Cella S G, Picotti G B, Müller E E
Life Sci. 1983 Jun 13;32(24):2785-92. doi: 10.1016/0024-3205(83)90400-9.
Intravenous administration of clonidine (CLO), (2,4 and 8/micrograms/Kg), a predominantly alpha 2-adrenergic receptor agonist, induced in unanesthetized dogs clear-cut and dose-related rises in plasma GH (cGH) levels. Pretreatment with the selective antagonist of alpha 1-adrenergic receptors prazosin (0.1 mg/Kg iv) left unaltered the cGH rise induced by 4/micrograms/Kg of CLO whilst blockade of alpha 2-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 alpha 2-adrenergic receptors and suggest that the latter are located presynaptically in relation to norepinephrine neurons.
静脉注射可乐定（CLO）（2、4和8微克/千克），一种主要作用于α2 - 肾上腺素能受体的激动剂，可使未麻醉犬的血浆生长激素（cGH）水平出现明显且与剂量相关的升高。预先静脉注射α1 - 肾上腺素能受体选择性拮抗剂哌唑嗪（0.1毫克/千克），不改变4微克/千克可乐定诱导的cGH升高，而静脉注射育亨宾（2.5毫克/千克）阻断α2 - 肾上腺素能受体则完全阻止了这种升高。在24小时前接受利血平（0.5毫克/千克静脉注射）治疗（一种脑内儿茶酚胺储存耗竭剂）的犬中，可乐定刺激cGH释放无效。这些数据表明，在犬中可乐定的生长激素释放作用是通过刺激α2 - 肾上腺素能受体实现的，并提示后者位于去甲肾上腺素能神经元的突触前部位。
