摘要
目的探讨7,8-二羟基黄酮（DHF）对高钾预收缩的去内皮血管的舒张作用及其机制。方法制备大鼠离体胸主动脉并去除内皮,以高钾溶液（60mmol/L的KCl）诱导血管收缩,平台期后以累积给药法加入终浓度1~300μmol/L的DHF,观察其舒张作用。在无钙-复钙实验中,观察100μmol/L的DHF预处理对高钾诱导的最大张力的影响。高钾预收缩前加入1.0μmol/L硝苯地平（Nif）孵育10min,观察Nif对DHF（300μmol/L）舒张作用的影响。结果 DHF在1~300μmol/L浓度范围内剂量依赖性抑制高钾诱导的血管收缩（F=119.7,P〈0.05）。复钙过程中,DHF预处理明显减少了高钾诱导的张力变化（t=4.395,P〈0.01）。高钾预收缩前加入Nif则显著抑制了DHF的舒张效应（t=2.308,P〈0.01）。结论 DHF对高钾预收缩的去内皮血管具有明显的舒张效应,该作用与其阻断细胞膜上电压依赖性钙通道有关。
Objective To investigate the vasorelaxing effect of 7,8-dihydroxyflavone（DHF）in high potassium-preconstricted rat aorta without endothelium and its mechanism. Methods An in vitro endothelium-denuded rat thoracic aorta was created for this study.When the vasoconstriction induced by 60 mmol/L KCl reached the peak level,different concentrations of DHF（1-300μmol/L）were added in a cumulative manner to observe its vasorelaxing effect.In Ca2＋recovery experiment,DHF（100μmol/L）was pre-incubated before adding KCl and CaCl2 to observe its influence on the changes of aorta tension.To estimate the involvement of voltage dependent calcium channel（VDCC）,1.0μmol/L Nifedipine（Nif,a selective VDCC blocker）was used before KCl plus DHF treatment. Results 1-300μmol/L DHF relaxed KCl-preconstricted aorta in a dose-dependent manner（F=119.7,P0.05）.Pretreatment with DHF markedly reduced the maximal tension induced by KCl during extracelluar Ca2＋recovery（t=4.395,P0.01）.Furthermore,Nifidepine pretreatment before KCl significantly attenuated the vasorelaxing effect of DHF（t=2.308,P0.01）. Conclusion DHF exerts vasorelaxing effect in KCl-preconstricted rat aorta without endothelium.This effect might be mediated by blocking VDCC and preventing the subsequent Ca2＋influx.
出处
《青岛大学医学院学报》
CAS
2015年第4期474-476,共3页
Acta Academiae Medicinae Qingdao Universitatis
基金
山东省自然科学基金资助项目(ZR2014CM014)
青岛大学医学院2014年大学生创新创业训练项目
