cardiac action potential


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cardiac action potential

the transmembrane potential in the heart, consisting of five phases: 0, the upstroke or rapid depolarization, which initiates the heartbeat in response to an influx of Na+; 1, early rapid repolarization; 2, plateau in response to an influx of Ca2+; 3, final rapid repolarization in response to an influx of K+; and 4, resting membrane potential and diastolic depolarization. Abnormalities of the heart or its conduction system that alter the cardiac action potential lead to the development of cardiac arrhythmias.
References in periodicals archive ?
1 High intracellular iron causes disturbance in the function of the sodium channels responsible for the upstroke (depolarisation) of the cardiac action potential.
In SCN5A mutations, the defect in sodium channels leads to decrease in the sodium current and a shortening of the cardiac action potential by blunting phase 0 depolarisation.
The trajectory of the cardiac action potential is divided into five distinct phases, which reflect changes in the predominant ionic current flowing during the cardiac cycle.
This improves the shape of the action potential to mimic the shape of a real cardiac action potential (see Figure 1(b)).
Models of this type have then been extensively studied and developed by physiologists for the cardiac action potential under the assumption of an equipotential cell, the variation in time of the membrane potential [V.
Congenital LQTS is caused by mutations in ion channels or related proteins that determine conduction of the cardiac action potential.
Thus, the most important toxic effect of TCAs is the slowing of depolarization of the cardiac action potential by inhibition of the sodium current and this delays propagation of depolarization through both myocardium and conducting tissue.
The effects of potassium channel gene regulation on ion currents, protein density, and the cardiac action potential have been demonstrated previously.
Molecular Basis of Cardiac Action Potential Repolarization: Yoram Rudy.
The shape and duration of the cardiac action potential are regulated by multiple ion channels (RyR2, SERCA2a, L-type calcium channel) that are subject to regulatory S-nitrosylation [13,15].
Both of these are considered as potentially fatal cardiac arrhythmia caused due to repolarisation disturbances of the cardiac action potential.
The hERG (human Ether-a-go-go Related Gene) encodes potassium channels, which are responsible for the normal repolarization of the cardiac action potential.