α2-Adrenergic stimulation enhances growth hormone secretion in the dog: a presynaptic mechanism?

ntravenous administration of clonidine (CLO), (2,4 and 8 ug/kg), a predominantly α2-adrenergic receptor agonist, induced in unanesthetized dogs clear-cut and dose -related rises in plasma GH (cGH) levels. Pretreatment with the selective antagonist of α1-adrenergic receptors prazosin (0.1 mg/Kg iv) left unaltered the cGH rise inducedby 4 ug/Kg of CLO whilst blockade of α2-adrenergic receptors by yohimbine (2.5 mg/Kg iv) completely prevented it. In dogs treated 24 h previously with reserpine (0.5 mg/Kg iv), a depletor of brain catecholamine stores, CLO was ineffective to stimulate cGH release. These data indicate that in the dog the GH-releasing effect of CLO occurs via stimulation of α2-adrenergic receptors and suggest that the latter are located presynaptically in relation to norepinephrine neurons.