L-型钙电流在血管紧张素Ⅱ诱导新生大鼠肥大心肌细胞中的功能和分子水平改变  

Molecular and Functional Changes in L-type Ca^(2+) Channel of Hypertrophied Cardiocytes in Neonatal Rats Induced by Angiotensin Ⅱ

作　　者：闫秋丽[1] 

机构地区：[1]武汉大学基础医学院,湖北武汉430074

出　　处：《湖北科技学院学报（医学版）》2012年第5期372-377,共6页Journal of Hubei University of Science and Technology(Medical Sciences)

摘　　要：目的探讨血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)诱导的新生大鼠肥大心肌细胞中L-型钙电流的功能和分子水平改变。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 AngⅡ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,AngⅡ还增加了L-型Ca2+通道α1C亚单位mRNA表达量。AngⅡ的这些作用都可被其1型受体阻断剂losartan所抑制。结论在AngⅡ诱导的新生大鼠肥大心肌中,L-型Ca2+通道的分子和功能水平发生了显著变化,这些变化是通过激活心肌细胞上AngⅡ1型受体所介导的。Objective To investigate the molecular and functional changes in L-type Ca^2＋ channel of hypertrophied cardiocytes in neonatal rats induced by angiotensin Ⅱ （Ang Ⅱ ）. Methods The in vitro model of cardiocyte hypertrophy was established in cultured cardiocytes from neonatal rats. Whole cell patch clamp was used to measure the L-type Ca^2＋ currents;Semi-quantitative RT-PCR was used to determine the mRNA expres- sion of L-type Ca^2＋ channel α1C subunits. Results In the hypertrophied cardiocytes 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 Ca^2＋ channel α1C subunits in card- iocytes. All these actions of Ang Ⅱ could be blocked by the angiotensin Ⅱ 1 type receptor blocker losartan. Conclusion Ang Ⅱ can induce significant changes in the molecular structure and function of L-type Ca^2＋ ehan- nels of hypertrophied cardiocytes, which may be 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 

分 类 号：R33-33[医药卫生—人体生理学]