Inhibitory action of the alpha 1-adrenergic receptor on growth hormone secretion in the dog

Intravenous administration of methoxamine (METHOX, 5 mg, iv), a specific α1-adrenergic agonist, reduced baseline GH levels of four unanesthetized beagle dogs 45 and 60 min post-injection and completely abolished the GH-releasing effect of the α2-adrenergic agonist clonidine (CLON, 4 µ/kg, iv). Prazosin (PRA, 0.1 mg/ kg, iv), an C α1-adrenergic antagonist, administered before METHOX re-instituted the GH-releasing effect of CLON. METHOX administered at the starting of an arginine infusion (ARG, 10% solution, 3.3 ml/min × 30 min) reduced consistently the GH releasing effect of the latter while, conversely, pretreatment with PRA, strikingly potentiated the GH-releasing effect of the amino acid (2 dogs). METHOX did not alter the GH-releasing effect of human pancreatic GH-releasing factor (hpGRF-40, 1,µg/kg, iv), though it consistently delayed the occurrence of the GH secretory peak following hpGRF-40. These data indicate that α1-adrenergic receptors located in the central nervous system, inhibit in the dog tonic and stimulated GH secretion.