L-型钙电流在血管紧张素Ⅱ诱导新生大鼠心肌细胞肥大中的作用  

The functional changes in L-type Ca^(2+) channel of hypertrophied cardiomyocytes in neonatal rats induced by angiotensin Ⅱ

作　　者：闫秋丽[1] 化维[1] 余良主[2] 

机构地区：[1]北京市昌平区华一医院,北京102208 [2]湖北科技学院,咸宁437100

出　　处：《中国应用生理学杂志》2013年第1期91-95,共5页Chinese Journal of Applied Physiology

摘　　要：目的:探讨血管紧张素II(Ang II)诱导的新生大鼠肥大心肌细胞中L-型钙电流的功能在分子水平改变。方法:在血管紧张素II诱导的新生大鼠肥大心肌细胞中,应用全细胞膜片钳技术检测L-型钙电流的密度及门控动力学变化;应用半定量RT-PCR技术检测L-型Ca2+通道α1C亚单位mRNA的表达量。结果:Ang II在引起新生大鼠心肌肥大的同时,也增加了心肌细胞ICa,L电流密度,但并不影响ICa,L电流的激活、失活和复活特征。另外,Ang II还增加了L-型Ca2+通道α1C亚单位mRNA表达量。Ang II的这些作用都可被其1型受体阻断剂losartan所抑制。结论:在Ang II诱导的新生大鼠肥大心肌中,L-型Ca2+通道的功能在分子水平发生了显著变化,这些变化是通过激活心肌细胞上Ang II 1型受体所介导的。Objective： To investigate the molecular and functional changes in Ltype Ca2＋ channel of hypertrophied cardiomyocytes in neonatal rats induced by angiotensin Ⅱ（Ang Ⅱ）.Methods： The in vitro model of cardiomyocyte hypertrophy was established in cultured cardiomyocytes from neonatal rats.Whole cell patch clamp was used to measure the L-type Ca2＋ currents.Semi-quantitative RT-PCR was used to determine the mRNA expression of L-type Ca2＋ channel α1C subunits.Results： In the hypertrophied cardiomyocytes induced by Ang Ⅱ,ICa,L densities were increased,whereas the features of ICa,L activation,inactivation or recovery from inactivation were not affected.Meanwhile,Ang Ⅱ increased the mRNA expression of L-type Ca2＋ channel α1C subunits in cardiomyocytes.All these actions of Ang Ⅱ could be blocked by the angiotensin Ⅱ 1 type receptor blocker losartan.Conclusion： During cardiomyocyte hypertrophy induced by Ang Ⅱ,there are significant changes in the molecule and function of L-type Ca2＋ channels,which are mediated by the angiotensin Ⅱ 1 type receptor.

关 键 词：血管紧张素Ⅱ 心肌肥厚 L-型Ca2+通道 大鼠 

分 类 号：R33-33[医药卫生—人体生理学]