Skip Navigation

Cardiovascular Research 2000 46(3):361-363; doi:10.1016/S0008-6363(00)00068-7
© 2000 by European Society of Cardiology
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Elvan, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Elvan, A.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2000, European Society of Cardiology

Reexpression of T-type Ca channels after myocardial infarction: does it play a role in cardiac excitation?

A. Elvan*

Diakonessenhuis Utrecht, Interne Geneeskunde, Bosboomstraat 3, 3582 KE Utrecht, The Netherlands

* Tel.: +31-30-2566-566; fax: +31-30-2566-738

Received 13 March 2000; accepted 13 March 2000

The first 10% of the full text of this article appears below.

See article by Huang et al. [5] (pages 442–449) in this issue.


   Introduction
 
Electrophysiological and myocardial remodeling plays an important role in the development of heart failure and arrhythmogenesis after myocardial infarction. Previous reports [1–4] have shown that the activation of signal transduction pathways after myocardial infarction involved in the initiation of cardiac hypertrophy follows a distinct pattern. Why do fetal and neonatal isogenes become reactivated under pathologic conditions? Recent studies [5–7] have taught us that expression and function of ion channels is very dynamic and can be affected at various levels depending on various physiologic and adverse stimuli. The pattern of cardiac excitation, pathologic stimuli such as ischemia or infarction and rate of impulse propagation have important effects on ion channel expression and properties. The number, biophysical characteristics and distribution of . . . [Full Text of this Article]


   Cardiac Ca2+ channels
 

   T-type Ca2+ channel in growth and hypertrophy
 

   Reexpression of fetal T-type Ca2+ channel isogenes
 

   Post-infarction myocardial remodeling and arrhythmogenesis
 

Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Circ. Res.Home page
C.-S. Chiang, C.-H. Huang, H. Chieng, Y.-T. Chang, D. Chang, J.-J. Chen, Y.-C. Chen, Y.-H. Chen, H.-S. Shin, K. P. Campbell, et al.
The CaV3.2 T-Type Ca2+ Channel Is Required for Pressure Overload-Induced Cardiac Hypertrophy in Mice
Circ. Res., February 27, 2009; 104(4): 522 - 530.
[Abstract] [Full Text] [PDF]

Home page
 Cardiovasc ResHome page
N. Laleve, M. C. Rebsamen, S. Barrere-Lemaire, E. Perrier, J. Nargeot, J.-P. Benitah, and M. F. Rossier
Aldosterone increases T-type calcium channel expression and in vitro beating frequency in neonatal rat cardiomyocytes
Cardiovasc Res, August 1, 2005; 67(2): 216 - 224.
[Abstract] [Full Text] [PDF]