Concept of "excitability"

[capostat]

Question from EK:

Cardiac muscle is excited by:

A. Parasympathetic nervous excitation
B. Constriction of T-tubules
C. Increased cytosolic sodium concentration
D. Increased cytosolic calcium concentration

The answer is D, but contractility isn't excitablity, or is it? If the answer choice for C, was "extracellular sodium concentration", that would be correct, right?

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[matth87]

Question from EK:

Cardiac muscle is excited by:

A. Parasympathetic nervous excitation
B. Constriction of T-tubules
C. Increased cytosolic sodium concentration
D. Increased cytosolic calcium concentration

The answer is D, but contractility isn't excitablity, or is it? If the answer choice for C, was "extracellular sodium concentration", that would be correct, right?

I picked D but I think C would be right as well, the unstable RMB in the SA node is due to a slow influx of Na+. This slow influx reaches threshold and then Ca+ Channels open to allow Ca+ in.

If muscle gets excited it contracts, so they are basically the same.

 

[capostat]

I picked D but I think C would be right as well, the unstable RMB in the SA node is due to a slow influx of Na+. This slow influx reaches threshold and then Ca+ Channels open to allow Ca+ in.

If muscle gets excited it contracts, so they are basically the same.

ok, i thought since excitability is a feature of neuronal cells, that only cells that can have action potentials are considered excitable. Like in the heart--those purkinje fibers and the bundle of His are cells that dont contract, but do pass action potentials.

 

[Charles_Carmichael]

ok, i thought since excitability is a feature of neuronal cells, that only cells that can have action potentials are considered excitable. Like in the heart--those purkinje fibers and the bundle of His are cells that dont contract, but do pass action potentials.

All cardiac cells are excitable, not just the conducting cells. Ventricular and atrial myocytes also have distinct action potentials associated with them (these are different from the action potentials of the conducting cells).

Cardiomyocytes have a plateau phase during their action potential that is due to an influx of calcium. Calcium is important in both the excitability and contraction of these cells. Excitation-contraction coupling in these cells translates the action potential into contraction.

During the plateau phase, calcium enters the cell but this amount of calcium is not enough to initiate contraction on its own. What it does though is that it triggers the release of more calcium from the sarcoplasmic reticulum; this process is called calcium-induced calcium release. It is this extra calcium that binds to troponin C and leads to contraction. The amount of tension developed is proportional to the intracellular calcium concentration. If there's more calcium intracellularly, more calcium is stored and more calcium is released when induced by the influx of calcium during the action potential; this leads to a stronger contraction.

So, calcium is important in both the action potential (excitation) and contraction of cardiac muscle cells. Hope this helps.

 

[capostat]

All cardiac cells are excitable, not just the conducting cells. Ventricular and atrial myocytes also have distinct action potentials associated with them (these are different from the action potentials of the conducting cells).

Cardiomyocytes have a plateau phase during their action potential that is due to an influx of calcium. Calcium is important in both the excitability and contraction of these cells. Excitation-contraction coupling in these cells translates the action potential into contraction.

During the plateau phase, calcium enters the cell but this amount of calcium is not enough to initiate contraction on its own. What it does though is that it triggers the release of more calcium from the sarcoplasmic reticulum; this process is called calcium-induced calcium release. It is this extra calcium that binds to troponin C and leads to contraction.

So, calcium is important in both the action potential (excitation) and contraction of cardiac muscle cells. Hope this helps.

yep... will note.

 

[Dr Gerrard]

Why is A not correct? Is it because the heart has the pacemaker and does not require nervous system stimulation?

I never understood what a T-tubule was either.

Also, is C wrong? I thought C would be correct, because it is the influx of Na ions that starts the action potential.

Then the calcium just comes in to maintain the potential, right??

 

[capn jazz]

Why is A not correct? Is it because the heart has the pacemaker and does not require nervous system stimulation?

I never understood what a T-tubule was either.

Also, is C wrong? I thought C would be correct, because it is the influx of Na ions that starts the action potential.

Then the calcium just comes in to maintain the potential, right??

The sympathetic NS excites cardiac muscle. The parasympathetic NS lowers the HR.

 

[Charles_Carmichael]

Why is A not correct? Is it because the heart has the pacemaker and does not require nervous system stimulation?

I never understood what a T-tubule was either.

Also, is C wrong? I thought C would be correct, because it is the influx of Na ions that starts the action potential.

Then the calcium just comes in to maintain the potential, right??

The SA node is actually constantly under parasympathetic stimulation. If it weren't the HR would be much faster.

