Skip Navigation

Cardiovascular Research 2003 57(2):468-476; doi:10.1016/S0008-6363(02)00715-0
© 2003 by European Society of Cardiology
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
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
Google Scholar
Right arrow Articles by Poitry, S.
Right arrow Articles by Baertschi, A. J
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Poitry, S.
Right arrow Articles by Baertschi, A. J
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2003, European Society of Cardiology

Differential sensitivity of atrial and ventricular KATP channels to metabolic inhibition

Serge Poitry, Laurianne van Bever, Fabrice Coppex, Angela Roatti and Alex J Baertschi*

Department of Physiology, Centre Médical Universitaire, Université de Genève, 1 rue Michel-Servet, 1211 Geneva 4, Switzerland

alex.baertschi{at}medecine.unige.ch

* Corresponding author. Tel.: +41-22-702-5347; fax: +41-22-702-5402.

Objective: The aim is to compare the activation of ATP-sensitive potassium channels (KATP channels) in intact and metabolically impaired atrial and ventricular myocytes. Methods: The KATP channel current is measured by whole cell and gramicidin-perforated patch clamp recordings in 164 cultured neonate rat cardiomyocytes. Results: In whole cell recordings with 84 µmol/l ADP in pipette, spontaneous activity is significantly higher in atrium than ventricle, and EC50 for the KATP channel opener diazoxide is 0.13 µmol/l (atrium) versus 3.1 µmol/l (ventricle). With an ATP-regenerating system in pipette, EC50 for diazoxide is 19.7 µmol/l (atrium) versus 54.9 µmol/l (ventricle). In gramicidin-perforated patch recordings, atrial myocytes respond significantly to 100 nmol/l of the mitochondrial protonophore CCCP, while ventricular myocytes do not. EC50 for diazoxide is 129 µmol/l (atrium) versus <2500 µmol/l (ventricle) for myocytes exposed to CCCP, and 676 versus <2500 µmol/l, respectively, without CCCP. Conclusions: (1) KATP channels are significantly more sensitive to metabolic inhibition in atrial than ventricular myocytes. (2) Sensitivity of atrium versus ventricle to the channel opener diazoxide increases from 3:1 to ≥24:1 with ADP or metabolic inhibition. If extended to intact hearts, the results would predict a higher atrial sensitivity to ischemia, and a high sensitivity of the ischemic atrium to KATP channel openers.

KEYWORDS Atrial function; K-ATP channel; Membrane currents; Myocytes


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




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.