E. Arvat et al., INTERACTION OF SALBUTAMOL AND GALANIN ON BOTH BASAL AND GROWTH-HORMONE RELEASING HORMONE-STIMULATED GROWTH-HORMONE SECRETION IN HUMANS, Journal of endocrinological investigation, 18(5), 1995, pp. 324-328
Beta adrenergic receptors mediate the inhibitory influence of catechol
amines on GH secretion in man, likely via stimulation of hypothalamic
somatostatin release. To further clarify the role of beta adrenergic r
eceptors in the neural control of GH secretion, in 7 normal females (a
ge 21-27 yr) we studied the interaction of salbutamol (SAL 0.08 mg/kg
orally), a beta 2-adrenergic agonist, with GHRH (1 mu g/kg iv) and/or
galanin (GAL 15 mu g/kg iv), a neuropeptide endowed with a GH-releasin
g effect which is likely mediated by concomitant stimulation of GHRH-
and inhibition of somatostatin-secreting neurons. SAL inhibited the GH
response to GHRH (AUC: 282.6 +/- 102.7 vs 1083.6 +/- 176.5 mu g/l/h,
p< 0.05) and, although not significantly, that to GAL (263.9 +/- 103.7
vs 418.4 +/- 70.4 mu g/l/h). GAL enhanced the GHRH-induced GH rise (2
129.5 +/- 362.2 mu g/l/h, p< 0.05) but SAL pretreatment inhibited this
effect (1249.8 +/- 257.1 mu g/l/h, p< 0.02) so that the GH response t
o the combined administration of GHRH, GAL and SAL overlapped with tha
t to the neurohormone alone. In conclusion, our results show that the
inhibitory influence of beta adrenergic activation on GH secretion ove
rrides the stimulatory one of galanin. They strenghten the view that i
n man beta-adrenergic receptors and galanin modulate GH secretion havi
ng opposite influences aimed to balance the function of the GH-IGF-I a
xis.