +/- 158.1 micrograms/L/h; p < 0.03). In group B, the GH response to GHRH was only blunted by inhaled SAL (938.6 +/- 284.6 vs 1378.8 +/- 315.6 micrograms/L/h; p < 0.02). In conclusion, our data show that in asthmatic children, therapeutical doses of SAL exert a marked inhibitory effect on GH secretion. Further studies are needed to exclude detrimental effects of chronic treatment with beta 2-agonists on GH secretion and growth velocity in asthmatic children.