physio question

[samtheman]

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High extracellular K concentrations depolarize the cell and inactivate the k channel by closing the inactivation h gate making the cell less excitable. Why doesn't this happen with a normal AP? I know that it has to do with a prolonging of the h gates being closed but I don't see why it is any different than a normal depolarization. Explanations please.

 

[engineeredout]

Depolarizing a cell causes the inactivation gates to close and go refractory, but at the same time depolarizing keeps the channels from returning to the resting state, so since there are fewer sodium channels in the resting state the cell is less excitable.

 

[samtheman]

Depolarizing a cell causes the inactivation gates to close and go refractory, but at the same time depolarizing keeps the channels from returning to the resting state, so since there are fewer sodium channels in the resting state the cell is less excitable.

Why doesn't this same scenerio play out with a normal AP when the cell initially gets depolarized to threshold. What is different in this case?

Thanks

 

[Igor4sugry]

You are thinking on the right track.

When an AP occurs and the cell depolarizes (say from -60 to +20) the sodium channels become inactive until the cell repolarizes once again (refractory period). During the refractory period an AP will not be conducted. So with an AP the Na channels do stay inactive, but only until repolarization occurs (which is fast)

With high levels of pottasium (a positive ion); the charge of the membrane is closer to zero (say instead of -60 its now -10). Once this occurs there are also Na channels that stay refractory (just like in the AP event). The only difference here is that the cell stays depolarized like this until K levels are corrected.

The main effect with high K levels is conduction problems (which is terrible for the heart conduction system). The slowing of conduction will show up on the EKG as a wide QT interval.

 

[greatnt249]

Why doesn't this same scenerio play out with a normal AP when the cell initially gets depolarized to threshold. What is different in this case?

Thanks

The high EC concentration of K+ makes the resting membrane potential of the cell more positive than what is physiologically normal, which depolarizes the cell and inactivates the Na+ channels. Unlike an AP, hyperkalemia doesn't cause a transitory depolarization; it's permanent until you can rid of the excess K+.

 

[samtheman]

Thanks guys.

 

[Dirt]

The simple answer is that the concentration gradient that normally leads to K+ efflux is decreased (Normally a lot of K+ intracellularly, a little extracellulary), therefore you get prolonged depolarization. It has nothing to do with inactivation gates.

 

[Sol Rosenberg]

The simple answer is that the concentration gradient that normally leads to K+ efflux is decreased (Normally a lot of K+ intracellularly, a little extracellulary), therefore you get prolonged depolarization. It has nothing to do with inactivation gates.

Incorrect. The correct answer was already given in posts 4 and 5.

 

[engineeredout]

The simple answer is that the concentration gradient that normally leads to K+ efflux is decreased (Normally a lot of K+ intracellularly, a little extracellulary), therefore you get prolonged depolarization. It has nothing to do with inactivation gates.