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Cardiac action potential
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===Phase 2=== This phase is also known as the "plateau" phase due to the [[membrane potential]] remaining almost constant, as the membrane slowly begins to repolarize. This is due to the near balance of charge moving into and out of the cell. During this phase [[KvLQT1|delayed rectifier potassium channels]] (I<sub>ks</sub>) allow potassium to leave the cell while L-type calcium channels (activated by the influx of sodium during phase 0) allow the movement of calcium ions into the cell. These calcium ions bind to and open more calcium channels (called ryanodine receptors) located on the sarcoplasmic reticulum within the cell, allowing the flow of calcium out of the SR. These calcium ions are responsible for the contraction of the heart.{{cn|date=May 2025}} Calcium also activates chloride channels called I<sub>to2</sub>, which allow Cl<sup>β</sup> to enter the cell. Increased calcium concentration in the cell also increases activity of the sodium-calcium exchangers, while increased sodium concentration (from the depolarisation of phase 0) increases activity of the sodium-potassium pumps. The movement of all these ions results in the membrane potential remaining relatively constant, with K<sup>+</sup> outflux, Cl<sup>β</sup> influx as well as Na<sup>+</sup>/K<sup>+</sup> pumps contributing to repolarisation and Ca<sup>2+</sup> influx as well as Na<sup>+</sup>/Ca<sup>2+</sup> exchangers contributing to depolarisation.<ref name="Grunnet M 2010b 1β48">{{Cite journal |last=Grunnet M |year=2010b |title=Repolarization of the cardiac action potential. Does an increase in repolarization capacity constitute a new anti-arrhythmic principle? |journal=Acta Physiologica |volume=198 |pages=1β48 |doi=10.1111/j.1748-1716.2009.02072.x |pmid=20132149 |doi-access=free}}</ref><ref name="santana 496" /> This phase is responsible for the large duration of the action potential and is important in preventing irregular heartbeat (cardiac arrhythmia). There is no plateau phase present in pacemaker action potentials.
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