Parasympathetic stimulation decreases heart rate by decreasing the rate of phase 4 depolarization (the unstable resting membrane potential) in the SA node. Parasympathetic stimulation has a negative effect on heart rate, conduction velocity, and force of contraction (negative chronotropic, negative dromotropic, and negative inotropic effects respectively if you're interested). The decrease in contractility is in the atria only though, since the ventricles are not really innervated with parasympathetic fibers. Overall, parasympathetic stimulation decreases excitability in the heart. Hope this helps.

 

[capostat]

Why is A not correct? Is it because the heart has the pacemaker and does not require nervous system stimulation?

I never understood what a T-tubule was either.

Also, is C wrong? I thought C would be correct, because it is the influx of Na ions that starts the action potential.

Then the calcium just comes in to maintain the potential, right??

The key word is "cytosolic". I got this one wrong too.

 

[Dr Gerrard]

Ahh, I get it. So if A said "Sympathetic nervous system" it would be correct, yeah?

What exactly is the "pacemaker" function for then?

Also, back to the other two questions, what are T-tubules? From my understanding, this is just the area between the sarcoplasmic reticulum, where the calcium ions are released. What is its significance though?

Also, why would C be wrong? I thought Ca ions just maintain the plateau.

EDIT: Capostat, I just saw your response. Isn't cytosolic correct though? Lots of sodium ions come into the cytosol to start the potential, correct? Or am I reading the question wrong here. Would cytosolic only be high AFTER the muscle is excited? That is, extracellular sodium would be high before and would lead to excitability?

Thanks for your help!

I am really sorry though, I never learned any physiology in my bio classes, so I have had to learn all of it this summer.

 

[G1SG2]

Ahh, I get it. So if A said "Sympathetic nervous system" it would be correct, yeah?

What exactly is the "pacemaker" function for then?

Also, back to the other two questions, what are T-tubules? From my understanding, this is just the area between the sarcoplasmic reticulum, where the calcium ions are released. What is its significance though?

Also, why would C be wrong? I thought Ca ions just maintain the plateau.

EDIT: Capostat, I just saw your response. Isn't cytosolic correct though? Lots of sodium ions come into the cytosol to start the potential, correct? Or am I reading the question wrong here. Would cytosolic only be high AFTER the muscle is excited? That is, extracellular sodium would be high before and would lead to excitability?

Thanks for your help!

I am really sorry though, I never learned any physiology in my bio classes, so I have had to learn all of it this summer.

T-tubules maximize the entry of calcium ions in the cell. The action potentials propagate down the T tubules and allow calcium to enter from the extracellular environment and also induce calcium release from the sarcoplasmic reticulum. I believe T-tubules allow the action potential to affect the entire cell, which may be too big/thick. The smooth muscle cell doesn't have T-tubules because it is relatively smaller. So, a depolarization on the surface of the smooth muscle cell can depolarize the entire cell and T-tubules are not needed.

 

[Charles_Carmichael]

Why is A not correct? Is it because the heart has the pacemaker and does not require nervous system stimulation?

I never understood what a T-tubule was either.

Also, is C wrong? I thought C would be correct, because it is the influx of Na ions that starts the action potential.

Then the calcium just comes in to maintain the potential, right??

Okay, I thought about this for a sec and here's my view on this:

If there's an increase in cytosolic Na+, the Na+ influx wouldn't be as great compared to normal. This should make the slope of the upstroke less steep.

Conduction velocity depends on the size of the inward current during the upstroke (either Na+ in atrial, ventricular, and Purkinje cells or Ca++ in the SA node). With an increased intracellular concentration of Na+, the influx of Na+ is less than normal (because of changes in the electrochemical gradient calculated using the Nernst equation). This means that there's a decrease in conduction velocity from one cardiomyocyte to an adjacent one. In the macroscopic view, this would mean that the heart would contract more slowly because the action potential is not spreading through the muscle as fast as it normally would.

On the other hand, an increase in cytosolic Ca++ would mean that there's an increase in the Ca++ stores in the sarcoplasmic reticulum. When Ca++ rushes in either in the upstroke of the SA node action potential or the plateau phase of the myocyte action potential, it would cause a greater release of Ca++ from the SR stores, which would be seen as an increase in the size of the inward current (note that as the levels of intracellular Ca++ increase, more and more Ca++ is stored and thus, more and more Ca++ is released from the SR during subsequent action potentials); this would cause an increase in conduction velocity and in the macroscopic view, would increase the rate of contractility of cardiac muscle. The action potential in spread throughout the cardiac muscle faster. Ca++ influx is very important in conduction velocity and the autonomic nervous system regulates conduction velocity by affecting Ca++ conductance into the cell (which increases or decreases intracellular Ca++) and K+ conductance out of the cell (in the case of parasympathetic stimulation). Hope this helps.

 

[Charles_Carmichael]

Ahh, I get it. So if A said "Sympathetic nervous system" it would be correct, yeah?

What exactly is the "pacemaker" function for then?

