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Extrarenal potassium homeostasis
Abstract
Normal potassium homeostasis is regulated by both renal and extrarenal mechanisms. Although chronic potassium balance is primarily regulated by the kidneys, acute potassium tolerance is largely determined by extrarenal tissues. During the first 4-6 h following an acute potassium load, only about 50% of the potassium is excreted by the kidneys. Of the remaining 50% that is retained, over 80% is translocated into cells, and this provides the primary defense against hyperkalemia. Potassium uptake by both liver and muscle and intestinal secretion of potassium are the most important mechanisms of extrarenal potassium disposal. Several hormones, including insulin and epinephrine, have been shown to play an important role in the maintenance of normal extrarenal potassium metabolism. These hormones function by enhancing potassium uptake by liver and muscle. There is also evidence that aldosterone is necessary in the maintenance of normal extrarenal potassium tolerance. Although the major extrarenal site of action of aldosterone has not yet been clearly defined, gastrointestinal potassium secretion and muscle transport of potassium are both affected by the hormone. Evidence exists that glucocorticoids may also have an effect on extrarenal potassium homeostasis. In addition to this hormonal regulation, cellular shifts of potassium are influenced by changes in acid-base balance. Extrarenal potassium tolerance is impaired in chronic renal insufficiency. These uremia-related changes are discussed in the context of our present understanding of normal extrarenal potassium metabolism.
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“After a K+ load, in the first 3–6 hours, only about 50% of the K+ load is excreted via urine; the remaining K+ load is excreted over the next 10 hours [1, 12].”
From A mathematical model of potassium homeostasis: Effect of feedforward and feedback controls (2022) · cites this paper as [12]
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“Potassium homeostasis is regulated by renal and extrarenal mechanisms, aected by acid-base balance and hormonal regulation by epinephrine, insulin, and aldosterone [42].”
BackgroundSeeliger, E., Wiegard, M., & Reinhardt, H. W. (2005) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.00676.2005 · Cited by 29
“It is conceivable that this exchange does not occur (to the same extent) on all cells, but (preferentially) on cells of specific tissues, since intracellular Na and K concentrations differ considerably among tissues (26), and compartmental redistributions of K during primary TBPotassium changes occur preferentially in…”
BackgroundEffects of Aldosterone on Urinary Kallikrein and Sodium Excretion during Fetal Life
Robillard, J., Nakamura, K. T., Lawton, W. J., et al. (1985) · Pediatric Research · doi:10.1203/00006450-198510000-00021 · Cited by 29
Garg, L. C., & Narang, N. (1985) · Journal of Clinical Investigation · doi:10.1172/jci112059 · Cited by 28
A Patient With Hyperkalemia and Metabolic Acidosis
Kurtzman, N. A., Gonzalez, J., DeFronzo, R. A., & Giebisch, G. (1990) · American Journal of Kidney Diseases · doi:10.1016/s0272-6386(12)80080-1 · Cited by 27
Self-citationSodium Zirconium Cyclosilicate ( ZS ‐9): A Novel Agent for the Treatment of Hyperkalemia
Linder, K. E., Krawczynski, M. A., & Laskey, D. (2016) · Pharmacotherapy The Journal of Human Pharmacology and Drug Therapy · doi:10.1002/phar.1797 · Cited by 26
“14 In individuals with normal kidney function, 95% of daily potassium load is eliminated in the urine, and the remaining 5% is excreted in the gut.(3) Under normal conditions, renal potassium handling depends on glomerular filtration rate and potassium secretion, both of which rely on the effects *Address for correspo…”
BackgroundPotassium Homeostasis and Hyperkalemic Syndromes
Clark, B. A., & Brown, R. S. (1995) · Endocrinology and Metabolism Clinics of North America · doi:10.1016/s0889-8529(18)30032-x · Cited by 26
Early physiologic responses to hemorrhagic hypotension
Filho, I. P. T., Torres, L. N., & Pittman, R. N. (2009) · Translational research · doi:10.1016/j.trsl.2009.09.001 · Cited by 24
Metadata
- Authors
- Bia, M. J., & DeFronzo, R. A.
- Venue
- American Journal of Physiology-Renal Physiology
- Publisher
- American Physiological Society
- Published
- 1981-04-01
- Volume
- 240
- Issue
- 4
- Pages
- F257-F268
- ISSN
- 1522-1466 (ISSN-L)
- 1931-857X
- OpenAlex
- W2216918211
- Cited by
- 249
- References
- 0
- Citations by year
- 2026: 5 · 2025: 2 · 2024: 6 · 2023: 3 · 2022: 6 · 2021: 5 · 2020: 6 · 2019: 1 · 2018: 4 · 2017: 7 · 2016: 7 · 2015: 2 · 2014: 4 · 2013: 6 · 2012: 5
- FWCI
- 7.65
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Physiology-Renal Physiology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Nephrology › Potassium and Related Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
- Health Sciences › Medicine › Nephrology › Parathyroid Disorders and Treatments
- Keywords
- hyperkalemia, aldosterone, insulin, epinephrine, glucocorticoids, acid-base balance, chronic renal insufficiency, uremia
- MeSH terms
- Aldosterone, Animals, Dogs, Epinephrine, Glomerular Filtration Rate, Glucagon, Homeostasis, Humans, Hydrocortisone, Insulin, Kidney, Kidney Failure, Chronic, Male, Norepinephrine, Potassium, Prednisone, Somatostatin, Rats
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