摘要
目的 研究血管紧张素 (1 7) [Ang (1 7) ]对正常豚鼠心室肌细胞膜L型钙内流 (ICa L)、延迟整流性钾流 (IK)、内向整流性钾流 (IK1 )和快钠内流 (INa)以及跨膜动作电位的影响 ,旨在探讨Ang (1 7)对心肌细胞的电生理作用。方法 应用膜片钳全细胞记录方法记录各项离子流和标准微电极技术记录动作电位。结果 (1 )Ang (1 7)可使ICa L呈浓度依赖性增加 ,选择性血管紧张素 (AT1 )受体阻滞剂缬沙坦 (Val)或非选择性血管紧张素受体阻滞剂Sarthran(Sar)均可以消除Ang (1 7)增加ICa L的作用。 (2 )Ang (1 7)可使IK呈浓度依赖性增加 ,Val不能拮抗Ang (1 7)增加IK的作用 ,而Sar可以拮抗Ang (1 7)的作用。 (3)Ang (1 7)对IK1 和INa无影响。 (4)Ang (1 7)可使动作电位时程 (APD30 、APD50 和APD90 )呈浓度依赖性缩短 ,2 μmol/LAng (1 7)使APD90 从 (1 52± 1 8 1 4 )ms缩短至 (1 36± 2 1 37)ms(n =5 ,P <0 0 5) ,对静息电位、动作电位幅度和最大除极速率无影响。结论 Ang (1 7)对心肌细胞复极电流IK作用不同于AngⅡ ,Ang (1 7)通过非AT1 受体促进IK,有助于心肌细胞复极 。
Objective To investigate the effects of angiotensin (1 7)[Ang (1 7)]on the cardiac electrophysiology including the membrane currents of I Ca L , I K I K1 , I Na and action potentials in guinea pig myocardium Methods Membrane currents were recorded with patch electrodes in a whole cell clamp configuration Action potentials(AP)were recorded with standard microelectrode techniques Results The present results showed that:1 I Ca L were increased from (-9 64±1 19)pA/pF to (-10 23±2 16,-11 45±2 78 and -12 76±1 76)pA/pF ( n =11, P <0 05 or 0 01)following administration of Ang (1 7) 0 5, 1 and 2 μmol/L, respectively These effects can be eliminated by specific AT 1 antagonist Valsartan or non specific AT antagonist Sarthran 2 Ang (1 7)(0 5, 1 and 2 μmol/L)also increased I K in a concentration dependent manner [ from (13 53±0 92)pA/pF to (15 67±1 74, 16 96±2 15 and 17 58±2 73)pA/pF, ( n =5, P all<0 05)] And I K.tail were increased from (3 03±0 92)pA/pF to(3 23± 1 14, 3 56±1 15 and 3 86±1 12) pA/pF( n =5, P all<0 05) The effects of Ang (1 7) on I K and I K.tail could be completely eliminated by Sarthran, but not by Valsartan 3 Ang (1 7)had no effects on I Na and I K1 4 The papillary muscles were driven at 1Hz APD 90 was shortened from (152±18 14) ms to (136±21 37) ms following administration of Ang (1 7)2 μmol/L( n =5, P <0 01) All the APD 30 ,APD 50 and APD 90 were shortened with a dose dependent manner, but the rest AP, amplitude of AP and maximal depolarization rate were not changed significantly Conclusions Ang (1 7) increase the amplitude of I K through a non specific AT receptor It will accelarate the repolarization of cardiac myocyte and be benefit to the stability of cardiac electrophysiology
出处
《中华心血管病杂志》
CAS
CSCD
北大核心
2002年第2期105-108,共4页
Chinese Journal of Cardiology
