potassium channels, cardiac muscle contraction

[yellowjellybean]

My BR book says "as the cardiac action potential begins, the permeability of potassium decreases as potassium channels close" and the potassium channel returns to their original state with repolarization.

I am confused because this is different from a neuronal action potential when the voltage gated K+ channels are late to open. What kind of channels are they talking about here, voltage gated or leaky?

Also, calcium is not involved in action potentials of pacemaker cells right?

Thank you

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[akim6890]

Calcium is required for cardiac muscle contraction but I don't know about the pacemaker cells. I think those are independent of calcium but I'm not sure. For potassium, maybe the book is referencing the end of repolarization prior to beginning of a new action potential.

 

[Leonardo Noto]

My BR book says "as the cardiac action potential begins, the permeability of potassium decreases as potassium channels close" and the potassium channel returns to their original state with repolarization.

I am confused because this is different from a neuronal action potential when the voltage gated K+ channels are late to open. What kind of channels are they talking about here, voltage gated or leaky?

Also, calcium is not involved in action potentials of pacemaker cells right?

Thank you

Okay, a few things.

1. The reason that the permeability of potassium decreases during the cardiac muscle action potential (unlike in skeletal muscle) is because it helps to prolong the depolarization of the cardiac muscle. This is important because heart muscle that repolarizes too quickly is at risk of becoming a foci for an arrhythmia, not something that the body is concerned about in skeletal muscle. You'll learn about it in med school, but this is one of the reasons why hyperkalemia--an excess of potassium in the blood--can cause heart arrhythmias (KCl is used in lethal injection executions, FYI). I'm not sure of the exact physiological explanation for the decrease in potassium permeability--my copy of Guyton's Textbook of Medical Physiology says that the mechanism has yet to be determined, but my edition is about 10 years old so maybe someone has figured it out by now. A little off topic, but just so you know, the best medical physiology textbook for medical school (but not for the MCAT!) is Guyton's and the review book that most people prefer is Lippincott's BRS Physiology.

2. It's easy to get this stuff confused because the action potentials in neurons, skeletal muscle, smooth muscle, cardiac muscle, and the pacemaker cells of the heart are all different--some are slightly different and some are quite a bit different from the generic neuronal action potential that we all learned in Introduction to Biology. To answer your second question, no, calcium IS involved in the action of the cardiac pacemaker cells. Slow leakage of sodium into the cells raises the resting potential in the SA (sinoatrial) node from -55mV to -40mV. At -40mV Ca-Na channels open and cause the action potential (both Ca and Na enter the cells moving down both their charge and concentration gradients) in the SA node that initiates a heart beat. Listed below is a good website that shows the depolarization cascade of the SA Node.

http://www.cvphysiology.com/Arrhythmias/A004.htm

This stuff is awfully complicated and the easiest way to remember it is to draw out some simplified diagrams and just try to remember the high points, not the minutiae.

Dr. Leonardo Noto
www.leonardonoto.com or follow me on Twitter @DrLeonardoNoto

 

[yellowjellybean]

Thank you so much for the clear explanation. Very interesting about the hyperkalemia/arrhythmia, can hypokalemia cause arrhythmia too? So is it the permeability of the leaky potassium channels that decrease during the cardiac AP? And do the voltage gated K+ channels delay in opening like in a neuronal AP?

Also I don't understand why skeletal/smooth muscle action potential isn't prolonged. There is still an influx of Ca2+, is just because there is no decrease in the permeability of potassium.

 

[Leonardo Noto]

Thank you so much for the clear explanation. Very interesting about the hyperkalemia/arrhythmia, can hypokalemia cause arrhythmia too? So is it the permeability of the leaky potassium channels that decrease during the cardiac AP? And do the voltage gated K+ channels delay in opening like in a neuronal AP?

Also I don't understand why skeletal/smooth muscle action potential isn't prolonged. There is still an influx of Ca2+, is just because there is no decrease in the permeability of potassium.

I'm going to hit these questions in a different order than you asked them, hope that's okay.

1) Hypokalemia--Hypokalemia can cause arrhythmias and screwy function of both skeletal and smooth muscle throughout the body, but it is usually more of a subacute problem, the "lets fix this in 24-48 hours" kind of thing versus the "holy crap!!!" medical emergency that severe hyperkalemia is. This is medical school knowledge though and I doubt that it will be useful for the MCAT.

2) The calcium that is important in skeletal muscle contraction doesn't ENTER the cell, it is already in the cell in the sarcoplasmic reticulum. Na entrance through acetylcholine-gated Na-channels depolarizes the cell, and b/c skeletal muscle cells are huge, this depolarization is carried into the interior of the myocyte (muscle cell) by T-tubules (special "electricity" channels)-->leading to release of calcium from the sarcoplasmic reticulum that activates the contractile units of the muscle cell (actin/myosin and friends). Knowing the Sliding Filament Model of muscle contraction is high yield for the MCAT and you should review it.

3) To the extent of my knowledge, slow voltage-gated potassium channels are involved in repolarizing skeletal muscle cells via the same mechanism that you learned in the generic "action potential" series in Introduction to Biology. Here is a website with a good diagram/explanation: http://www.getbodysmart.com/ap/muscletissue/contraction/actionpotentials/tutorial.html. Cardiac muscle is different because the potassium permeability is particularly delayed--this is because it is dangerous for cardiac muscle to repolarize too quickly d/t the threat of arrhythmias.

4) Here's a great website that compares cardiac and skeletal muscle action potentials (scroll down to the second page/slide #12). http://facstaff.unca.edu/cnicolay/BIO338/338-22-heart-AP.pdf

Dr. Leonardo Noto
www.leoanrdonoto.com or follow me on Twitter @DrLeonardoNoto