Yamahara J, Kobayashi G, Matsuda H, Fujimura H
Kyoto Pharmaceutical University, Japan.
Eur J Pharmacol. 1988 Oct 11;155(1-2):139-43. doi: 10.1016/0014-2999(88)90411-6.
The effect of evocarpine (EVO), a quinolone alkaloid isolated from Evodiae fructus, on Ca2+-blocking activity has been examined. In the isolated rat thoracic aorta evocarpine significantly inhibited the contraction induced by 60 mM K+ with an IC50 of 9.8 microM, and that induced by external Ca2+ in the depolarized muscle in concentrations of 10-100 microM. The relaxant effect of evocarpine and verapamil was antagonized by Bay K8644. The increase of 45Ca2+-influx induced by 60 mM K+ was significantly inhibited by 100 microM evocarpine. In the isolated rabbit thoracic aorta 100 microM evocarpine had no effect on the norepinephrine-induced contraction in normal medium or on the phasic contraction in Ca2+-free medium or on the transient relaxation induced by activation of the Na+ pump. The content of cyclic AMP or cyclic GMP was unchanged. These results suggest that evocarpine inhibits Ca2+ influx through voltage-dependent calcium channels.
从吴茱萸果实中分离得到的喹诺酮生物碱吴茱萸次碱（EVO）对Ca2+阻断活性的影响已被研究。在离体大鼠胸主动脉中，吴茱萸次碱显著抑制60 mM K+诱导的收缩，IC50为9.8 microM，并且在10 - 100 microM浓度下抑制去极化肌肉中外源性Ca2+诱导的收缩。吴茱萸次碱和维拉帕米的舒张作用被Bay K8644拮抗。100 microM吴茱萸次碱显著抑制60 mM K+诱导的45Ca2+内流增加。在离体兔胸主动脉中，100 microM吴茱萸次碱对正常培养基中去甲肾上腺素诱导的收缩、无钙培养基中的相性收缩或钠泵激活诱导的瞬时舒张均无影响。环磷酸腺苷（cAMP）或环磷酸鸟苷（cGMP）的含量没有变化。这些结果表明，吴茱萸次碱通过电压依赖性钙通道抑制Ca2+内流。
