摘要
目的 探讨血管紧张素Ⅱ (AngⅡ )对心肌细胞内向整流性钾流 (IK1)的调节作用及其机制。方法 应用膜片钳技术研究AngⅡ对豚鼠单个心肌细胞IK1的影响。结果 AngⅡ促进IK1,内向整流作用减弱。单通道记录表明 ,IK1的加大是由AngⅡ激活了一种非常态钾电流 ,这不受Losartan和Glibenclamide (ATP敏感性钾通道阻滞剂 )的影响。结论 这种非常态钾电流由AT2 受体介导 ,可能是IK1的非常态激活或AngⅡ经AT2
Objective Patch-clamp electrophysiologic techniques were used to study the effects of the biologic active transmiter-AngiotensinⅡ (AngⅡ) on inward rectifier potassium current (IK 1) in single guinea pig myocytes and to assess the effects among the transmiter-receptor-channel.Methods Single emzyne-isolated ventricular cells were used to study the effects of AngⅡ on IK 1.Results The results showed that AngⅡ increased both inward and outward currents of IK 1 and decreased inward rectification in whole cell recording.Single channel recording showed that the increase of IK 1 was attributed to the abnormal burst opening current with a larger unit amplitude.These changes were inversible by using Losartan and Glibenclamide (a ATP sensitive potassium channel inhibitor).Conclusion It suggest that AngⅡ elicited abnormal potassium current characterized by burst opening is mediated by AT 2 receptor subtype,which was caused by abnormal activation of IK 1 or AngⅡ.
出处
《苏州医学院学报》
2000年第4期314-316,327,共4页
Acta Academiae Medicinae Suzhou
