Chiou W F, Chou C J, Liao J F, Sham A Y, Chen C F
National Research Institute of Chinese Medicine, Taipei, Hsien, Taiwan.
Eur J Pharmacol. 1994 May 12;257(1-2):59-66. doi: 10.1016/0014-2999(94)90694-7.
The mechanisms underlying the rutaecarpine-induced vasodilatation were studied using isolated rat mesenteric arterial ring segments. The results showed that rutaecarpine (0.1 microM to 0.1 mM) produced a dose-dependent vasorelaxing response in our preparations, which were precontracted with phenylephrine. This vasodilator effect was significantly attenuated by removal of the endothelium, treatment with L-NG-nitro-arginine, a nitric oxide synthase inhibitor, and methylene blue, a guanylyl cyclase inhibitor, but not by treatment with atropine, triprolidine and yohimbine. Rutaecarpine pretreatment (1 microM to 0.1 mM) reduced both the phasic (fast) and tonic (slow) phases of phenylephrine-induced contractions, suggesting that a reduction in intracellular calcium might be involved. It is thus concluded that while the vasorelaxing effect of rutaecarpine appeared to be endothelium-dependent and to involve nitric oxide and guanylyl cyclase, neither muscarinic receptors, histamine H1 receptors nor alpha 2-adrenoceptors are involved. Moreover, a direct effect on the vascular smooth muscle cell, possibly through a reduction in intracellular Ca2+, can not be excluded.
利用离体大鼠肠系膜动脉环段研究了吴茱萸次碱诱导血管舒张的机制。结果表明，在我们用去氧肾上腺素预收缩的标本中，吴茱萸次碱（0.1微摩尔/升至0.1毫摩尔/升）产生了剂量依赖性的血管舒张反应。去除内皮、用一氧化氮合酶抑制剂L-NG-硝基精氨酸和鸟苷酸环化酶抑制剂亚甲蓝处理后，这种血管舒张作用显著减弱，但用阿托品、曲普利啶和育亨宾处理则无此作用。吴茱萸次碱预处理（1微摩尔/升至0.1毫摩尔/升）可降低去氧肾上腺素诱导收缩的相性（快速）和紧张性（缓慢）阶段，提示可能涉及细胞内钙的减少。因此得出结论，虽然吴茱萸次碱的血管舒张作用似乎依赖于内皮且涉及一氧化氮和鸟苷酸环化酶，但毒蕈碱受体、组胺H1受体和α2-肾上腺素受体均未参与。此外，不能排除其对血管平滑肌细胞有直接作用，可能是通过降低细胞内Ca2+来实现的。
