Shen D L, Jin G Z, He Y F, Zhang Z D, Sun Z, Lu Y Q, Yang Z C
Shanghai Institute of Materia Medica, Chinese Academy of Sciences.
Zhongguo Yao Li Xue Bao. 1991 Nov;12(6):514-8.
Iv (-)-SPD lowered the blood pressure in anesthetized rat, the ED50 value was 5.1 +/- 2.5 mg.kg-1. In the experiments of rat and rabbit aortic strips, (-)-SPD 0.3-100.0 mumol.L-1 inhibited the contraction initiated by clonidine (alpha 2) and phenylephrine (alpha 1) and shifted the dose-response curve to the right parallely without change in maximum response. The inhibitory ratio of (-)-SPD acting on alpha 2/alpha 1 adrenergic receptors was about 7.2, and (-)-SPD thus was predominant inhibition on alpha 2 adrenergic receptors. In the experiment of aortic strips from reserpinized rabbits, the inhibition of (-)-SPD on contraction evoked by clonidine was diminished markedly. The results suggest that (-)-SPD stimulated mainly the alpha 2-adrenergic receptors of presynaptic nerve endings. Moreover (-)-SPD 1 mumol.L-1 inhibited the release of intracellular Ca2+ initiated by NE. (-)-SPD 3-30 mumol.L-1 blocked the voltage-dependent Ca2+ channel.
静脉注射（-）-SPD可降低麻醉大鼠的血压，半数有效剂量（ED50）值为5.1±2.5mg·kg-1。在大鼠和兔主动脉条实验中，0.3 - 100.0μmol·L-1的（-）-SPD可抑制可乐定（α2）和去氧肾上腺素（α1）引发的收缩，并使剂量反应曲线平行右移，最大反应无变化。（-）-SPD作用于α2/α1肾上腺素能受体的抑制率约为7.2，因此（-）-SPD对α2肾上腺素能受体的抑制作用占主导。在利血平化兔的主动脉条实验中，（-）-SPD对可乐定诱发收缩的抑制作用明显减弱。结果表明，（-）-SPD主要刺激突触前神经末梢的α2肾上腺素能受体。此外，1μmol·L-1的（-）-SPD可抑制去甲肾上腺素引发的细胞内Ca2+释放。3 - 30μmol·L-1的（-）-SPD可阻断电压依赖性Ca2+通道。
