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.
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].