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This Article Full Text Full Text (PDF) All Versions of this Article: 89/3/237    most recent expphysiol.2003.027052v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Tan, J. H. C. Articles by Saint, D. A. Search for Related Content PubMed PubMed Citation Articles by Tan, J. H. C. Articles by Saint, D. A. Related Collections Heart/Cardiac Muscle

School of Molecular and Biomedical Sciences, University of Adelaide, Adelaide, SA 5005, Australia

Mechanoelectric feedback (MEF) is the process by which mechanical forces on the myocardium induce electrical responses. It is thought that MEF is important in controlling the beat to beat force of contraction in the ventricle, in response to fluctuations in load, and it may also play a role in controlling the dispersion of repolarization. The transduction mechanism for MEF is via stretch sensitive ion channels in the surface membrane of myocytes. Two types of stretch sensitive channels have been described; a non-selective cation channel, and a potassium selective channel. TREK-1 is a member of the recently cloned tandem pore potassium channels that has been shown to be mechanosensitive and to be expressed in rat heart. Here we report that the gene expression level of TREK-1, quantified using real-time RT-PCR against glyceraldehyde phosphate dehydrogenase (GAPDH) as a comparator gene, was found to be 0.34 ± 0.14 in endocardial cells compared to 0.02 ± 0.02 in epicardial cells (P < 0.05). To confirm that this is reflected in a different current density, whole cell TREK-1 currents, activated by chloroform, were recorded with patch clamp techniques in epicardial and endocardial cells. TREK-1 current density in epicardial and endocardial cells was 0.21 ± 0.06 pA/pF and 0.8 ± 0.27 pA/pF, respectively (P 0.05). We discuss the implications of this differential expression of TREK-1 for controlling action potential repolarization when the myocardium is stretched. We hypothesize that the gene expression of TREK-1 is controlled by the different amounts of stretch experienced by muscle cells across the ventricular wall.

(Received 18 December 2003; accepted after revision 9 January 2004; first published online 17 February 2004)
Corresponding author D. A. Saint: School of Molecular and Biomedical Sciences, University of Adelaide, Adelaide, SA 5005, Australia. Email: david.saint{at}adelaide.edu.au