• 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

Calcium currents in normal and hypertrophied isolated feline ventricular myocytes.

作者信息

Kleiman R B, Houser S R

机构信息

Department of Physiology, Temple University School of Medicine, Philadelphia, Pennsylvania 19140.

出版信息

Am J Physiol. 1988 Dec;255(6 Pt 2):H1434-42. doi: 10.1152/ajpheart.1988.255.6.H1434.

DOI:10.1152/ajpheart.1988.255.6.H1434
PMID:2849320
Abstract

The magnitude and kinetics of the slow inward calcium current (Isi) were compared in single right ventricular myocytes that were isolated from normal cats and cats with right ventricular hypertrophy. Peak inward current density was greater in hypertrophy than normal myocytes (-20.4 +/- 15.3 vs. -10.4 +/- 8.8 microA/cm2, P less than 0.05). When we blocked early outward currents with intracellular CsCl, however, the peak magnitude of Isi was shown to be similar in hypertrophy and normal myocytes (-16.4 +/- 11.2 vs. -12.7 +/- 3.0 microA/cm2, P = NS). The increased net inward current in hypertrophy was thus due to a decrease in Cs-sensitive early outward current rather than an increase in the magnitude of Isi. The fast component of inactivation of Isi was similar in hypertrophy and normal myocytes, but the slow component was delayed in hypertrophy (slow time constant; tau slow = 75.9 +/- 14.7 ms vs. tau slow = 60.6 +/- 4.9 ms, P less than 0.05). These abnormalities of Isi may contribute to the prolonged duration of the action potential and of contraction in hypertrophied myocardium, but a defect in excitation-contraction coupling distal to Isi appears to produce the diminished magnitude of contraction.

摘要

相似文献

1
Calcium currents in normal and hypertrophied isolated feline ventricular myocytes.
Am J Physiol. 1988 Dec;255(6 Pt 2):H1434-42. doi: 10.1152/ajpheart.1988.255.6.H1434.
2
Outward currents in hypertrophied feline ventricular myocytes.肥厚型猫心室肌细胞中的外向电流。
Prog Clin Biol Res. 1990;334:65-83.
3
Outward currents in normal and hypertrophied feline ventricular myocytes.正常和肥厚猫心室肌细胞中的外向电流。
Am J Physiol. 1989 May;256(5 Pt 2):H1450-61. doi: 10.1152/ajpheart.1989.256.5.H1450.
4
The electrophysiological characteristics of hypertrophied ventricular myocytes from the spontaneously hypertensive rat.自发性高血压大鼠肥厚心室肌细胞的电生理特性
J Hypertens. 1993 Jun;11(6):611-22. doi: 10.1097/00004872-199306000-00005.
5
T-type Ca2+ current is expressed in hypertrophied adult feline left ventricular myocytes.T型钙电流在成年猫左心室肥厚心肌细胞中表达。
Circ Res. 1993 Oct;73(4):777-82. doi: 10.1161/01.res.73.4.777.
6
Electrical remodeling of membrane ionic channels of hypertrophied ventricular myocytes from spontaneously hypertensive rats.自发性高血压大鼠肥厚心室肌细胞膜离子通道的电重构
Chin Med J (Engl). 2000 Jul;113(7):584-7.
7
Characteristics of single Ca(2+) channel kinetics in feline hypertrophied ventricular myocytes.猫肥厚性心室肌细胞中单个Ca(2+)通道动力学的特征
Chin Med J (Engl). 2002 Apr;115(4):502-8.
8
Enhanced functional expression of transient outward current in hypertrophied feline myocytes.肥厚型猫心肌细胞瞬时外向电流的功能表达增强。
Cardiovasc Drugs Ther. 1993 Aug;7 Suppl 3:611-9. doi: 10.1007/BF00877628.
9
Regional distribution of hyperpolarization-activated current (If) and hyperpolarization-activated cyclic nucleotide-gated channel mRNA expression in ventricular cells from control and hypertrophied rat hearts.正常和肥大大鼠心脏心室细胞中超级化激活电流(If)的区域分布及超级化激活环核苷酸门控通道mRNA表达
J Physiol. 2003 Dec 1;553(Pt 2):395-405. doi: 10.1113/jphysiol.2003.041954. Epub 2003 Sep 26.
10
Reduction of calcium-independent transient outward potassium current density in DOCA salt hypertrophied rat ventricular myocytes.
Pflugers Arch. 1994 May;427(1-2):47-55. doi: 10.1007/BF00585941.

