Török T L, Bunyevácz Z, Nguyen T T, Magyar K
J Pharm Pharmacol. 1984 Feb;36(2):107-10. doi: 10.1111/j.2042-7158.1984.tb03003.x.
High concentrations of selegiline[-)-deprenyl) (greater than 10(-5) M) enhanced the nerve stimulation (2 Hz)-evoked release of [3H]noradrenaline from the isolated main pulmonary artery of the rabbit. This facilitation of stimulation-evoked [3H]noradrenaline release by selegiline was reduced by exogenous (-)-noradrenaline, an agonist of presynaptic alpha 2-adrenoceptors. This inhibitory action of (-)-noradrenaline was partly antagonized by yohimbine, a selective alpha 2-adrenoceptor blocker. When the stimulation-evoked [3H]noradrenaline release had already been increased by inhibition of Na+-pump (K+-free solution), selegiline further enhanced the nerve-evoked release of labelled neurotransmitter.
高浓度的司来吉兰[(-)-丙炔苯丙胺]（大于10⁻⁵M）增强了神经刺激（2赫兹）诱发的兔离体主肺动脉中[³H]去甲肾上腺素的释放。司来吉兰对刺激诱发的[³H]去甲肾上腺素释放的这种促进作用，被外源性(-)-去甲肾上腺素（一种突触前α₂-肾上腺素能受体激动剂）所减弱。(-)-去甲肾上腺素的这种抑制作用被育亨宾（一种选择性α₂-肾上腺素能受体阻滞剂）部分拮抗。当通过抑制钠泵（无钾溶液）使刺激诱发的[³H]去甲肾上腺素释放已经增加时，司来吉兰进一步增强了神经诱发的标记神经递质的释放。
