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目的:研究缬沙坦对血管紧张素Ⅱ(AngⅡ)引起人心房肌细胞离子电流改变的调节作用。方法:经典两步酶解法分离单个心房肌细胞,膜片钳全细胞法记录离子电流。结果:AngⅡ(300nmol/L)使快速内向钠电流(INa)从(-15.83±1.62)电流(pA)/电容(pF)降到(-6.35±1.83)pA/pF(P<0.01),其作用不能被缬沙坦(10μmol/L)抑制;使L型钙电流(ICa-L)从(-4.5±1.64)pA/pF增加到(-5.5±1.95)pA/pF(P<0.05),其作用能被缬沙坦抑制;指令电位-120mV时使内向整流性钾电流(IK1)从(-3.49±1.03)pA/pF增加到(-5.47±1.83)pA/pF(P<0.01),+10mV~+50mV时其外向电流成分随电压而增加,其作用不能被缬沙坦抑制。AngⅡ对超速激活延迟整流性钾电流(IKur)和瞬间外向钾电流(Ito1)无显著影响。结论:AngⅡ对人心房肌细胞ICaL有促进作用并可被缬沙坦抑制;增加IK1,抑制INa,其作用不能被缬沙坦抑制。
AIM: To investigate the regulatory effect of valsartan on changes of ion current in human atrial myocytes induced by angiotensin Ⅱ (Ang Ⅱ). Methods: The single atrial myocytes were isolated by classical two - step enzymatic method. Whole - cell patch clamp method was used to record the ion current. RESULTS: AngⅡ (300 nmol / L) decreased INa from (-15.83 ± 1.62) pA / pF to (-6.35 ± 1.83) pA / pF (P <0.01) The effect was not inhibited by valsartan (10μmol / L); the L-type calcium current (ICa-L) was increased from (-4.5 ± 1.64) pA / pF to (-5.5 ± 1.95) pA / pF Its action could be inhibited by valsartan; when the command potential was -120mV, the inward rectifier potassium current (IK1) increased from (-3.49 ± 1.03) pA / pF to (-5.47 ± 1.83) pA / pF The external current component increases with voltage when + 10mV ~ + 50mV, and its effect can not be inhibited by valsartan. AngⅡ had no significant effect on delayed activation of delayed rectifier potassium current (IKur) and transient outward potassium current (Ito1). CONCLUSION: AngⅡ can promote ICaL in human atrial myocytes and can be inhibited by valsartan. Increasing IK1 and inhibiting INa can not be inhibited by valsartan.