Let's see how you are doing on cardiac action potentials. The first thing to note is that cardiac action potentials are much, much longer than neuronal action potentials.
QUESTION: But what's the significance of this? Why is a long action potential important in the heart?
Fill in your answer below:
There are two general types of cardiac action potentials. Let's first look at the type found in regular ventricular muscle fibers, which are the type of workaday muscle fibers that do the actual pumping of the blood. (The second type of cardiac action potential is found in the small number of muscle fibers that automatically generate action potentials. This is covered in the section below.)
Look at the figure to the right, which shows the times that three types of ion channels are open.
(The designations of "A, B, C" are for the purpose of this webpage only. Incidentally, these are only the most important channels. We are not discussing all of the known ion channels.)
In all these ion channels, which is the factor (one word) that controls the gate?
Lidocaine blocks the opening of channel A, which cause the rapid depolarization at the start of the action potential. What ion moves through this channel and where else might you find a similar channel?
Channel B creates the long plateau phase and the ion is different than that for channel A. Perforce, what does the ion have to be?
Channel C performs the same function as the similar channel in neuronal action potentials. Thus, what does the ion have to be?
To the right you see the action potential in an SA node.
First, note that there is no fast Na+ channel and thus the action potential begins more slowly. But, as before, the prolonged depolarization of the action potential is due to a voltage gated Ca++ channel and the repolarization is due to the usual voltage-gated K+ channel.
Next, note the slow upward movement of the membrane potential between action potentials. As we saw above, this is not seen in healthy regular venticular muscle cells. The horizontal line represents the threshold.
What is this slow upward movement of the membrane potential called?
The pacemaker potential is due to the interplay of Na+, Ca++ and K+ ion channels. As you have anticipated, slow opening of Na+ and Ca++ channels tend to promote the slow depolarization.
(The Na+ channel is interesting in that it is "funny"; that is, it is an exception because it is a voltage gated ion channel that opens with repolarization rather than depolarization.)
Do you expect the K+ channel to be opening or closing during the pacemaker potential?
Acetylcholine and norepinephrine influence the pacemaker potential by opening ion channels. The receptors for both neurotransmitters activate trimeric G proteins, which then open the corresponding ion channels.
Recall that parasympathetic neurons slow the heart rate. Thus, what type of ion channel would you expect acetylcholine to open?
Following the same logic, you can readily deduce that the most important ion channel opened by norepinephrine has an equilibrium potential above threshold. This indeed is the case, since the most important ion channel opened by norepinephrine is Ca++. With the opening of Ca++ channels, the pacemaker potential climb towards threshold more quickly.
Assume a friend of yours is given adenosine to terminate an episode of superventricular tachycardia (see webpage on arrhythmias). Suppose I tell you that the adenosine affects a type K+ channel (which is not a voltage gated channel, but opens via a G protein). Think for a second and then go ahead and bark out whether adenosine causes this channel to open or to close.
Suppose someone is told to do the Valsalva maneuver as an attempt to terminate an episode of supraventricular tachycardia. Why does this make sense?