Extracellular Potassium Homeostasis: Insights from Hypokalemic Periodic Paralysis
Open accessAbstract
Extracellular potassium makes up only about 2% of the total body's potassium store. The majority of the body potassium is distributed in the intracellular space, 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(+)-adenosine triphosphatase 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 are reviewed.
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An increase in aldosterone concentration leads to a modest increase in Na+-K+-ATPase abundance, which increases K+ flux into cells.
“An increase in ALD concentration leads to a modest increase in Na+-K+-ATPase abundance, which increases K+ flux into cells [30–32].”
From A mathematical model of potassium homeostasis: Effect of feedforward and feedback controls (2022) · cites this paper as [30]
The Regulation of Abundance section reports relatively modest effects of aldosterone on skeletal-muscle Na⁺-K⁺-ATPase and higher pump-subunit abundance correlated with aldosterone levels in patients with hyperaldosteronism. It also reports that aldosterone treatment decreased pump abundance in animals, so the claim is too general. The same section says pump upregulation enhances muscle potassium uptake. (LLM, conf=0.86)
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“5 L [20] Vinterstitial interstitial fluid volume 10 L [20] Vmax maximum K + flow into cells 130 mEq/min [21] Km half maximal activation 1.”
BackgroundPathophysiologic approach in genetic hypokalemia: An update
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- Authors
- Cheng, C.-J., Kuo, E., & Huang, C.-L.
- Affiliations
- Tri-Service General Hospital (TW)
- The University of Texas Southwestern Medical Center (US)
- Corresponding author
- Huang, Chou-Long
- ORCID
- Cheng, Chih-Jen
- Venue
- Seminars in Nephrology
- Publisher
- Elsevier BV
- Published
- 2013-05
- Volume
- 33
- Issue
- 3
- Pages
- 237-247
- ISSN
- 0270-9295 (ISSN-L)
- PMC
- PMC4131448
- OpenAlex
- W2133790757
- Cited by
- 107
- References
- 85
- Citations by year
- 2026: 10 · 2025: 10 · 2024: 7 · 2023: 12 · 2022: 7 · 2021: 9 · 2020: 5 · 2019: 7 · 2018: 12 · 2017: 14 · 2016: 3 · 2015: 6 · 2014: 4 · 2013: 1
- FWCI
- 0.73
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Seminars in Nephrology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (DK85726, DK59530, DK79328, R01DK059530, P30DK079328, R01DK085726)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Potassium and Related Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
- Keywords
- hypokalemic periodic paralysis, skeletal muscle, potassium transport, Na+/K+-ATPase, inwardly rectifying potassium channels, potassium channel mutations, potassium intake, muscle activity, circulating hormones
- MeSH terms
- Sodium-Potassium-Exchanging ATPase, Animals, Extracellular Space, Homeostasis, Humans, Potassium, Muscle, Skeletal, Muscle Fibers, Skeletal, Hypokalemic Periodic Paralysis, Potassium Channels, Inwardly Rectifying
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