World Library  
Flag as Inappropriate
Email this Article

Cardiac transient outward potassium current

Article Id: WHEBN0027037063
Reproduction Date:

Title: Cardiac transient outward potassium current  
Author: World Heritage Encyclopedia
Language: English
Subject: Electrophysiology
Collection: Cardiac Electrophysiology, Electrophysiology
Publisher: World Heritage Encyclopedia

Cardiac transient outward potassium current

The cardiac action potential has five phases. Ito1 is active during phase 1, causing a fast repolarization of the action potential

The cardiac transient outward potassium current (referred to as Ito1 or Ito[1] ) is one of the ion currents across the cell membrane of heart muscle cells. It is the main contributing current during the repolarizing phase 1 of the cardiac action potential. It is a result of the movement of positively charged potassium (K+) ions from the intracellular to the extracellular space. Ito1 is complemented with Ito2 resulting from Cl- ions to form the transient outward current Ito.


Ito1 is rapidly activated and deactivated.[2] It is activated after the fast increase of the membrane potential following the phase 0 of the cardiac action potential. Once activated, (K+) ions from inside the cells flow to the extracellular space. This outward flow of positively charged ions constitutes the Ito1 and causes the transmembrane voltage to decrease.This decrease of the transmembrane potential is known as repolarization. Ito1 is then quickly deactivated, stopping the repolarization and ending the phase 1 of the action potential.

Ito1 is Ca2+-independent[3] and has been clearly demonstrated in myocytes from different cardiac regions and species.[3] There are two kinetic variants of cardiac Ito1: fast Ito1, called Ito1,f, and slow Ito, called Ito1,s. The channel responsible for Ito1,f is formed by assembly of Kv4.2 (KCND2) subunits, Kv4.3 (KCND3) subunits or a combination of the two, while the channel responsible for Ito1,s is composed of Kv1.4 (KCNA4) subunits.[2] In addition, several regulatory subunits and pathways modulating the level and biophysical properties of cardiac Ito have been identified.[2]

Ito1 affects the opening of Ca2+ channels during Phase 2 of the Action Potential. As a result, changes in Ito1 modulate changes in the action potential duration.[2]

Role in disease

  • Reduction in Ito1 density is associated with prolonged action potentials and is a common finding in cardiac disease .[3]
  • Ito1 density is significantly lower in the cells of a failing heart in comparison to the cells of a healthy heart.[4]
  • There is correlation between decreased Ito1 density and atrial fibrillation.[5]
  • An increase in the Ito1 density caused by a mutation in Kv4.3 can be the cause of Brugada Syndrome.[6]


  1. ^ Niwa, Noriko; Nerbonne, Jeanne M. (January 2010). "Molecular determinants of cardiac transient outward potassium current (Ito) expression and regulation". Journal of Molecular and Cellular Cardiology 48 (1): 12–25.  
  2. ^ a b c d Wettwer, E.; Amos, G.; Gath, J.; Zerkowski, H.-R.; Reidemeister, J.-C.; Ravens, U. (1 September 1993). "Transient outward current in human and rat ventricular myocytes". Cardiovascular Research 27 (9): 1662–1669.  
  3. ^ a b c Oudit GY, Kassiri Z, Sah R, Ramirez RJ, Zobel C, Backx PH (May 2001). "The molecular physiology of the cardiac transient outward potassium current (I(to)) in normal and diseased myocardium". J. Mol. Cell. Cardiol. 33 (5): 851–72.  
  4. ^ Beuckelmann, D. J.; Nabauer, M.; Erdmann, E. (1 August 1993). "Alterations of K+ currents in isolated human ventricular myocytes from patients with terminal heart failure". Circulation Research 73 (2): 379–385.  
  5. ^ Brandt, M (October 2000). "The Ultrarapid and the Transient Outward K+Current in Human Atrial Fibrillation. Their Possible Role in Postoperative Atrial Fibrillation". Journal of Molecular and Cellular Cardiology 32 (10): 1885–1896.  
  6. ^ Giudicessi, John R.; Ye, Dan; Tester, David J.; Crotti, Lia; Mugione, Alessandra; Nesterenko, Vladislav V.; Albertson, Richard M.; Antzelevitch, Charles; Schwartz, Peter J.; Ackerman, Michael J. (July 2011). "Transient outward current (Ito) gain-of-function mutations in the KCND3-encoded Kv4.3 potassium channel and Brugada syndrome". Heart Rhythm 8 (7): 1024–1032.  
This article was sourced from Creative Commons Attribution-ShareAlike License; additional terms may apply. World Heritage Encyclopedia content is assembled from numerous content providers, Open Access Publishing, and in compliance with The Fair Access to Science and Technology Research Act (FASTR), Wikimedia Foundation, Inc., Public Library of Science, The Encyclopedia of Life, Open Book Publishers (OBP), PubMed, U.S. National Library of Medicine, National Center for Biotechnology Information, U.S. National Library of Medicine, National Institutes of Health (NIH), U.S. Department of Health & Human Services, and, which sources content from all federal, state, local, tribal, and territorial government publication portals (.gov, .mil, .edu). Funding for and content contributors is made possible from the U.S. Congress, E-Government Act of 2002.
Crowd sourced content that is contributed to World Heritage Encyclopedia is peer reviewed and edited by our editorial staff to ensure quality scholarly research articles.
By using this site, you agree to the Terms of Use and Privacy Policy. World Heritage Encyclopedia™ is a registered trademark of the World Public Library Association, a non-profit organization.

Copyright © World Library Foundation. All rights reserved. eBooks from Project Gutenberg are sponsored by the World Library Foundation,
a 501c(4) Member's Support Non-Profit Organization, and is NOT affiliated with any governmental agency or department.