Molecular basis of functional voltage-gated K+ channel diversity in the mammalian myocardium

J Physiol. 2000 Jun 1;525 Pt 2(Pt 2):285-98. doi: 10.1111/j.1469-7793.2000.t01-1-00285.x.


In the mammalian heart, Ca2+-independent, depolarization-activated potassium (K+) currents contribute importantly to shaping the waveforms of action potentials, and several distinct types of voltage-gated K+ currents that subserve this role have been characterized. In most cardiac cells, transient outward currents, Ito,f and/or Ito,s, and several components of delayed reactivation, including IKr, IKs, IKur and IK,slow, are expressed. Nevertheless, there are species, as well as cell-type and regional, differences in the expression patterns of these currents, and these differences are manifested as variations in action potential waveforms. A large number of voltage-gated K+ channel pore-forming (alpha) and accessory (beta, minK, MiRP) subunits have been cloned from or shown to be expressed in heart, and a variety of experimental approaches are being exploited in vitro and in vivo to define the relationship(s) between these subunits and functional voltage-gated cardiac K+ channels. Considerable progress has been made in defining these relationships recently, and it is now clear that distinct molecular entities underlie the various electrophysiologically distinct repolarizing K+ currents (i.e. Ito,f, Ito,s, IKr, IKs, IKur, IK,slow, etc.) in myocyardial cells.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Action Potentials
  • Animals
  • Humans
  • In Vitro Techniques
  • Ion Channel Gating
  • Models, Molecular
  • Myocardium / metabolism*
  • Potassium Channels / chemistry*
  • Potassium Channels / metabolism*


  • Potassium Channels