Potassium cation (BioCAD00000016547)

blood cerebrospinal fluid (csf) saliva urine

Metabolite Card

Formula: K (38.9637)
SMILES: [K+]

Synonyms [en]

potassium ion; potassium(1+); Potassium cation; potassium(1+) ion; Potassium; Kalium

Reviewed

Last reviewed on 2024-06-28.

Cite this Page

Potassium cation. 数据之源,洞见之始. SMRUCC genomics institute, a synthetic life researcher from China. https://biocad_registry.innovation.ac.cn/s/(-)-arctiin (retrieved 2026-01-03) (CAD Registry RN: BioCAD00000016547). Licensed under the Attribution-Noncommercial 4.0 International License (CC BY-NC 4.0).

Note

Potassium 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. (PMID: 17883675).

Entity Information

DBLinks

Other DBLinks
  • CAS Registry Number: 125352-08-1
  • CAS Registry Number: 138363-30-1
  • CAS Registry Number: 13966-00-2
  • CAS Registry Number: 24203-36-9
  • CAS Registry Number: 7440-09-7
  • PubChem: 5462222
  • PubChem: 6328542
  • PubChem: 813
  • ChEBI: ChEBI:26216
  • ChEBI: ChEBI:29103
  • HMDB: HMDB0000586
  • KEGG: C00238
  • BioCyc: K+
  • NCBI MeSH: liver regeneration factor 1
  • NCBI MeSH: Potassium
  • NCBI MeSH: Potassium-40
  • Wikipedia: Potassium
  • DrugBank: DB01345
  • DrugBank: DB14500
  • Coconut NaturalProduct: CNP0580715.0
  • Coconut NaturalProduct: CNP0586268.0

Class / Ontology

Metabolic Network
ID EC Number Name
BioCyc:TRANS-RXN-336 electrogenic potassium:proton antiport
BioCyc:TRANS-RXN-2 7.2.2.6 K+ + WATER + ATP --> K+ + Pi + ADP + PROTON
BioCyc:TRANS-RXN-42 potassium:proton antiport
BioCyc:TRANS-RXN-188 sodium:potassium symport
BioCyc:TRANS-RXN-3 K+:proton symport
Rhea:RHEA:16778 7.2.2.6 K+(out) + ATP + H2O => K+(in) + ADP + phosphate + H+
Rhea:RHEA:16779 7.2.2.6 K+(in) + ADP + phosphate + H+ => K+(out) + ATP + H2O
Rhea:RHEA:16780 7.2.2.6 K+(out) + ATP + H2O <=> K+(in) + ADP + phosphate + H+
Rhea:RHEA:18354 7.2.2.13 K+(out) + Na+(in) + ATP + H2O => K+(in) + Na+(out) + ADP + phosphate + H+
Rhea:RHEA:18355 7.2.2.13 K+(in) + Na+(out) + ADP + phosphate + H+ => K+(out) + Na+(in) + ATP + H2O
Rhea:RHEA:18356 7.2.2.13 K+(out) + Na+(in) + ATP + H2O <=> K+(in) + Na+(out) + ADP + phosphate + H+
Rhea:RHEA:22045 7.2.2.19 K+(out) + ATP + H2O + H+(in) => K+(in) + ADP + phosphate + 2 H+(out)
Rhea:RHEA:22046 7.2.2.19 K+(in) + ADP + phosphate + 2 H+(out) => K+(out) + ATP + H2O + H+(in)
Rhea:RHEA:22047 7.2.2.19 K+(out) + ATP + H2O + H+(in) <=> K+(in) + ADP + phosphate + 2 H+(out)
Rhea:RHEA:28491 K+(in) + H+(in) => K+(out) + H+(out)
Rhea:RHEA:28492 K+(out) + H+(out) => K+(in) + H+(in)
Rhea:RHEA:28493 K+(in) + H+(in) <=> K+(out) + H+(out)
Rhea:RHEA:29464 K+(in) => K+(out)
Rhea:RHEA:29465 K+(out) => K+(in)
Rhea:RHEA:29466 K+(in) <=> K+(out)
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Organism Source

Taxonomy Source

Pathway Synthetic

pathway id name
BioCyc:HUMAN_PWY-6938 NADH repair
BioCyc:HUMAN_PWY66-367 ketogenesis
BioCyc:HUMAN_PWY-5177 glutaryl-CoA degradation
BioCyc:HUMAN_ILEUDEG-PWY isoleucine degradation
BioCyc:HUMAN_TRYPTOPHAN-DEGRADATION-1 tryptophan degradation
BioCyc:HUMAN_PWY66-401 superpathway of tryptophan utilization
BioCyc:META_PWY-7151 polymethylated quercetin glucoside biosynthesis II - quercetagetin series (Chrysosplenium)
BioCyc:META_PWY-7013 (S)-propane-1,2-diol degradation
BioCyc:META_PWY-6277 superpathway of 5-aminoimidazole ribonucleotide biosynthesis
BioCyc:META_PWY-6387 UDP-N-acetylmuramoyl-pentapeptide biosynthesis I (meso-diaminopimelate containing)
BioCyc:META_GLUDEG-II-PWY L-glutamate degradation VII (to butanoate)
BioCyc:META_PWY-5920 superpathway of b heme biosynthesis from glycine
BioCyc:META_P142-PWY pyruvate fermentation to acetate I
BioCyc:META_PWY-6141 archaetidylserine and archaetidylethanolamine biosynthesis
BioCyc:META_PWY0-1335 NADH to cytochrome bo oxidase electron transfer I
BioCyc:META_PWY-6703 preQ0 biosynthesis
BioCyc:META_PWY-5695 inosine 5'-phosphate degradation
BioCyc:META_P163-PWY L-lysine fermentation to acetate and butanoate
BioCyc:META_PWY-7006 4-amino-3-hydroxybenzoate degradation
BioCyc:META_PWY-7384 anaerobic energy metabolism (invertebrates, mitochondrial)
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