Question

(Select all correct answers; one or more than one answer may be correct.) In cases of renal failure, plasma (extracellular) concentrations of K⁺ may increase from normal levels of 4-5 mM to 10 to 12 mM. From what you know of the effects of increasing extracellular K⁺ on the membrane potential (E_K = RT/zF x ln[K_o/K_i) and the effects of membrane potential on the HCN channel (hint, remember what H stands for), you would expect the increased extracellular concentration of K⁺ to:

Group of answer choices:

decrease the rate of rise of the ramp potential for the pacemaker action potential.

decrease cardiac output.

hyperpolarize the membrane potential.

increase the rate of rise of the ramp potential for the pacemaker action potential.

decrease heart rate.

depolarize the resting membrane potential in the pacemaker cells.

Answer 1

Answer: The correct statements are: decrease the rate of rise of the ramp potential for the pacemaker action potential, decrease cardiac output, hyperpolarize the membrane potential, decrease heart rate and depolarize the resting membrane potential in the pacemaker cells.

In case of renal failure, the extracellular concentration of K⁺ increases about three times from normal levels of 4-5 mM to 10-12 mM. This increase in extracellular concentration of K⁺ ions will depolarize the resting membrane potential (decrease the membrane potential) in the pacemaker cells This is because the increase in K⁺ concentration will reduce the equilibrium potential for potassium and this will mean that less potassium will diffuse out of the cell, leaving the interior more positive. There will be a decrease in the rate of rise of the ramp potential for the pacemaker action potential, thus it will reduce the strength of conduction. The high concentration of K⁺ ions in plasma will decrease heart rate which in turn will decrease the cardiac output. As cardiac output is the product of heart beat and stroke volume, so decrease in the heart rate will automatically decrease the cardiac output. HCN channels are activated by membrane hyperpolarization which mediates the influx of Na⁺ or K⁺ non-selectively.