Skip Navigation

Cardiovascular Research 1998 40(3):508-515; doi:10.1016/S0008-6363(98)00204-1
© 1998 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 Iost, N.
Right arrow Articles by Papp, J. Gy.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Iost, N.
Right arrow Articles by Papp, J. Gy.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 1998, European Society of Cardiology

Delayed rectifier potassium current in undiseased human ventricular myocytes

Norbert Iosta, László Virága, Miklós Opincariub, János Szécsib, András Varróa and Julius Gy. Pappa,*

aDepartment of Pharmacology, Albert Szent-Györgyi Medical University, Szeged, Hungary
bDepartment of Cardiac Surgery, Albert Szent-Györgyi Medical University, Szeged, Hungary

* Corresponding author. Tel.: +36-62-311-760, +36-62-455-681; fax: +36-62-321-107; e-mail: papp@phcol.szote.u-szeged.hu

Objective: The purpose of the study was to investigate the properties of the delayed rectifier potassium current (IK) in myocytes isolated from undiseased human left ventricles. Methods: The whole-cell configuration of the patch-clamp technique was applied in 28 left ventricular myocytes from 13 hearts at 35°C. Results: An E-4031 sensitive tail current identified the rapid component of IK (IKr) in the myocytes, but there was no evidence for an E-4031 insensitive slow component of IK (IKs). When nifedipine (5 µM) was used to block the inward calcium current (ICa), IKr activation was fast ({tau}=31.0±7.4 ms, at +30 mV, n=5) and deactivation kinetics were biexponential and relatively slow ({tau}1 =600.0±53.9 ms and {tau}2=6792.2±875.7 ms, at –40 mV, n=7). Application of CdCl2 (250 µM) to block ICa altered the voltage dependence of the IKr considerably, slowing its activation ({tau}=657.1±109.1 ms, at +30 mV, n=5) and accelerating its deactivation ({tau}=104.0±18.5 ms, at –40 mV, n=8). Conclusions: In undiseased human ventricle at 35°C IKr exists having fast activation and slow deactivation kinetics; however, there was no evidence found for an expressed IKs. IKr probably plays an important role in the frequency dependent modulation of repolarization in undiseased human ventricle, and is a target for many Class III antiarrhythmic drugs.

KEYWORDS Cell isolation; K-channel; Human myocytes; Ventricular arrhythmias


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
 J. Physiol.Home page
A. Varro, B. Balati, N. Iost, J. Takacs, L. Virag, D. A Lathrop, L. Csaba, L. Talosi, and J. G. Papp
The role of the delayed rectifier component IKs in dog ventricular muscle and Purkinje fibre repolarization
J. Physiol., February 15, 2000; 523(1): 67 - 81.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.