Potassium concentration and action potentials Watch

Lucofthewoods
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When the concentration of concentration is too low or high, why do action potentials stop firing?
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ThatGuy107
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Concentration of concentration? Do you mean on potassium?
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Lucofthewoods
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Oops yeah sorry typo
(Original post by ThatGuy107)
Concentration of concentration? Do you mean on potassium?
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ThatGuy107
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Potassium ions are involved in the re-establishing the resting potential, so no potassium ions = no resting potential so an action potential cannot be generated.
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bobby147
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(Original post by Lucofthewoods)
When the concentration of concentration is too low or high, why do action potentials stop firing?
They don’t stop firing ,who told you that ?

High potassium levels reduces the resting membrane potential of the myocyte by making it more positive.The number of voltage gated sodium channels opened depends on the membrane potential,so a lower membrane potential means less sodium influx during depolarisations.Repolarisation phase increases as more reflux potassium channels opens ,stimulated by high extracellular potassium levels.

For low potassium levels,Sodium potassium pump works less well,so so sodium and calcium levels build inside the cell, leading to depolarisation for a long time.Since potassium levels determine resting potential and it’s so low,resting potential is more positive,so it gets depolarised more easily since the threshold is longer and when it does ,it lasts long and can be self sustaining.

Basically both situations can lead to arrthymias ,where the cardiac action potential is disturbed and so no longer normal.
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Jpw1097
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(Original post by bobby147)
They don’t stop firing ,who told you that ?

High potassium levels reduces the resting membrane potential of the myocyte by making it more positive.The number of voltage gated sodium channels opened depends on the membrane potential,so a lower membrane potential means less sodium influx during depolarisations.Repolarisation phase increases as more reflux potassium channels opens ,stimulated by high extracellular potassium levels.

For low potassium levels,Sodium potassium pump works less well,so so sodium and calcium levels build inside the cell, leading to depolarisation for a long time.Since potassium levels determine resting potential and it’s so low,resting potential is more positive,so it gets depolarised more easily since the threshold is longer and when it does ,it lasts long and can be self sustaining.

Basically both situations can lead to arrthymias ,where the cardiac action potential is disturbed and so no longer normal.
Exactly. Hyperkalaemia (high potassium levels) increases the resting membrane potential (it becomes less negative) as they reduce the efflux of potassium ions out of the cell (by reducing the potassium gradient across the cell membrane). You may think that depolarising the cell increases the likelihood of an action potential firing, and it does up to a certain point, but as the resting membrane potential increases, this actually inactivates voltage-gated sodium channels as these channels need the cell membrane to repolarise to become reactivated. Therefore fewer activated sodium channels = higher threshold potential (i.e. the membrane potential at which an action potential can be fired).

Hypokalaemia (low potassium levels) causes the resting membrane potential to become more negative. This is because more potassium ions leave the cell as there is a greater gradient across the cell membrane as the concentration of potassium outside the cell is lower. This essentially hyperpolarises the cell, making an action potential less likely to fire as the resting membrane potential is further away from the threshold potential - so a much bigger stimulus is needed to reach the threshold potential (similar to the relative refractory period).
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