【摘要】 目的观察血管紧张素Ⅱ(AngiotensinⅡAⅡ)抑制人脐静脉内皮细胞株ECV304细胞的大电导钙激活钾通道(Maxi-conductancecalcium-activatedpotassiumchannelBKCa)效应与AⅡ受体、蛋白激酶C(ProteinKinaseCPKC)和一氧化氮(NitricOxideNO)的关系,以及中药银杏叶提取物Gingkoleafextract对AⅡ抑制BKCa效应的影响。方法细胞贴附式膜片箝技术。结果AⅡ受体拮抗剂saralasin(10-7mol/L)可对抗AⅡ(10-7mol/L)的抑制效应;PKC的激动剂佛波酯(5×10-8mol/LPhorbolester)可加重AⅡ的抑制效应;NO(10-10mol/L,sod-iumnitroprussideSNP)则削弱AⅡ的抑制作用。中药银杏叶提取物(800μg/ml)可激活BKCa并可对抗AⅡ的抑制效应。结论AⅡ对ECV304BKCa的抑制是由AⅡ受体介导的,PKC参与其中。NO与银杏叶提取物对ECV304BKCa免受AⅡ的抑制具有保护作用。更多还原

【Abstract】 Objective To observe the cellular mechanism of AⅡinhibition on Maxi-conduct ance calcium activ ated potassium channel(BK Ca )in ECV304cell membrane.Method Using the cell-attached con f-ig uration of patch clamp technique.Results AⅡreceptor antagonist saralasin(10 -7 mol/L)may block the inhibitory effect of AⅡ(10 -7 mol/L).Phorbol ester(5×10 -8 mol/L)potentiated the effect of AⅡ,while NO(10 -10 mol/L SNP)decreased the effect of AⅡand gingko leaf extract(800μg/ml )activated BK Ca and opposed the effects of AⅡ.Conclusion AⅡreceptor mediates the inhibito ry effect of AⅡon BK Ca in ECV304,and PKC is involved in this inhibition.NO and ginkgo leaf ext ract protect BK Ca from the inhibition of AⅡ.更多还原