原花色素对大鼠阻力血管舒张作用机制研究

中国临床药理学与治疗学 ›› 2010, Vol. 15 ›› Issue (2): 170-174.

原花色素对大鼠阻力血管舒张作用机制研究

王燕锋¹, 彭晓晖², 张晨瑶¹, 赵欣¹, 王燕颖¹

¹黑龙江省医院药剂部,哈尔滨 150036,黑龙江;
²大庆油田总医院普外科,大庆 163001,黑龙江

收稿日期:2009-05-12 修回日期:2009-09-05 出版日期:2010-02-26 发布日期:2020-09-18
通讯作者: 王燕颖,女,博士,副主任医师,研究方向:消化系统疾病临床及内镜诊断及治疗。
作者简介:王燕锋,男,本科,主管药师,研究方向:临床药理学。Tel: 15946006896 E-mail:liuyuzhe1972@163.net

Research of the mechanism about proanthocyanidins’s diastolic function to rat resistance vessel

WANG Yan-feng¹, PENG Xiao-hui², ZHANG Chen-yao¹, ZHAO Xin¹, WANG Yan-ying¹

¹ Department of Dispensary, Heilongjiang Provincial Hospital, Haerbin 150036,Heilongjiang, China;
² Department of General surgery, General Hospital of Daqing Oil Field, Daqing 163001,Heilongjiang, China

Received:2009-05-12 Revised:2009-09-05 Online:2010-02-26 Published:2020-09-18

摘要/Abstract

摘要： 目的:通过大鼠离体肠系膜动脉网(MAB)和肠系膜动脉(MA)环,研究原花色素(PRF)的舒张作用和机制。方法:分离大鼠MAB和MA,并将其制成血管环,使用微血管张力系统测定血管张力变化。结果:PRF能使经去氧肾上腺素(PE)预收缩的MAB环浓度依赖性舒张,舒张率为73%(相对于对照组),该舒张作用能够被一氧化氮合酶抑制剂(L-NOARG)以及高K⁺溶液所削弱,并且可被加入L-NOARG的KCl溶液完全阻断,但吲哚美辛、阿托品、育亨宾、吡啦明、BACl₂、格列苯脲、哇巴因、4-氨基吡啶不能影响这种舒张作用。PRF对PE预收缩的离体MA环所表现出来的浓度依赖性舒张作用,且该作用被去除内皮、鸟苷酸环化酶抑制剂ODQ、北非蝎毒素、与北非蝎毒素合用蜂毒明肽所阻断,但是并不受单独使用的蜂毒明肽和HOE140影响。结论:PRF的舒张作用与NO-cGMP通路和钙依赖性钾通道激活所引起的超级化有关。

关键词: 原花色素, 一氧化氮, 钾通道

Abstract: AIM: The present study was designed to investigate the relaxing effects and mechanism of PRF in rat mesenteric arterial bed(MAB) and isolated mesenteric artery(MA). METHODS: Isolated the MAB and MA of the rat,and the MAB and MA were cuted into artery rings, the tension of MAB and MA rings was measured by Myograph System. RESULTS: PRF could induce a concentration-dependent relaxation of MAB rings which was pre-contracted with phenylephrine(Phe), the relaxation rate was 70%(compared to the control). This effect was significantly reduced by the nitric oxide(NO) Synthase inhibitor N-nitro-L-arginine(L-NOARG) or high K⁺ solution and completely inhibited by KCl plus L-NOARG. But the vasorelaxant effect could not be altered by indometacin,atropine,yohimbine,pyrilamine K channel inhibitor: BACl₂, glibenclamide,ouabain,4-aminopyridine. In Phe pre-contracted MA rings, PRF also induced a concentration-dependent relaxation,which was inhibited by endothelial removal, charybdotoxin(ChTx), and ChTx plus apamin, respectively.Moreover the relaxant functiont was not altered by HOE140 and apamin given alone. CONCLUSION: The vasorelaxing effect of PRF is dependent upon the NO-cGMP pathway and in combinaton with hyperpolarization due to activation of Ca²⁺-dependent K⁺ channels.

Key words: Proanthocyanidins, Nitricoxide, K channel

中图分类号:

R965.2

王燕锋, 彭晓晖, 张晨瑶, 赵欣, 王燕颖. 原花色素对大鼠阻力血管舒张作用机制研究[J]. 中国临床药理学与治疗学, 2010, 15(2): 170-174.

WANG Yan-feng, PENG Xiao-hui, ZHANG Chen-yao, ZHAO Xin, WANG Yan-ying. Research of the mechanism about proanthocyanidins’s diastolic function to rat resistance vessel[J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2010, 15(2): 170-174.

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