血管紧张素Ⅱ抑制ECV304细胞BKca效应的细胞机制及银杏叶提取物的作用

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-conductance calcinm-activated potassiun channel,BKCa)效应与AⅡ受体、蛋白激酶C(ProteinKinase C,PKC)和一氧化氮(Nitric Oxide,NO)的关系,以及中药银杏叶提取物(Gingko leaf extract)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(10-7 mol/L)可对抗AⅡ(10-7mol/L)的抑制效应;PKC的激动剂佛波酯(5×10-8 mol/L,Phorbolester)可加重AⅡ的抑制效应;NO(10-10mol/L.sod-ium nitroprusside,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ECV304 BKCa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ECV304 BKCa免受AⅡ的抑制具有保护作用.

The cellular mechanism of angiotensin II inhibition on BKCa of ECV304 cell and the protective effect of gingko leaf extract

OBJECTIVE: To observe the cellular mechanism of A II inhibition on Maxi-conductance calcium activated potassium channel (BKCa) in ECV304 cell membrane. METHOD: Using the cell-attached configuration of patch clamp technique. RESULTS: A II receptor antagonist saralasin (10(-7) mol/L) may block the inhibitory effect of A II (10(-7) mol/L). Phorbol ester (5 x 10(-8) mol/L) potentiated the effect of A II, while NO (10(-10) mol/L SNP) decreased the effect of A II and gingko leaf extract (800 micrograms/ml) activated BKCa and opposed the effects of A II. CONCLUSION: A II receptor mediates the inhibitory effect of A II on BKCa in ECV304, and PKC is involved in this inhibition. NO and ginkgo leaf extract protect BKCa from the inhibition of A II.