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Extracellular Potassium Homeostasis: Insights from Hypokalemic Periodic Paralysis
Journal article   Peer reviewed

Extracellular Potassium Homeostasis: Insights from Hypokalemic Periodic Paralysis

Chih-Jen Cheng, Elizabeth Kuo and Chou-Long Huang
Seminars in nephrology, Vol.33(3), pp.237-247
05/2013
DOI: 10.1016/j.semnephrol.2013.04.004
PMCID: PMC4131448
PMID: 23953801
url
http://doi.org/10.1016/j.semnephrol.2013.04.004View
Open Access

Abstract

The extracellular potassium makes up only about 2% of the total body potassium store. The majority of the body potassium is distributed in the intracellular space, and of which about 80% is in skeletal muscle. Movement of potassium in and out of skeletal muscle thus plays a pivotal role in extracellular potassium homeostasis. The exchange of potassium between the extracellular space and skeletal muscle is mediated by specific membrane transporters. These include potassium uptake by Na + , K + -ATPase and release by inward rectifier K + channels. These processes are regulated by circulating hormones, peptides, ions, and by physical activity of muscle as well as dietary potassium intake. Pharmaceutical agents, poisons and disease conditions also affect the exchange and alter extracellular potassium concentration. Here, we review extracellular potassium homeostasis focusing on factors and conditions that influence the balance of potassium movement in skeletal muscle. Recent findings that mutations of a skeletal muscle-specific inward rectifier K + channel cause hypokalemic periodic paralysis provide interesting insights into the role of skeletal muscle in extracellular potassium homeostasis. These recent findings will be reviewed.
Hypokalemia-induced paradoxical depolarization Hypokalemic periodic paralysis Na+, K+-ATPase Inward rectifier K+ channel Kir Skeletal muscle Thyrotoxic periodic paralysis

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