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This Article Full Text Full Text (PDF) All Versions of this Article: 288/3/H1113    most recent 00882.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (5) Citing Articles via Google Scholar Google Scholar Articles by Lin, X. Articles by Veenstra, R. D. Search for Related Content PubMed PubMed Citation Articles by Lin, X. Articles by Veenstra, R. D.

Dynamic model for ventricular junctional conductance during the cardiac action potential

¹Department of Pharmacology, State University of New York Upstate Medical University, Syracuse, New York; and ²Department of Pediatrics, University of Chicago, Chicago, Illinois

Submitted 26 August 2004 ; accepted in final form 25 October 2004

The ventricular action potential was applied to paired neonatal murine ventricular myocytes in the dual whole cell configuration. During peak action potential voltages >100 mV, junctional conductance (g_j) declined by 50%. This transjunctional voltage (V_j)-dependent inactivation exhibited two time constants that became progressively faster with increasing V_j. G_j returned to initial peak values during action potential repolarization and even exceeded peak g_j values during the final 5% of repolarization. This facilitation of g_j was observed <30 mV during linearly decreasing V_j ramps. The same behavior was observed in ensemble averages of individual gap junction channels with unitary conductances of 100 pS or lower. Immunohistochemical fluorescent micrographs and immunoblots detect prominent amounts of connexin (Cx)43 and lesser amounts of Cx40 and Cx45 proteins in cultured ventricular myocytes. The time dependence of the g_j curves and channel conductances are consistent with the properties of predominantly homomeric Cx43 gap junction channels. A mathematical model depicting two inactivation and two recovery phases accurately predicts the ventricular g_j curves at different rates of stimulation and repolarization. Functional differences are apparent between ventricular myocytes and Cx43-transfected N2a cell gap junctions that may result from posttranslational modification. These observations suggest that gap junctions may play a role in the development of conduction block and the genesis and propagation of triggered arrhythmias under conditions of slowed conduction (<10 cm/s).

gap junctions; connexin43; voltage gating; inactivation; kinetics; repolarization

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