Phase 2 is characterized by a net balance between inward (depolarizing) and outward (repolarizing) ion currents maintaining the myocyte in a depolarized state. During this phase, Ca++ enters the cell, causing Ca++ release from intracellular stores and linking electrical depolarization with mechanical contraction. Interestingly, the current flow during the plateau phase is small, and therefore, perturbations in any of the currents participating in this phase (either through genetic mutations or pharmacologically) may result in profound alterations in the action potential. Ca++ enters the cell through voltage-dependent channels highly selective for Ca++ that open when the membrane is depolarized above -40 mV. The channel (L-type calcium channel) possesses slow inactivation kinetics resulting in a long-lasting current.
Outward repolarizing K+ currents oppose the effect of the inward ICa++ on the plateau phase. This current is carried predominantly through delayed rectifier potassium channels (IK).These channels are voltage sensitive, with slow inactivation kinetics. Three distinct subpopulations of IK with differing activation and inactivation kinetics have been described. A rapidly activating subset (IKr), a slowly inactivating subset (IKs), and an ul-tra-rapidly activating subset to date are identified only in atrial tissue (IKur).
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