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This Article Full Text Full Text (PDF) All Versions of this Article: 90/1/111    most recent expphysiol.2004.028712v1 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 Volk, T. Articles by Ehmke, H. Search for Related Content PubMed PubMed Citation Articles by Volk, T. Articles by Ehmke, H. Related Collections Heart/Cardiac Muscle

¹ Institut für Physiologie, Universitätskrankenhaus Eppendorf, Martinistraße 52, 20246 Hamburg, Germany ² University Laboratory of Physiology, University of Oxford, Parks Road, Oxford OX1 3PT, UK ³ Institut für Zelluläre und Molekulare Physiologie, Friedrich-Alexander-Universität Erlangen-Nürnberg, Waldstraße 6, 91054 Erlangen, Germany

A decrease of the transient outward potassium current (I_to) has been observed in cardiac hypertrophy and contributes to the altered shape of the action potential (AP) of hypertrophied ventricular myocytes. Since the shape and duration of the ventricular AP are important determinants of the Ca²⁺ influx during the AP (Q_Ca), we investigated the effect of ascending aortic stenosis (AS) on Q_Ca in endo- and epicardial myocytes of the left ventricular free wall using the AP voltage-clamp technique. In sham-operated animals, Q_Ca was significantly larger in endocardial compared to epicardial myocytes (803 ± 65 fC pF^–1, n = 27 vs. 167 ± 32 fC pF^–1, n = 38, P < 0.001). Ascending aortic stenosis significantly increased Q_Ca in epicardial myocytes (368 ± 54 fC pF^–1, n = 42, P < 0.05), but did not alter Q_Ca in endocardial myocytes (696 ± 65 fC pF^–1, n = 26). Peak and current–voltage relation of the AP-induced Ca²⁺ current were unaffected by AS. However, the time course of the current–voltage relation was significantly prolonged in epicardial myocytes of AS animals. Model calculations revealed that the increase in Q_Ca can be ascribed to a prolonged opening of the activation gate, whereas an increase in inactivation prevents an excessive increase in Q_Ca. In conclusion, AS significantly increased AP-induced Ca²⁺ influx in epicardial but not in endocardial myocytes of the rat left ventricle.

(Received 20 July 2004; accepted after revision 27 September 2004; first published online 4 October 2004)
Corresponding author T. Volk: Institut für Zelluläre und Molekulare Physiologie, Friedrich-Alexander-Universität Erlangen-Nürnberg, Waldstraße 6, 91054 Erlangen, Germany. Email: tilmann.volk{at}physiologie2.med.uni-erlangen.de