Pathway: Phase 2 - plateau phase
Reactions in pathway: Phase 2 - plateau phase :
Phase 2 - plateau phase
Phase 2 of the cardiac action potential is the plateau phase which is sustained by a balance of Ca2+ influx through L-type Ca2+ channels (LTCCs) and K+ efflux through the slow delayed rectifier K+ channel 1 (KCNQ1). This phase sustains muscle contraction (Park & Fishman 2011, Grant 2009).
The normal sequence of contraction of atria and ventricles of the heart require activation of groups of cardiac cells. The mechanism must elicit rapid changes in heart rate and respond to changes in autonomic tone. The cardiac action potential controls these functions. Action potentials are generated by the movement of ions through transmembrane ion channels in cardiac cells. Like skeletal myocytes (and axons), in the resting state, a given cardiac myocyte has a negative membrane potential. In both muscle types, after a delay (the absolute refractory period), K+ channels reopen and the resulting flow of K+ out of the cell causes repolarisation. The voltage-gated Ca2+ channels on the cardiac sarcolemma membrane are generally triggered by an influx of Na+ during phase 0 of the action potential. Cardiac muscle cells are so tightly bound that when one of these cells is excited the action potential spreads to all of them. The standard model used to understand the cardiac action potential is the action potential of the ventricular myocyte (Park & Fishman 2011, Grant 2009).
The action potential has 5 phases (numbered 0-4). Phase 4 describes the membrane potential when a cell is not being stimulated. The normal resting potential in the ventricular myocardium is between -85 to -95 mV. The K+ gradient across the cell membrane is the key determinant in the normal resting potential. Phase 0 is the rapid depolarisation phase in which electrical stimulation of a cell opens the closed, fast Na+ channels, causing a large influx of Na+ creating a Na+ current (INa+). This causes depolarisation of the cell. The slope of phase 0 represents the maximum rate of potential change and differs in contractile and pacemaker cells. Phase 1 is the inactivation of the fast Na+ channels. The transient net outward current causing the small downward deflection (the "notch" of the action potetial) is due to the movement of K+ and Cl- ions. In pacemaker cells, this phase is due to rapid K+ efflux and closure of L-type Ca2+ channels. Phase 2 is the plateau phase which is sustained by a balance of Ca2+ influx and K+ efflux. This phase sustains muscle contraction. Phase 3 of the action potential is where a concerted action of two outward delayed currents brings about repolarisation back down to the resting potential (Bartos et al. 2015).
The action potential has 5 phases (numbered 0-4). Phase 4 describes the membrane potential when a cell is not being stimulated. The normal resting potential in the ventricular myocardium is between -85 to -95 mV. The K+ gradient across the cell membrane is the key determinant in the normal resting potential. Phase 0 is the rapid depolarisation phase in which electrical stimulation of a cell opens the closed, fast Na+ channels, causing a large influx of Na+ creating a Na+ current (INa+). This causes depolarisation of the cell. The slope of phase 0 represents the maximum rate of potential change and differs in contractile and pacemaker cells. Phase 1 is the inactivation of the fast Na+ channels. The transient net outward current causing the small downward deflection (the "notch" of the action potetial) is due to the movement of K+ and Cl- ions. In pacemaker cells, this phase is due to rapid K+ efflux and closure of L-type Ca2+ channels. Phase 2 is the plateau phase which is sustained by a balance of Ca2+ influx and K+ efflux. This phase sustains muscle contraction. Phase 3 of the action potential is where a concerted action of two outward delayed currents brings about repolarisation back down to the resting potential (Bartos et al. 2015).
In this module, the processes by which calcium binding triggers actin - myosin interactions and force generation in smooth and striated muscle tissues are annotated.