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Cardiac action potential
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===Phase 3=== During phase 3 (the "rapid repolarization" phase) of the action potential, the L-type [[voltage dependent calcium channel|Ca<sup>2+</sup> channels]] close, while the [[KvLQT1|slow delayed rectifier]] (I<sub>Ks</sub>) [[potassium channels|K<sup>+</sup> channels]] remain open as more potassium leak channels open. This ensures a net outward positive current, corresponding to negative change in [[membrane potential]], thus allowing more types of K<sup>+</sup> channels to open. These are primarily the [[HERG|rapid delayed rectifier]] K<sup>+</sup> channels (I<sub>Kr</sub>) and the [[Inward-rectifier potassium ion channel|inwardly rectifying]] K<sup>+</sup> current, I<sub>K1</sub>. This net outward, positive current (equal to loss of positive charge from the cell) causes the cell to repolarize. The delayed rectifier K<sup>+</sup> channels close when the membrane potential is restored to about -85 to -90 mV, while I<sub>K1</sub> remains conducting throughout phase 4, which helps to set the resting membrane potential<ref name="Kubo2005">{{Cite journal |last=Kubo |first=Y |last2=Adelman |first2=JP |last3=Clapham |first3=DE |last4=Jan |first4=LY |last5=Karschin |first5=A |last6=Kurachi |first6=Y |last7=Lazdunski |first7=M |last8=Nichols |first8=CG |last9=Seino |first9=S |last10=Vandenberg |first10=CA |display-authors=4 |year=2005 |title=International Union of Pharmacology. LIV. Nomenclature and molecular relationships of inwardly rectifying potassium channels |journal=Pharmacol Rev |volume=57 |issue=4 |pages=509β26 |doi=10.1124/pr.57.4.11 |pmid=16382105 |s2cid=11588492 |ref={{sfnref|Kubo et al.|2005}}}}</ref> Ionic pumps as discussed above, like the [[sodium-calcium exchanger]] and the [[Na+/K+-ATPase|sodium-potassium pump]] restore ion concentrations back to balanced states pre-action potential. This means that the intracellular calcium is pumped out, which was responsible for cardiac myocyte contraction. Once this is lost, the contraction stops and the heart muscles relax.{{cn|date=May 2025}} In the sinoatrial node, this phase is also due to the closure of the L-type calcium channels, preventing inward flux of Ca<sup>2+</sup> and the opening of the rapid delayed rectifier potassium channels (I<sub>Kr</sub>).<ref name="pmid14693686">{{Cite journal |vauthors=Clark RB, Mangoni ME, Lueger A, Couette B, Nargeot J, Giles WR |date=May 2004 |title=A rapidly activating delayed rectifier K+ current regulates pacemaker activity in adult mouse sinoatrial node cells |journal=American Journal of Physiology. Heart and Circulatory Physiology |volume=286 |issue=5 |pages=H1757β66 |doi=10.1152/ajpheart.00753.2003 |pmid=14693686}}</ref>
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