Skip Navigation

Cardiovascular Research 2001 52(2):236-245; doi:10.1016/S0008-6363(01)00395-9
© 2001 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 Knopp, A.
Right arrow Articles by Benndorf, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Knopp, A.
Right arrow Articles by Benndorf, K.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2001, European Society of Cardiology

Mitochondria are the main ATP source for a cytosolic pool controlling the activity of ATP-sensitive K+ channels in mouse cardiac myocytes

Andreas Knopp, Stephan Thierfelder, Bettina Doepner and Klaus Benndorf*

Institut für Physiologie, Abt. Herz-Kreislauf-Physiologie, Friedrich-Schiller-Universität Jena, D-07740 Jena, Germany

* Corresponding author. Tel.: +49-3641-934-351; fax: +49-3641-933-202 kben{at}mti-n.uni-jena.de

Objective: The aim was to identify the major ATP source controlling the activity of sarcolemmal KATP channels in ventricular cardiomyocytes. Methods: KATP-channel current (IKATP) was measured with the patch-clamp technique in either the whole-cell (glycogenolysis blocked by 10 mmol/l EGTA), cell-attached, or inside-out configuration. Results: In the absence of any substrate, IKATP (amplitude 31±4 nA; n=5) appeared spontaneously 520±160 s (n=6) after whole-cell access. This latency was shortened by exposure to anoxia (117±33 s, n=32) and even more by uncoupling (1–10 µmol/l FCCP; 25±3 s; n=13) while the amplitude was unchanged. During metabolic inhibition the latency was remarkably prolonged when the F1F0-ATPase was blocked by oligomycin, suggesting that under those conditions the F1F0-ATPase is the major ATP consumer. Glucose (5.5–20.0 mmol/l) in the bath solution did not affect the amplitude of IKATP but prolonged its latency compared to respective substrate-free conditions. However, IKATP was blocked immediately by mitochondrial substrates. FCCP also induced large IKATP in cell-attached measurements in either the absence or presence of glucose and oligomycin. Conclusions: The activity of KATP channels in cardiomyocytes of mice is controlled by a cytosolic [ATP] pool for which oxidative phosphorylation is the predominant ATP source.

KEYWORDS Energy metabolism; Glycolysis; Hypoxia/anoxia; K-ATP channel; Mitochondria; Oxidative phosphorylation


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.