Look at the figure to the right, which shows the times that five types of ion channels are open. (The designations of "A, B, C, D, E" are for the purpose of this webpage only.)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.
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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 five types of ion channels are open. (The designations of "A, B, C, D, E" are for the purpose of this webpage only.)
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?
The last three channels (C, D, E) are all K+ channels. We are primarily interested in channel C, which performs to same function as the related channel in action potentials. (Channel D creates the downward blip near the beginning of the action potential, which is a minor effect. Channel E is a K+ voltage gated ion channel with an unusual feature. It closes on depolarization. Thus it is closed during the plateau of the action potential, making it easier for the Ca++ channel to keep the cell depolarized at that level. )
To the right you see the action potential in an SA node and the times that four voltage gated ion channels are open. First, 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.
What is this slow upward movement of the membrane potential called?
Next note that there is no fast Na+ channel and thus the action potential begins more slowly.
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QUESTION: Channel A here is nonetheless a Na+ channel, but it is called "funny". Why is this? (I am not looking for a gag here) And, what is its role? Fill in your answer below: |
Channels B and C are Ca++ channels. The first helps the action potential get started. The second creates the prolonged portion of the action potential, just as it does in the ventricular action potential (i.e. see channel B above in ventricular muscle.)
The last is a K+ channel. As usual, the opening of this type of channel causes repolarization .
But here this K+ channel plays an additional role, and helps create the pacemaker potential. Why does it do this?
Assume a friend of yours is given adenosine to terminate an episode of superventricular tachycardia. 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.
What I hope your cat, roommate, or etc heard.
Acetylcholine has the same action on K+ channels as adenosine, although acting via a different receptor. Suppose someone is told to do the Valsalva maneuver as an attempt to terminate an episode of supraventricular tachycardia. Why does this make sense?