Periodic paralysis and the sodium-potassium pump.
Analysis of the pathophysiology of hypokalemic paralysis, as it occurs in barium poisoning, chronic potassium deficiency, and thyrotoxicosis, suggests that these disorders may have a similar mechanism. An increased ratio of muscle sodium permeability to potassium permeability reduces the ionic diffusion potential, while the resting membrane potential is sustained by an increase of Na-K pump electrogenesis. The result is that potassium entry (the sum of active and passive influx) exceeds potassium efflux; this causes a large shift of extracellular potassium into muscle until the Na-K pump turns off, leading to depolarization and paralysis. The primary defect in familial hypokalemic periodic paralysis, as in the example of barium poisoning, may be a marked reduction of muscle permeability to potassium.
D000818:Animals; D001001:Anura; D001464:Barium / Q000506:poisoning; D002908:Chronic Disease; D004285:Dogs; D006801:Humans; D006980:Hyperthyroidism / Q000150:complications; D007473:Ion Channels / Q000502:physiology*; D010243:Paralysis / Q000139:chemically induced / Q000209:etiology / Q000235:genetics / Q000503:physiopathology*; D010507:Periodicity; D011191:Potassium Deficiency / Q000150:complications; D051381:Rats
D007473:Ion Channels; D001464:Barium