中文摘要：

目的将在老鼠 mesenteric 动脉和为它负责的机制调查 paeonol 的 vasodilative 效果。方法老鼠被使麻木并且牺牲。优异 mesenteric 动脉被移开，没有支持者织物把了并且把长圆柱的片断切了成 2.0 公里。动脉戒指的等轴的紧张被一个肌动描记器系统在 vitro 记录。 paeonol (到 3.16 mmol/L 的 17.8 mol/L )的集中松驰曲线被钾氯化物( KCl )在动脉戒指 precontracted 上记录，集中收缩 KCl ， 5-hydroxytryptamine ( 5-HT )， noradrenaline ( NA )或钙氯化物( CaCl2 )弯面对 paeonol 被记录( 104.5 ， 103.8 ， 103.5 mol/L )分别地。并且也， paeonol 的 concentrationrelaxation 曲线分别地与 KCl 在戒指 precontracted 上面对不同的钾隧道禁止者和 propranolol 被记录。为了调查细胞内部的 Ca2+ 的角色，免除 Ca2+ 店， NA (100 mol/L ) 导致的收缩和在 Ca2+ 免费媒介的 CaCl2 (2 mmol/L ) 分别地面对 paeonol 被观察。结果 Paeonol 以一种集中依赖者方式由 KCl 放松了动脉戒指 precontracted， vasodilatation 效果没被内皮细胞层剥光影响。 Paeonol 重要减少 KCl ， CaCl2 ， NA 和 5-HT 导致的最大的收缩( Emax )，以及 Emax 在Ca2+免费媒介由 NA 和 CaCl2 导致了，建议 paeonol 经由禁止细胞外的Ca2+流入扩大了动脉由电压依赖者调停了钙隧道，并且调停受体的Ca2+流入和版本。而且，任何一个都没 glibenclamide， tetraethylammonium，钡 chlorded 和 propranolol 影响导致 paeonol 的 vasodilatation，显示 vasodilatation 是没贡献 ATP 敏感的钾隧道，激活钙的钾隧道，里面地修正的钾隧道，和 -adrenoceptor。结论 Paeonol 经由禁止电压依赖者钙在老鼠 mesenteric 动脉导致非内皮细胞层 dependent-vasodilatation 调停隧道的细胞外的 Ca2+ 流入和调停受体的 Ca2+ 流入和版本。

英文摘要：

To investigate the vasodilative effect of paeonol in rat mesenteric artery and the mechanisms responsible for it. Methods： Rats were anaesthetized and sacrificed. The superior mesenteric artery was removed, dissected free of adherent tissue and cut into 2.0 mm long cylindrical segments. Isometric tension of artery rings was recorded by a myograph system in vitro. Concentration-relaxation curves of paeonol （17.8 μmol/L to 3.16 mmol/L） were recorded on artery rings precontracted by potassium chloride （KCI） and concentration-contraction curves of KCI, 5-hydroxytryptamine （5-HT）, noradrenaline （NA） or calcium chloride （CaCI2） were recorded in the presence of paeonol （10^-4.5, 10^-3.8, 10^-3.5 tool/L） respectively. And also, concentration- relaxation curves of paeonol were recorded in the presence of different potassium channel inhibitors and propranolol on rings precontracted with KCI respectively. To investigate the role of intracellular Ca2. release from Ca2. store, the contraction induced by NA （100μmol/L） and CaCI2 （2 mmol/L） in Ca^2＋ free medium was observed in the presence of paeonol respectively. Results： Paeonol relaxed artery rings precontracted by KCI in a concentration-dependent manner and the vasodilatation effect was not affected by endothelium denudation. Paeonol significant decreased the maximum contractions （Emax） induced by KCI, CaCl2, NA and 5-HT, as well as Emax induced by NA and CaCI2 in Ca^2＋-free medium, suggesting that paeonol dilated the artery via inhibiting the extracellular Ca2. influx mediated by voltage-dependent calcium channel, and receptor-mediated Ca^2＋-influx and release. Moreover, none of glibenclamide, tetraethylammonium, barium chlorded and propranolol affected the paeonol-induced vasodilatation, indicating that the vasodilatation was not contributed to ATP sensitive potassium channel, calcium-activated potassium channel, inwardly rectifying potassium channel, and β-adrenoceptor. Conclusion： Paeonol induces non-endothelium depende