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Record Information
Creation Date2014-08-29 06:30:31 UTC
Update Date2014-12-24 20:26:47 UTC
Accession NumberT3D4344
Common NamePotassium
ClassSmall Molecule
DescriptionPotassium is an essential electrolyte. Potassium balance is crucial for regulating the excitability of nerves and muscles and so critical for regulating contractility of cardiac muscle. Although the most important changes seen in the presence of deranged potassium are cardiac, smooth muscle is also affected with increasing muscle weakness, a feature of both hyperkalaemia and hypokalaemia. Physiologically, it exists as an ion in the body. Potassium (K+) is a positively charged electrolyte, cation, which is present throughout the body in both intracellular and extracellular fluids. The majority of body potassium, >90%, are intracellular. It moves freely from intracellular fluid (ICF) to extracellular fluid (ECF) and vice versa when adenosine triphosphate increases the permeability of the cell membrane. It is mainly replaced inside or outside the cells by another cation, sodium (Na+). The movement of potassium into or out of the cells is linked to certain body hormones and also to certain physiological states. Standard laboratory tests measure ECF potassium. Potassium enters the body rapidly during food ingestion. Insulin is produced when a meal is eaten; this causes the temporary movement of potassium from ECF to ICF. Over the ensuing hours, the kidneys excrete the ingested potassium and homeostasis is returned. In the critically ill patient, suffering from hyperkalaemia, this mechanism can be manipulated beneficially by administering high concentration (50%) intravenous glucose. Insulin can be added to the glucose, but glucose alone will stimulate insulin production and cause movement of potassium from ECF to ICF. The stimulation of alpha receptors causes increased movement of potassium from ICF to ECF. A noradrenaline infusion can elevate serum potassium levels. An adrenaline infusion, or elevated adrenaline levels, can lower serum potassium levels. Metabolic acidosis causes a rise in extracellular potassium levels. In this situation, excess of hydrogen ions (H+) are exchanged for intracellular potassium ions, probably as a result of the cellular response to a falling blood pH. Metabolic alkalosis causes the opposite effect, with potassium moving into the cells. (1).
Compound Type
  • Animal Toxin
  • Food Toxin
  • Industrial/Workplace Toxin
  • Inorganic Compound
  • Metabolite
  • Metal
  • Natural Compound
Chemical Structure
Potassium (ion)
Potassium (K+)
Potassium alloy
Potassium cation
Potassium ion
Potassium ion (K+)
Potassium ion (K1+)
Potassium ion(+)
Potassium ion(1+)
Potassium monocation
Potassium(1+) ion
Potassium(I) cation
Chemical FormulaK
Average Molecular Mass39.098 g/mol
Monoisotopic Mass38.963 g/mol
CAS Registry Number7440-09-7
IUPAC Namepotassium(1+) ion
Traditional Namepotassium(1+) ion
InChI IdentifierInChI=1S/K/q+1
Chemical Taxonomy
Description belongs to the class of inorganic compounds known as homogeneous alkali metal compounds. These are inorganic compounds containing only metal atoms,with the largest atom being a alkali metal atom.
KingdomInorganic compounds
Super ClassHomogeneous metal compounds
ClassHomogeneous alkali metal compounds
Sub ClassNot Available
Direct ParentHomogeneous alkali metal compounds
Alternative ParentsNot Available
  • Homogeneous alkali metal
Molecular FrameworkNot Available
External Descriptors
Biological Properties
StatusDetected and Not Quantified
Cellular Locations
  • Cytoplasm
  • Extracellular
  • Golgi apparatus
Biofluid LocationsNot Available
Tissue LocationsNot Available
Lactose DegradationSMP00457 Not Available
Trehalose DegradationSMP00467 Not Available
Fanconi-bickel syndromeSMP00572 Not Available
ApplicationsNot Available
Biological Roles
Chemical RolesNot Available
Physical Properties
AppearanceWhite powder.
Experimental Properties
Melting Point63.2°C
Boiling PointNot Available
SolubilityNot Available
LogPNot Available
Predicted Properties
pKa (Strongest Acidic)3.09ChemAxon
Physiological Charge1ChemAxon
Hydrogen Acceptor Count0ChemAxon
Hydrogen Donor Count0ChemAxon
Polar Surface Area0 ŲChemAxon
Rotatable Bond Count0ChemAxon
Refractivity0 m³·mol⁻¹ChemAxon
Polarizability1.78 ųChemAxon
Number of Rings0ChemAxon
Rule of FiveYesChemAxon
Ghose FilterYesChemAxon
Veber's RuleYesChemAxon
MDDR-like RuleYesChemAxon
Spectrum TypeDescriptionSplash KeyDeposition DateView
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 10V, Positivesplash10-000i-9000000000-560fc6f738e9570ec8a22015-09-15View Spectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 20V, Positivesplash10-000i-9000000000-560fc6f738e9570ec8a22015-09-15View Spectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 40V, Positivesplash10-000i-9000000000-560fc6f738e9570ec8a22015-09-15View Spectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 10V, Negativesplash10-000i-9000000000-bcbe5ea7d5d32f6a95982015-09-15View Spectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 20V, Negativesplash10-000i-9000000000-bcbe5ea7d5d32f6a95982015-09-15View Spectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 40V, Negativesplash10-000i-9000000000-bcbe5ea7d5d32f6a95982015-09-15View Spectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 10V, Positivesplash10-000i-9000000000-e11fed6c31524d9e4d2c2021-09-22View Spectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 20V, Positivesplash10-000i-9000000000-e11fed6c31524d9e4d2c2021-09-22View Spectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 40V, Positivesplash10-000i-9000000000-e11fed6c31524d9e4d2c2021-09-22View Spectrum
Toxicity Profile
Route of ExposureNot Available
Mechanism of ToxicityNot Available
MetabolismNot Available
Toxicity ValuesNot Available
Lethal DoseNot Available
Carcinogenicity (IARC Classification)No indication of carcinogenicity to humans (not listed by IARC).
Uses/SourcesThis is an endogenously produced metabolite found in the human body. It is used in metabolic reactions, catabolic reactions or waste generation.
Minimum Risk LevelNot Available
Health EffectsNot Available
SymptomsNot Available
TreatmentNot Available
Normal Concentrations
Not Available
Abnormal Concentrations
Not Available
DrugBank IDDB01345
PubChem Compound IDNot Available
ChEMBL IDNot Available
ChemSpider IDNot Available
UniProt IDNot Available
ChEBI ID26216
BioCyc IDK%2b
CTD IDNot Available
Stitch IDNot Available
PDB IDNot Available
ACToR IDNot Available
Wikipedia LinkPotassium
Synthesis Reference

