Inward Rectifying Potassium Current

http://tmedweb.tulane.edu/pharmwiki/doku.php/introduction_to_cardiac_physiology_
electrophysiology

The inward potassium rectifying current (Ik) is what distinguishes a cardiac muscle cell from other muscle cells and nerve cells.  It causes a delay in the refractory period which allows for the crucial entry of calcium during the plateau phase of the action potential.

How does it work?

Ionic basis for the resting and action potential in a ventricular heart cell. The action potential is divided into phases 0 through 4. Each phase results from a change in the balance of inward and outward ionic currents that become activated upon membrane depolarization. The primary currents underlying each phase are: phase 0: Na current (I_Na); phase 1: transient outward K current (I_to); phase 2: L-type Ca current(I_Ca); phase 3: delayed rectifier K currents (I_Kr & I_Ks); phase 4: inwardly rectifying K current (I_K1). The change in dominant conductance during each phase produce either net depolarization or hyperpolarization, and give the action potential its characteristic shape.

Mechanism for inward rectification. When the voltage across the cell membrane becomes positive to E_K there is a driving force for K ions to leave the cell & create an outward current. However, as K ions leave the cell, Mg²⁺ ions and/or other impermeant substances in the cytoplasm get swept into the channel opening and block the efflux of ions from the cell (top left). This phenomenon produces a sharp bend in the current-voltage relationship (right panel), which would otherwise be linear and follow Ohm’s law: IK = ΔV/R (where ΔV = V_m – E_K). The linear slope predicted for a “non-rectifying” IV relationship is indicated by the dashed line, and reflects a constant voltage-independent channel conductance. In the absence of rectification (dashed line), there would be a huge outward K current generated at positive voltages, producing a very short APD, and this would not allow time for Ca influx, which is necessary for excitation-contraction coupling to occur in cardiac muscle.

Effect of hyperkalemia