HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) 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 HighWire Citing Articles via Google Scholar Google Scholar Articles by McAllister, R. E. Articles by Noble, D. Search for Related Content PubMed PubMed Citation Articles by McAllister, R. E. Articles by Noble, D.

1. In normal Tyrode solution the initial inward sodium current which is produced in Purkinje fibres in response to a sudden depolarization is followed by a very slow change in current in an outward direction. The magnitude and speed of onset of this slow change both increase with the strength of the depolarization.

2. On repolarization, a transient outward current is observed (Deck & Trautwein, 1964). The initial magnitude of this outward current also increases with the strength and duration of the preceding depolarization, with a time course similar to the time course of the slow change in current during depolarization.

3. Evidence is presented for the view that the slow change in current during depolarization represents the onset of delayed potassium rectification and that the decline in outward current following repolarization represents its decay.

4. Removal of sodium ions greatly increases the threshold of the slow outward current. In the presence of sodium ions 15 mV depolarization is sufficient to produce an appreciable current. In the absence of sodium ions at least 50 mV depolarization is required and, in some fibres, no delayed rectification is observed even when the membrane potential is made positive.

5. Prolonged depolarization of the membrane by outward current changes the quiescent membrane potential in a positive direction. This change in potential is attributed to an accumulation of potassium ions in a space immediately outside the cell membrane, which equilibrates slowly with the extracellular fluid. It is shown that this effect is very small during depolarizations of the magnitude and duration of the normal action potential.

6. It is concluded that the results are consistent with the view that repolarization of the Purkinje fibre action potential is initiated by a slow increase in K conductance similar to, but much smaller and slower than, that observed in nerve fibres.

This article has been cited by other articles:

				D. M. Roden and T. Yang Protecting the Heart Against Arrhythmias: Potassium Current Physiology and Repolarization Reserve Circulation, September 6, 2005; 112(10): 1376 - 1378. [Full Text] [PDF]

				T. W. Claydon, S. Y. Makary, K. M. Dibb, and M. R. Boyett K+ Activation of Kir3.1/Kir3.4 and Kv1.4 K+ Channels Is Regulated by Extracellular Charges Biophys. J., October 1, 2004; 87(4): 2407 - 2418. [Abstract] [Full Text] [PDF]

				A. E. Martynyuk, T. E. Morey, L. Belardinelli, and D. M. Dennis Hyperkalemia Enhances the Effect of Adenosine on IK,ADO in Rabbit Isolated AV Nodal Myocytes and on AV Nodal Conduction in Guinea Pig Isolated Heart Circulation, January 19, 1999; 99(2): 312 - 318. [Abstract] [Full Text] [PDF]

				A. M. Choy, C. C. Lang, D. M. Chomsky, G. H. Rayos, J. R. Wilson, and D. M. Roden Normalization of Acquired QT Prolongation in Humans by Intravenous Potassium Circulation, October 7, 1997; 96(7): 2149 - 2154. [Abstract] [Full Text]

				M. R. Rosen Cellular Electrophysiologic Basis of Cardiac Arrhythmias Angiology, May 1, 1977; 28(5): 289 - 299. [PDF]