John B. Sardisco, “Production of potassium sulfate and hydrogen chloride.” U.S. Patent US4045543, issued 1865.

General References
  1. Brooks G: Potassium additive algorithm for use in continuous renal replacement therapy. Nurs Crit Care. 2006 Nov-Dec;11(6):273-80. [17883675 ]
  2. Schaafsma A, de Vries PJ, Saris WH: Delay of natural bone loss by higher intakes of specific minerals and vitamins. Crit Rev Food Sci Nutr. 2001 May;41(4):225-49. [11401244 ]
  3. Preuss HG: Diet, genetics and hypertension. J Am Coll Nutr. 1997 Aug;16(4):296-305. [9263178 ]
  4. Beede DK: Mineral and water nutrition. Vet Clin North Am Food Anim Pract. 1991 Jul;7(2):373-90. [1893277 ]
Gene Regulation
Up-Regulated GenesNot Available
Down-Regulated GenesNot Available


General Function:
Steroid hormone binding
Specific Function:
This is the catalytic component of the active enzyme, which catalyzes the hydrolysis of ATP coupled with the exchange of sodium and potassium ions across the plasma membrane. This action creates the electrochemical gradient of sodium and potassium ions, providing the energy for active transport of various nutrients.
Gene Name:
Uniprot ID:
Molecular Weight:
112895.01 Da
  1. Silva E, Gomes P, Soares-da-Silva P: Overexpression of Na(+)/K (+)-ATPase parallels the increase in sodium transport and potassium recycling in an in vitro model of proximal tubule cellular ageing. J Membr Biol. 2006;212(3):163-75. Epub 2007 Feb 28. [17334838 ]
  2. Li C, Geering K, Horisberger JD: The third sodium binding site of Na,K-ATPase is functionally linked to acidic pH-activated inward current. J Membr Biol. 2006;213(1):1-9. Epub 2007 Mar 8. [17347782 ]
  3. Stanely Mainzen Prince P, Karthick M: Preventive effect of rutin on lipids, lipoproteins, and ATPases in normal and isoproterenol-induced myocardial infarction in rats. J Biochem Mol Toxicol. 2007;21(1):1-6. [17366541 ]
  4. Simon WA, Herrmann M, Klein T, Shin JM, Huber R, Senn-Bilfinger J, Postius S: Soraprazan: setting new standards in inhibition of gastric acid secretion. J Pharmacol Exp Ther. 2007 Jun;321(3):866-74. Epub 2007 Mar 16. [17369284 ]
  5. Iannello S, Milazzo P, Belfiore F: Animal and human tissue Na,K-ATPase in normal and insulin-resistant states: regulation, behaviour and interpretative hypothesis on NEFA effects. Obes Rev. 2007 May;8(3):231-51. [17444965 ]