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作 者:方卉[1] 林浩[2] 王利娟[1] 庞秀萍[1] 韩晓华[1]
机构地区:[1]青岛大学医学院生理学教研室,山东青岛266071 [2]青岛大学医学院
出 处:《青岛大学医学院学报》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
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.
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