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|本期目录/Table of Contents|

U69 593对家兔心室肌细胞L型Ca2+电流的影响(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2003年第3期
页码:
193-195,198
栏目:
实验研究
出版日期:
2003-05-01

文章信息/Info

Title:
Effect of U69 593 on L-type calcium currentin isolated rabbit ventricular myocytes
作者:
周京军1; 肖国胜2; 高瞻1; 于军1; 朱妙章1
1.第四军医大学生理学教研室,陕西西安710032;2.华中科技大学同济医学院附属协和医院心内科,湖北武汉430022
Author(s):
ZHOUJing-jun1; XIAOGuo sheng2;  GaoZhan1;  YuJun1;  ZHUMiao-zhang1
1.Department of Physiology,Fourth Military Medical University,Xi'an,Shaan xi710032,China;2.Department of Cardiology,Union Hospital,Tong ji Medical College,Hua zhong University of Science and Technology,Wu han,Hu bei430022,China
关键词:
U69593; 电压依赖性钙电流; 心室肌细胞
Keywords:
U69 593; voltage dependent L-type calcium current; ventricular myocytes
分类号:
Q463
DOI:
-
文献标识码:
A
摘要:
目的:研究U69593对家兔心室肌细胞L型Ca2+电流(ICa·L)的影响。方法:采用全细胞膜片钳技术记录家兔 心室肌细胞ICa·L。结果:在-20～ +40mV测试电压范围内,100nmol/LU69593显著增加ICa·L,以+10mV为 最大激活电压,其峰值ICa·L由加药前-7.1±0.4pA/pF增至-8.3±0.5pA/pF(P<0.01,n=8)。100nmol/L U69593不影响ICa·L电压依赖性激活与失活特性。结论:U69593可增加家兔心室肌细胞ICa·L。
Abstract:
AIM:To investigate the effect of U69 593 on the L-type calcium current(ICa·L) in isolated rabbit ventricular myocytes.METHODS:ICa·L was recorded by using the whole cell voltage clamp technique.RESULTS:U69 593 at 100 nmol/L significantly increased ICa·L at the test potential from-20mVto+40mV.The peak of ICa·L was increased from-7.1±0.4pA/pFto-8.3±0.5pA/pF with maximal activation potential at +10mV(by18.3%±3.5%,P<0.01vscontrol,n=8).The steady-state activation and inactivation of ICa·L was not affected by 100 nmol/L U69 593. CONCLUSION: The present study demonstrated that U69 593 increased ICa·L inisolated rabbit ventricular myocyte

参考文献/References

[1]Bers DM.Cardiac excitation-contraction coupling[J].Nature, 2002, 415 (6868):198-205.

[2] TaiKK, JinWQ, ChanTK, et al. Characterization of [3H] U69 593binding sites in the rat heart by receptor binding assays[J].J Mol Cell Cardiol,1991,23(11):1297-1302.

[3] Ventura C,Spurgeon H,Lakatta EG,et al.Kappa and delata opioid receptor stimulation affects cardiacmyocyte function and Ca2+ release from an intracellular pool in myocytes and neurons [J]. CircRes,1992,70(1):66-81.

[4]Li GR,Baumgarten CM.Modulation of cardiac Na+ current by gadolinium,ablockerofstretch induced arrhythmias[J].Am J Physiol (Heart Circ Physiol), 2001,280(1):H272-H279.

[5] Hamill OP,Marty A,Neher E,et al.Improved patch clamp techniques for high resolution current recording from cells and cell-free membrane patches [J]. Pflugers Arch,1981,391(2):85-100.

[6] Li GR,Yang B,Feng J,et al. Transmembrane ICa contributes to rate- dependent changes of action potentialsin human ventricular myocytes [J]. Am J Physiol, 1999, 276 (1Pt2):H98-H106.

[7] Utz J,Eckert R,Trautwein W.Inhibition of L-type calcium currents in guinea pig ventricular myocytes by the kappa-opioid agonist U50488H does not involve binding to opiate receptors [J].J Pharmacol Exp Ther,1995,274(2):627-633.

[8] BersDM, Perez-Reyes E.Ca2+ channels in cardiac myocytes: Structure and function in Ca influx and intracellular Ca2+ release [J]. Cardiovasc Res, 1999, 42 (2): 339-360

备注/Memo

备注/Memo:
收稿日期：2002-11-9.
更新日期/Last Update: 2003-05-01