Action potentials in myocardial contractile cells
Do you know what prevents tetany from occurring in cardiac muscle cells? In this last episode
of this Chalk Talk course on action potentials, we’ll wrap this up with the series of events
that occur during and following an action potential in myocardial contractile cells.
Sustained or tetanic contraction of myocardial contractile cells would be life-threatening
and is prevented by special properties of their action potential, leading to a significantly
longer refractory period and preventing re-excitation before muscle contraction is over.
The resting potential of myocardial contractile cells is around -90 millivolts. It’s almost
exclusively maintained by potassium ion efflux through delayed rectifier potassium channels.
In contrast to other cell types, action potentials in myocardial contractile cells aren’t triggered
by a transmitter but by electrochemical stimulation. The depolarization of a neighbouring cell
results in some positive ions moving from their cytosol into the myocardial contractile
cell through gap junctions. Thereby, the excess negative charge decreases and the membrane
potential increases. If it exceeds around -65 millivolts, the potassium channels close
and the voltage-gated sodium channels open. These sodium channels enable the rapid influx
of sodium ions into the cell, leading to rapid depolarization. Reaching a membrane potential
of about -40 millivolts, the sodium channels close again, resulting in the termination
of sodium influx after only approximately one millisecond. The maximum attainable membrane
potential is approximately +20 millivolts.
As with neurons and skeletal muscle cells, repolarization follows. However, initially,
only partial repolarization takes place in myocardial contractile cells. A transitory
efflux of potassium ions through transient and ultrafast potassium channels in conjunction
with an influx of negatively charged chloride ions lowers the positive intracellular charge.
The membrane potential decreases to about 0 millivolts and is maintained for approximately
200 to 400 milliseconds in the plateau phase. For this to occur, the repolarizing potassium
and chloride currents are counterbalanced by the slow influx of calcium into the cell.
The responsible L-type calcium channels are also voltage-dependent and activated at values
exceeding -40 millivolts but open with a significant delay. As soon as the calcium channels close,
the repolarizing ion currents dominate again, resulting in the final repolarization of the
myocardial contractile cell. During this part of repolarization, the rapid and slow potassium
channels are primarily involved. Also, the delayed rectifier potassium channels contribute
to restoring the resting potential in the myocardial contractile cell. In cardiomyocytes,
afterhyperpolarization doesn’t occur, similar to skeletal muscle cells.
Instead, a long refractory period ensures the correct functioning of myocardial contractile
cells. The absolute refractory period, during which sodium channels are inactive, lasts
until the end of the plateau phase. During final cell repolarization, the voltage-dependent
sodium channels return to their active state. However, they’re only completely activatable
once the resting potential is re-established.
To sum it up, there are several similarities in the formation of action potentials in the
three different cell types that we’ve discussed in this Chalk Talk series: namely, neurons,
skeletal muscle cells, and myocardial contractile cells. Check out parts two and three of our
course if you want to learn more about how the action potential of neurons and muscle
cells differ to that of myocardial contractile cells.