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.
α2-Adrenergic stimulation enhances growth hormone secretion in the dog: a presynaptic mechanism? / S.G. Cella, G.B. Picotti, E.E. Müller. - In: LIFE SCIENCES. - ISSN 0024-3205. - 32:24(1983), pp. 2785-2792.
Titolo: | α2-Adrenergic stimulation enhances growth hormone secretion in the dog: a presynaptic mechanism? |
Autori: | |
Settore Scientifico Disciplinare: | Settore BIO/14 - Farmacologia |
Data di pubblicazione: | 1983 |
Rivista: | |
Tipologia: | Article (author) |
Digital Object Identifier (DOI): | http://dx.doi.org/10.1016/0024-3205(83)90400-9 |
Appare nelle tipologie: | 01 - Articolo su periodico |