THERAPEUTIC 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 so matotropic function, likely via stimulation of hypothalamic somatostat in release. Accordingly, salbutamol (SAL), a beta2-agonist, given iv a bolishes the GH response to GH-releasing hormone (GHRH) in adults. Tak ing into account that in bronchial asthma an alteration in the beta-ad renergic neural control of airways has been hypothesized, we aimed to verify whether, in asthmatic children, beta-adrenergic activation inhi bits or not GH secretion. To this goal, we studied the effect of thera peutical 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 underwe nt a GHRH test (1 mug/kg iv). Moreover, in 7 children (group A), SAL w as administered orally (0.125 mg/kg) 1 h before GHRH, while in 8 (grou p 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 mug/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 mug/L/h; p<0.02). In conclusion, our data show that in asthmatic child ren, therapeutical doses of SAL exert a marked inhibitory effect on GH secretion. Further studies are needed to exclude detrimental effects of chronic treatment with beta2-agonists on GH secretion and growth ve locity in asthmatic children.