I have read in many sources that ischemia-induced depolarization is due to the opening of ATP-sensitive potassium channels and inactivation of Na/K exchangers [1,2]. However, K-atp channels are inward-rectifiers and their extensive opening should cause extracellular hypokalemia besides the fact that in low [ATP]i during ischemia, Mg++ ions are free (not complexed with ATP), and magnesium ions are outward potassium current blockers (i,e, they increase the rectifying power of k-atp, Kir, K-Ach channels)[3,4]. this would cause extracellular hypokalemic depolarization. What is the source of hyperkalemia then?


1 Answer 1


Inward-rectifying means positive current passes more easily in the inward direction, however it won't flow differently than the membrane voltage and reversal potential dictate. See for example https://en.m.wikipedia.org/wiki/Inward-rectifier_potassium_channel

The only time you'll have potassium flowing in to a cell, rather than out, is if the cell is very hyperpolarized, beyond the reversal potential for potassium, which is more negative than the resting potential.

Open potassium channels will almost always reduce intracellular potassium concentration as potassium flows out of the cell. Without ATP to fuel the sodium-potassium pump, there's no way to restore the lost potassium.

The existence of a negative resting membrane potential is due to relative concentrations of potassium (high inside cells) and the existence of primarily potassium conductance in the membrane, which means a few positive ions leak out to make the inside negative. If you don't maintain that concentration gradient, the cell is going to depolarize.

  • $\begingroup$ I'd also suggest an honorable mention of the chloride anions that stayed within the membrane in the last graph. $\endgroup$
    – X Zhang
    Commented Jun 9, 2022 at 7:19
  • $\begingroup$ i will try to explain what i understood. So, when the K+ channels open during repolarization the permeability is so high that according to goldmann's equation the resting membrane potential (RMP) is closer to K+ reversal potential(hyperpolarization) But as repolarization ends the fast and slow rectifyer channels close so the RMP shifts to a more positive voltage and then K-leak channels and K1 (inward rectifyer) channels open and since they are not as abunduntly opened as the channels during repolarization......... $\endgroup$
    – kljiuklk 1
    Commented Jun 9, 2022 at 11:38
  • $\begingroup$ ..... the RMP is still more positive than it was at end of repolarization. this causes the correction of RMP to the pre-depolarization state. So the main function of K1 is to allow rapid influx of k+ ions to correct hyperpolarization as fast as possible and thne k+ leak channels maintain their efflux. Am I right? $\endgroup$
    – kljiuklk 1
    Commented Jun 9, 2022 at 11:40
  • $\begingroup$ @kljiuklk1 Unless the membrane voltage is more negative than the potassium reversal potential (which can never happen by potassium flowing alone, no matter what channels are open), potassium net flow is always out of the cell. There's no "rapid influx of potassium ions". Leak channels are always open. Recovery from hyperpolarization happens because other ions (mostly sodium) are leaking in faster than potassium is leaking out. $\endgroup$
    – Bryan Krause
    Commented Jun 9, 2022 at 16:42
  • $\begingroup$ @BryanKrause, but if that is the case then why the correction of hyperpolarization is attributed to K1 channels. And why would there be an inward rectifyer if potassium is always flowing out even at hyperpolarized state? $\endgroup$
    – kljiuklk 1
    Commented Jun 10, 2022 at 19:39

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