Action potential in cardiac muscle

The resting membrane potential of individual

mammalian cardiac muscle cells is about 90 mV (interior negative to exterior

. This potential is determined by the selective

permeability of the cell membrane to various ions. The membrane is most permeable to K+ and relatively impermeable to other ions.

 Depolarization proceeds rapidly, and an overshoot

is present, as in skeletal muscle and nerve, but this is followed by a plateau before the membrane potential returns to the baseline.
In mammalian hearts, depolarization lasts about 2

ms, but the plateau phase and repolarization last 200 ms or more.
Repolarization is therefore not complete until the

contraction is half over.

 As in other excitable tissues, changes in the external

K+ concentration affect the resting membrane potential of cardiac muscle, whereas changes in the external Na+ concentration affect the magnitude of the action potential
The initial rapid depolarization and the overshoot

(phase 0) are due to opening of voltage-gated Na+ channels similar to that occurring in nerve and skeletal muscle

 The initial rapid repolarization (phase 1) is due to

closure of Na+ channels.small downward deflection of the action potential is due to the movement of K+ and Clions, slower but prolonged opening of voltage-gated Ca2+ channels. This "plateau" phase of the cardiac action potential is sustained by a balance between inward movement of Ca2+ (ICa) through L-type calcium channels and outward movement of K+ through the slow delayed rectifier potassium channels

The subsequent prolonged plateau (phase 2) is due to a

Final repolarization (phase 3) to the resting membrane

potential (phase 4) is due to closure of the Ca2+ channels and K+ efflux through various types of K+ channels.

Action potential and automaticity of SA node

Cells within the sinoatrial (SA) node are the

primary pacemaker site within the heart. These cells are characterized as having no true resting potential, but instead generate regular, spontaneous action potentials. SA nodal action potentials are divided intothree phases:
1. phase 0, upstroke of the action potential;

2. phase 3, the period of repolarization;

3. and phase 4, the period of spontaneous

depolarization that leads to subsequent generation of a new action potential

 Phase 0 depolarization primarily is due to

increased gCa through L-type calcium channels.

These voltage-operated channels open when

the membrane is depolarized to a threshold voltage of about 40 mV.

Because the movement of Ca through calcium

channels is not rapid (hence, the term slow calcium channels), the rate of depolarization (the slope of phase 0) is much slower than that found in other cardiac cells

 Depolarization causes voltage-operated,

delayed rectifier potassium channels to open,

the increased gK repolarizes the cell toward

the equilibrium potential for K (phase 3).

At the same time, the slow inward Ca

channels that opened during phase 0 become inactivated, thereby decreasing gCa and contributing to the repolarization.
Phase ends when the membrane potential

reaches about 65 mV.

 At the end of repolarization, when the membrane

potential is very negative (about -60 mV), ion channels open that conduct slow, inward (depolarizing) Na+ currents. These currents are called"funny" currents and abbreviated as "If". These depolarizing currents cause the membrane potential to begin to spontaneously depolarize, thereby initiating Phase 4 Thus, the resting potential gradually rises between each two heartbeats. When the potential reaches a threshold voltage of about -40 millivolts, the calcium channels become activated, thus causing the action potential. Therefore, basically, the inherent leakiness of the sinus nodal fibers to sodium and calcium ions causes their self-excitation.