Differences in Kir currents that underlie differences in K ⁺ handling between WT and periodic paralysis muscle. Shown are the Kir IV relationships at baseline and 10 min after lowering K_ex. At baseline E_K of WT was −88.0 mV and Vm was −86.8 mV such that net outward Kir current was small (black dot). 10 min after removing 3 mmol of extracellular K⁺, K_ex was 1.4 mM, such that E_K had hyperpolarized to −106.3 mV while Vm had only hyperpolarized to −90.1 mV because of the large Cl⁻ conductance. The moderately larger difference between E_K and Vm resulted in increased net outward Kir current (red dot) despite the reduction in maximal outward Kir current. HyperKPP muscle behaved identically to WT muscle when K_ex was lowered and Kir currents are identical to WT (not shown). In hypoKPP baseline, Vm was −79.3 mV, and there was a large outward Kir current (black dot). 10 min after removing 3 mmol of extracellular K⁺, K_ex was 0.3 mM such that E_K was −150.9 mV. Vm was depolarized to −70.7 mV due to the almost complete closure of Kir channels since Vm had become extremely depolarized relative to E_K. The closure of Kir channels resulted in almost no outward Kir current (red dot). In Andersen–Tawil syndrome baseline Vm was −84.2 mV with a small outward Kir current (black dot). 10 min after removal of 3 mmol of  extracellular K⁺, K_ex was 0.6 mM, E_K was −136.1 mV, Vm was −82.0 mV, and Kir channels had closed such that outward Kir current was almost 0 (red dot).