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A potassium channel opener is a type of drug which facilitates ion transmission through potassium channels.

Examples[edit]

Some examples include:

Class Subclasses Activators
Calcium-activated

6T & 1P

[citation needed]
Inwardly rectifying

2T & 1P

[citation needed]
  • none
[citation needed]
[citation needed]
Tandem pore domain

4T & 2P

[citation needed]
Voltage-gated

6T & 1P

See also[edit]

References[edit]

  1. ^ Mizutani S, Prasad SM, Sellitto AD, Schuessler RB, Damiano RJ, Lawton JS (August 2005). "Myocyte volume and function in response to osmotic stress: observations in the presence of an adenosine triphosphate-sensitive potassium channel opener". Circulation. 112 (9 Suppl): I219–23. doi:10.1161/CIRCULATIONAHA.104.523746. PMID 16159820.
  2. ^ Wang T (February 2003). "The effects of the potassium channel opener minoxidil on renal electrolytes transport in the loop of henle". J. Pharmacol. Exp. Ther. 304 (2): 833–40. doi:10.1124/jpet.102.043380. PMID 12538840. S2CID 6948410.
  3. ^ Sudo H, Yogo K, Ishizuka N, Otsuka H, Horie S, Saito K (November 2008). "Nicorandil, a potassium channel opener and nitric oxide donor, improves the frequent urination without changing the blood pressure in rats with partial bladder outlet obstruction". Biol. Pharm. Bull. 31 (11): 2079–82. doi:10.1248/bpb.31.2079. PMID 18981577.
  4. ^ Stojnic N, Gojkovic-Bukarica L, Peric M, et al. (June 2007). "Potassium channel opener pinacidil induces relaxation of the isolated human radial artery". J. Pharmacol. Sci. 104 (2): 122–9. doi:10.1254/jphs.FP0061434. PMID 17538231.[dead link]
  5. ^ Rundfeldt C (October 1997). "The new anticonvulsant retigabine (D-23129) acts as an opener of K+ channels in neuronal cells". European Journal of Pharmacology. 336 (2–3): 243–9. doi:10.1016/S0014-2999(97)01249-1. PMID 9384239.
  6. ^ Main MJ, Cryan JE, Dupere JR, Cox B, Clare JJ, Burbidge SA (August 2000). "Modulation of KCNQ2/3 potassium channels by the novel anticonvulsant retigabine". Molecular Pharmacology. 58 (2): 253–62. doi:10.1124/mol.58.2.253. PMID 10908292. S2CID 11112809.
  7. ^ a b c d e f Enyedi P, Czirják G (Apr 2010). "Molecular background of leak K+ currents: two-pore domain potassium channels" (PDF). Physiological Reviews. 90 (2): 559–605. doi:10.1152/physrev.00029.2009. PMID 20393194. S2CID 9358238.
  8. ^ a b c d e f Lotshaw DP (2007). "Biophysical, pharmacological, and functional characteristics of cloned and native mammalian two-pore domain K+ channels". Cell Biochemistry and Biophysics. 47 (2): 209–56. doi:10.1007/s12013-007-0007-8. PMID 17652773. S2CID 12759521.
  9. ^ a b Fink M, Lesage F, Duprat F, Heurteaux C, Reyes R, Fosset M, Lazdunski M (Jun 1998). "A neuronal two P domain K+ channel stimulated by arachidonic acid and polyunsaturated fatty acids". The EMBO Journal. 17 (12): 3297–308. doi:10.1093/emboj/17.12.3297. PMC 1170668. PMID 9628867.
  10. ^ Goldstein SA, Bockenhauer D, O'Kelly I, Zilberberg N (Mar 2001). "Potassium leak channels and the KCNK family of two-P-domain subunits". Nature Reviews. Neuroscience. 2 (3): 175–84. doi:10.1038/35058574. PMID 11256078. S2CID 9682396.
  11. ^ Sano Y, Inamura K, Miyake A, Mochizuki S, Kitada C, Yokoi H, Nozawa K, Okada H, Matsushime H, Furuichi K (Jul 2003). "A novel two-pore domain K+ channel, TRESK, is localized in the spinal cord". The Journal of Biological Chemistry. 278 (30): 27406–12. doi:10.1074/jbc.M206810200. PMID 12754259. S2CID 22656809.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  12. ^ Czirják G, Tóth ZE, Enyedi P (Apr 2004). "The two-pore domain K+ channel, TRESK, is activated by the cytoplasmic calcium signal through calcineurin" (PDF). The Journal of Biological Chemistry. 279 (18): 18550–8. doi:10.1074/jbc.M312229200. PMID 14981085. S2CID 21219622.
  13. ^ Meadows HJ, Randall AD (Mar 2001). "Functional characterisation of human TASK-3, an acid-sensitive two-pore domain potassium channel". Neuropharmacology. 40 (4): 551–9. doi:10.1016/S0028-3908(00)00189-1. PMID 11249964. S2CID 20181576.
  14. ^ Patel AJ, Honoré E, Lesage F, Fink M, Romey G, Lazdunski M (May 1999). "Inhalational anesthetics activate two-pore-domain background K+ channels". Nature Neuroscience. 2 (5): 422–6. doi:10.1038/8084. PMID 10321245. S2CID 23092576.
  15. ^ Gray AT, Zhao BB, Kindler CH, Winegar BD, Mazurek MJ, Xu J, Chavez RA, Forsayeth JR, Yost CS (Jun 2000). "Volatile anesthetics activate the human tandem pore domain baseline K+ channel KCNK5". Anesthesiology. 92 (6): 1722–30. doi:10.1097/00000542-200006000-00032. PMID 10839924. S2CID 45487917.
  16. ^ Rogawski MA, Bazil CW (Jul 2008). "New molecular targets for antiepileptic drugs: alpha(2)delta, SV2A, and K(v)7/KCNQ/M potassium channels". Current Neurology and Neuroscience Reports. 8 (4): 345–52. doi:10.1007/s11910-008-0053-7. PMC 2587091. PMID 18590620.
  17. ^ Premoli I, Rossini PG, Goldberg PY, Posadas K, Green L, Yogo N, Pimstone S, Abela E, Beatch GN, Richardson MP (November 2019). "TMS as a pharmacodynamic indicator of cortical activity of a novel anti-epileptic drug, XEN1101". Annals of Clinical and Translational Neurology. 6 (11): 2164–2174. doi:10.1002/acn3.50896. PMC 6856596. PMID 31568714. XEN1101 is a novel positive allosteric modulator ("opener") of the potassium channel KCNQ2/3 (Kv7.2/7.3) currently being developed by Xenon Pharmaceuticals Inc. for the treatment of focal epilepsy.