引用本文的文献

1
Differential expression of genes participating in cardiomyocyte electrophysiological remodeling via membrane ionic mechanisms and Ca-handling in human heart failure.通过心肌细胞膜离子机制和钙处理参与心肌电生理重构的基因在人类心力衰竭中的差异表达。
Mol Cell Biochem. 2020 Jan;463(1-2):33-44. doi: 10.1007/s11010-019-03626-4. Epub 2019 Sep 13.
2
Substrates and potential therapeutics of ventricular arrhythmias in heart failure.心力衰竭中心律失常的底物和潜在治疗方法。
Eur J Pharmacol. 2018 Aug 15;833:349-356. doi: 10.1016/j.ejphar.2018.06.024. Epub 2018 Jun 27.
3
Role of STIM1 (Stromal Interaction Molecule 1) in Hypertrophy-Related Contractile Dysfunction.
基质相互作用分子1(STIM1)在肥厚相关收缩功能障碍中的作用
Circ Res. 2017 Jul 7;121(2):125-136. doi: 10.1161/CIRCRESAHA.117.311094. Epub 2017 Jun 7.
4
Kvβ1.1 (AKR6A8) senses pyridine nucleotide changes in the mouse heart and modulates cardiac electrical activity.Kvβ1.1(AKR6A8)可感知小鼠心脏中吡啶核苷酸的变化,并调节心脏电活动。
Am J Physiol Heart Circ Physiol. 2017 Mar 1;312(3):H571-H583. doi: 10.1152/ajpheart.00281.2016. Epub 2016 Dec 16.
5
Role of RyR2 phosphorylation in heart failure and arrhythmias: protein kinase A-mediated hyperphosphorylation of the ryanodine receptor at serine 2808 does not alter cardiac contractility or cause heart failure and arrhythmias.兰尼碱受体2(RyR2)磷酸化在心力衰竭和心律失常中的作用:蛋白激酶A介导的兰尼碱受体在丝氨酸2808处的过度磷酸化不会改变心脏收缩力,也不会导致心力衰竭和心律失常。
Circ Res. 2014 Apr 11;114(8):1320-7; discussion 1327. doi: 10.1161/CIRCRESAHA.114.300569.
6
Ca(2+) influx through L-type Ca(2+) channels and transient receptor potential channels activates pathological hypertrophy signaling.钙离子经 L 型钙离子通道和瞬时受体电位通道内流激活病理性肥大信号转导。
J Mol Cell Cardiol. 2012 Nov;53(5):657-67. doi: 10.1016/j.yjmcc.2012.08.005. Epub 2012 Aug 21.
7
Autoregulation of cardiac l-type calcium channels.心脏 L 型钙通道的自身调节。
Trends Cardiovasc Med. 2009 Nov;19(8):268-71. doi: 10.1016/j.tcm.2010.02.009.
8
Electrophysiological remodeling in heart failure.心力衰竭中的电生理重构。
J Mol Cell Cardiol. 2010 Apr;48(4):619-32. doi: 10.1016/j.yjmcc.2010.01.009. Epub 2010 Jan 20.
9
Cooperative regulation of Ca(v)1.2 channels by intracellular Mg(2+), the proximal C-terminal EF-hand, and the distal C-terminal domain.细胞内镁离子、近端C末端EF手型结构域和远端C末端结构域对Ca(v)1.2通道的协同调节
J Gen Physiol. 2009 Aug;134(2):81-94. doi: 10.1085/jgp.200910209. Epub 2009 Jul 13.
10
Long-term improvement of QT dispersion is unaffected by short-term changes in blood pressure during treatment of systemic hypertension with enalapril.使用依那普利治疗系统性高血压期间,QT离散度的长期改善不受血压短期变化的影响。
Ann Noninvasive Electrocardiol. 2003 Jan;8(1):47-54. doi: 10.1046/j.1542-474x.2003.08108.x.