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Provides a mechanistic explanation for how hypokalemia increases arrhythmia risk through altered ion selectivity of K2P1 channels.
New evidence reveals that the common electrolyte disorder hypokalemia can induce K2P1 channels that are normally selective for K+ to break the rules and conduct Na+. This defiant behavior leads to paradoxical depolarization of many cells in the heart, increasing the risk for lethal arrhythmia. The new research resolves a mystery uncovered 50 years ago and bestows an array of new riddles. Here, I discuss how K2P1 might achieve this alchemy--through stable residence of the K+ selectivity filter in a Na+-conductive state between its open and C-inactive configurations--and predict that other K+ channels and environmental stimuli will be discovered to produce the same excitatory misconduct.
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Steven A. Goldstein (2011) studied this question.
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