From my understanding of myocardial ischemic contractile failure, ischemia causes increased extracellular K+ concentration due to the ATP-sensitive K+ channels opening (as they need ATP to stay closed). It is evident during ischemia, that the lack of oxygen inhibits the ability of the myocardial cell to generate ATP.

So, if K+ is leaving the cell and going into the ECF, shouldn't the resting membrane potential of the cells become more negative instead of positive (a positive ion going into ECF makes the electrical gradient larger, thus more negative) ? However myocardial ischemic contractile failure supposedly causes the RMP to become less negative due to the lowering of the potassium equilibrium potential.

Can someone explain to me how and why the potassium equilibrium potential is lowered and the reason why the RMP is becoming less negative please?



1 Answer 1


Your understanding about the mechanism by which the K+ ions leak out of the cardiac cell during ischaemia is correct.

But, regarding the latter part, lets discuss what is the situation of K+ ions in a normal cardiac cell.

In a normal cardiac cell, the concentration of K+ ions is more inside compared to the outside of the cell (150mM inside as compared to 4mM outside) and this gradient produces a potential of -96mV (equilibrium potential of K+ ions) across the membrane according to the Nernst equation. This means that there is no net movement of K+ ions across the membrane at this potential.

Now, in a normal cell other ions (Na+, Ca2+, Cl-) also play a role in the generation of a resting membrane potential but their contribution is on the lower side.

Now, if the K+ ions move out of the normal cell, the gradient will decrease and thus the equilibrium potential will also be reduced(becoming less negative or depolarised) and that is why if K+ ions leak out of the cell, the membrane potential becomes less negative.

In case of cardiac ischaemia, the lack of ATP inactivates the Na+ - K+ ATPase transporter which in a normal cell would repolarize the cell and re-establish the resting membrane potential.

For reference:- https://journals.physiology.org/doi/full/10.1152/advan.00105.2016

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