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Comment
. 2008 Dec 15;586(24):5849-52.
doi: 10.1113/jphysiol.2008.163089. Epub 2008 Oct 27.

Delayed-rectifier potassium currents and the control of cardiac repolarization: Noble and Tsien 40 years after

Stanley Nattel  1
Affiliations
Comment

Delayed-rectifier potassium currents and the control of cardiac repolarization: Noble and Tsien 40 years after

Stanley Nattel. J Physiol. .
No abstract available

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Figures

Figure 1
Figure 1. Schematic representation of the cardiac action potential and the consequences of repolarization abnormalities
A, the normal cardiac action potential, with corresponding delayed-rectifier currents (rapid, IKr, and slow, IKs, along with the corresponding Noble/Tsien nomenclature, ix1 and ix2), intracellular Ca2+ signal and cell shortening indicating contractile function (the horizontal dashed lines indicate 0 current, 0 intracellular [Ca2+] and reference cell-length values, respectively). Repolarization timing is determined largely by IKr, which is much larger than IKs over the course of the normal action potential. The relatively long cardiac action plateau allows sufficient Ca2+ to enter via L-type Ca2+ channels to maintain sarcoplasmic reticulum Ca2+ stores, essential for cardiac contractility. B, reduced repolarizing current delays repolarization and prolongs the action potential. When action potential prolongation is excessive, reactivation of Ca2+ currents provides enough inward current to generate early afterdepolarizations (dotted action potential). C, increased repolarizing current accelerates repolarization and shortens action potential duration. Action potential abbreviation reduces the refractory period, allowing re-entrant arrhythmias to emerge (for more detailed discussion, see Nattel et al. 2007).
See this image and copyright information in PMC

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