• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

Inactivation-resistant channels underlying the persistent sodium current in rat ventricular myocytes.

作者信息

Ju Y K, Saint D A, Gage P W

机构信息

John Curtin School of Medical Research, Australian National University, Canberra.

出版信息

Proc Biol Sci. 1994 May 23;256(1346):163-8. doi: 10.1098/rspb.1994.0065.

DOI:10.1098/rspb.1994.0065
PMID:8029241
Abstract

Single-channel sodium currents that could be blocked with TTX were elicited by depolarizing voltage pulses in either cell-attached or inside-out patches from rat ventricular myocytes. A transient burst of channels was followed by late-opening (persistent) channels with low open probability. Conditioning depolarizing pre-pulses that inactivated transient channels and 'chattering' late-opening channels had no effect on persistent channels. The open probability of persistent channels reached a maximum at more negative potentials than transient channels. Between -70 mV and -40 mV, the average open time of persistent channels increased, whereas the average open time of transient channels did not change significantly, so the open times of the two channels diverged as the potential became more positive. The conductance of transient and persistent channels was similar, and the conductance of both kinds of channel increased at more depolarized potentials.

摘要

相似文献

1
Inactivation-resistant channels underlying the persistent sodium current in rat ventricular myocytes.
Proc Biol Sci. 1994 May 23;256(1346):163-8. doi: 10.1098/rspb.1994.0065.
2
Hypoxia increases persistent sodium current in rat ventricular myocytes.缺氧增加大鼠心室肌细胞的持续性钠电流。
J Physiol. 1996 Dec 1;497 ( Pt 2)(Pt 2):337-47. doi: 10.1113/jphysiol.1996.sp021772.
3
A persistent sodium current in rat ventricular myocytes.大鼠心室肌细胞中的持续性钠电流。
J Physiol. 1992;453:219-31. doi: 10.1113/jphysiol.1992.sp019225.
4
The effects of propofol on macroscopic and single channel sodium currents in rat ventricular myocytes.丙泊酚对大鼠心室肌细胞宏观和单通道钠电流的影响。
Br J Pharmacol. 1998 Jun;124(4):655-62. doi: 10.1038/sj.bjp.0701876.
5
Effects of nitric oxide donors, S-nitroso-L-cysteine and sodium nitroprusside, on the whole-cell and single channel currents in single myocytes of the guinea-pig proximal colon.一氧化氮供体S-亚硝基-L-半胱氨酸和硝普钠对豚鼠近端结肠单个肌细胞全细胞电流和单通道电流的影响。
Br J Pharmacol. 1998 Feb;123(3):505-17. doi: 10.1038/sj.bjp.0701605.
6
Gating of cardiac Na+ channels in excised membrane patches after modification by alpha-chymotrypsin.经α-糜蛋白酶修饰后,在分离的膜片上心脏钠通道的门控。
Biophys J. 1994 Jul;67(1):161-71. doi: 10.1016/S0006-3495(94)80465-5.
7
Inward sodium current at resting potentials in single cardiac myocytes induced by the ischemic metabolite lysophosphatidylcholine.
Circ Res. 1992 Nov;71(5):1231-41. doi: 10.1161/01.res.71.5.1231.
8
Patch clamp analysis of Na channel gating in mammalian myocardium: reconstruction of double pulse inactivation and voltage dependence of Na currents.哺乳动物心肌中钠通道门控的膜片钳分析:钠电流双脉冲失活及电压依赖性的重构
Gen Physiol Biophys. 1988 Aug;7(4):353-77.
9
Modulation of single cardiac sodium channels by DPI 201-106.DPI 201-106对单个心脏钠通道的调节作用
Gen Physiol Biophys. 1987 Oct;6(5):409-24.
10
Effects of epoxyeicosatrienoic acids on the cardiac sodium channels in isolated rat ventricular myocytes.环氧二十碳三烯酸对离体大鼠心室肌细胞心脏钠通道的影响。
J Physiol. 1999 Aug 15;519 Pt 1(Pt 1):153-68. doi: 10.1111/j.1469-7793.1999.0153o.x.

引用本文的文献

1
Multiple mechanisms underlie increased cardiac late sodium current.多种机制导致心脏晚期钠电流增加。
Heart Rhythm. 2019 Jul;16(7):1091-1097. doi: 10.1016/j.hrthm.2019.01.018. Epub 2019 Jan 21.
2
Inhibition of the -Subunit of Phosphoinositide 3-Kinase in Heart Increases Late Sodium Current and Is Arrhythmogenic.抑制磷酯酰肌醇 3-激酶亚单位可增加心肌晚期钠电流并致心律失常。
J Pharmacol Exp Ther. 2018 Jun;365(3):460-466. doi: 10.1124/jpet.117.246157. Epub 2018 Mar 21.
3
Post-transcriptional silencing of SCN1B and SCN2B genes modulates late sodium current in cardiac myocytes from normal dogs and dogs with chronic heart failure.
转录后 SCN1B 和 SCN2B 基因沉默调节正常犬和慢性心力衰竭犬心肌细胞中的晚期钠电流。
Am J Physiol Heart Circ Physiol. 2011 Oct;301(4):H1596-605. doi: 10.1152/ajpheart.00948.2009. Epub 2011 Jun 24.
4
Riluzole protects against cardiac ischaemia and reperfusion damage via block of the persistent sodium current.利鲁唑通过阻断持续钠电流来防止心脏缺血再灌注损伤。
Br J Pharmacol. 2010 Jul;160(5):1072-82. doi: 10.1111/j.1476-5381.2010.00766.x.
5
Contributions of ion channel currents to ventricular action potential changes and induction of early afterdepolarizations during acute hypoxia.急性缺氧期间离子通道电流对心室动作电位变化及早期后去极化诱导的作用。
Circ Res. 2009 Dec 4;105(12):1196-203. doi: 10.1161/CIRCRESAHA.109.202267. Epub 2009 Oct 29.
6
Molecular identity of the late sodium current in adult dog cardiomyocytes identified by Nav1.5 antisense inhibition.通过Nav1.5反义抑制鉴定成年犬心肌细胞中晚钠电流的分子特性。
Am J Physiol Heart Circ Physiol. 2008 Aug;295(2):H667-76. doi: 10.1152/ajpheart.00111.2008. Epub 2008 Jun 13.
7
Acute hypoxia differentially regulates K(+) channels. Implications with respect to cardiac arrhythmia.急性缺氧对钾离子通道有不同的调节作用。与心律失常的关系。
Eur Biophys J. 2005 Jul;34(5):369-76. doi: 10.1007/s00249-005-0462-3. Epub 2005 Feb 22.
8
Kinetic diversity of single-channel burst openings underlying persistent Na(+) current in entorhinal cortex neurons.内嗅皮层神经元持续性钠电流中单通道爆发式开放的动力学多样性。
Biophys J. 2003 Nov;85(5):3019-34. doi: 10.1016/S0006-3495(03)74721-3.
9
An antisense oligonucleotide against H1 inhibits the classical sodium current but not ICa(TTX) in rat ventricular cells.针对H1的反义寡核苷酸可抑制大鼠心室细胞中的经典钠电流,但不影响ICa(TTX)。
J Physiol. 2003 Mar 1;547(Pt 2):435-40. doi: 10.1113/jphysiol.2002.035246. Epub 2003 Jan 24.
10
Fine gating properties of channels responsible for persistent sodium current generation in entorhinal cortex neurons.内嗅皮层神经元中负责持续性钠电流产生的通道的精细门控特性。
J Gen Physiol. 2002 Dec;120(6):855-73. doi: 10.1085/jgp.20028676.