Also, back to the other two questions, what are T-tubules? From my understanding, this is just the area between the sarcoplasmic reticulum, where the calcium ions are released. What is its significance though?

Also, why would C be wrong? I thought Ca ions just maintain the plateau.

EDIT: Capostat, I just saw your response. Isn't cytosolic correct though? Lots of sodium ions come into the cytosol to start the potential, correct? Or am I reading the question wrong here. Would cytosolic only be high AFTER the muscle is excited? That is, extracellular sodium would be high before and would lead to excitability?

Thanks for your help!

I am really sorry though, I never learned any physiology in my bio classes, so I have had to learn all of it this summer.

The pacemaker function is there so that the beating of the heart is not dependent on external stimulation. If you cut off the nerve supply to the heart, it should still be pumping blood.

Ca++ is very important in both the electrophysiology and contractility of cardiac cells. The upstroke of the SA node action potential (which generates the heart rate) is dependent on Ca++ influx, not Na+. And the Ca++ influx during the plateau phase of the myocytes couples the action potential to contraction; it's a link between excitability and contractility.

And if A said "Sympathetic stimulation" there would be two answers that would be correct (A and D) because A increases Ca++ influx and thus, increases the intracellular Ca++ levels (more Ca++ is stored in the SR).

 

[capostat]

Ahh, I get it. So if A said "Sympathetic nervous system" it would be correct, yeah?

What exactly is the "pacemaker" function for then?

Also, back to the other two questions, what are T-tubules? From my understanding, this is just the area between the sarcoplasmic reticulum, where the calcium ions are released. What is its significance though?

Also, why would C be wrong? I thought Ca ions just maintain the plateau.

EDIT: Capostat, I just saw your response. Isn't cytosolic correct though? Lots of sodium ions come into the cytosol to start the potential, correct? Or am I reading the question wrong here. Would cytosolic only be high AFTER the muscle is excited? That is, extracellular sodium would be high before and would lead to excitability?

Thanks for your help!

I am really sorry though, I never learned any physiology in my bio classes, so I have had to learn all of it this summer.

I didnt really give it much thought, i guess. Na+ IS ultimately high inside the cell during a depolarization. I'm not so sure that a high extracellular concentration would cause cardiac excitability. But reading Kaushik's response, made sense--it's about the inward flux. and maybe there has to be a propagation that is linked with that high sodium. so you cant just have high sodium inside the cell and expect excitability. Calcium probably works that way, but not sodium. maybe?

 

[Charles_Carmichael]

I didnt really give it much thought, i guess. Na+ IS ultimately high inside the cell during a depolarization. I'm not so sure that a high extracellular concentration would cause cardiac excitability. But reading Kaushik's response, made sense--it's about the inward flux. and maybe there has to be a propagation that is linked with that high sodium. so you cant just have high sodium inside the cell and expect excitability. Calcium probably works that way, but not sodium. maybe?

The inward flux of Ca++ (ie. the slope of the inward Ca++ current, dV/dt) shouldn't really be affected by increased intracellular Ca++ because the Ca++ is, for the most part, taken up by the SR and stored in there until the next action potential induces the release of Ca++ from these stores to initiate contraction.

Na+, on the other hand, is not removed from the cytosol by the SR or anything like that. So it should affect the dV/dt of the inward Na+ current (which would affect the size of the inward current).

At least, this is what makes sense to me. Hope this helps.

 

[capn jazz]

If there's a high intracellular Ca2+ concentration, wouldn't LESS Ca2+ flow out of the SR down the concentration gradient?

 

[Charles_Carmichael]

If there's a high intracellular Ca2+ concentration, wouldn't LESS Ca2+ flow out of the SR down the concentration gradient?

The Ca++ is uptaken by the SR. For example, in the presence of sympathetic stimulation, Ca++ conductance increases. This brings more Ca++ into the cell but during this first action potential, the contractility does not increase. The Ca++ is taken up into the SR and upon the subsequent action potential, more Ca++ is released and a stronger contraction results (this is known as the positive staircase effect).

So, with an increase in intracellular Ca++, there's an increase in SR Ca++ as the SR takes up the Ca++ from the cytosol. As more and more Ca++ enters the cell (for example, with sympathetic stimulation, which increases Ca++ conductance), more and more Ca++ is taken up by the SR until a maximal value is reached.

Ca++ is actively taken up by the SR via a Ca++ ATPase, so it's being taken up into the SR against its gradient.

Edit: How I'm explaining is what makes sense to me. Since Ca++ is actively pumped OUT of the cytosol into the SR, a higher intracellular concentration of Ca++ wouldn't affect the outflow of Ca++ from the SR (because the majority of Ca++ is stored in the SR, not the cytosol). If you see something wrong with my reasoning, point it out. I love CV physio!