Biophysical properties and molecular basis of cardiac rapid and slow delayed rectifier potassium channels

Cell Physiol Biochem. 1999;9(4-5):201-16. doi: 10.1159/000016317.

Abstract

Normal cardiac action potential repolarization is dependent on activation of several K(+) currents, including I(Kr) and I(Ks). I(Kr) activates rapidly at positive potentials, exhibits inward rectification caused by C-type inactivation, and is potently blocked by methanesulfon-anilide antiarrhythmic drugs and several other common medications. I(Ks) activates very slowly, does not inactivate and is blocked by some benzodiazepines and a chromanol. HERG encodes subunits that form channels that mediate I(Kr). KVLQT1 and minK encode subunits that coassemble to form channels that mediate I(Ks). Mutations in any of these genes cause long QT syndrome, a disorder of cardiac repolarization that predisposes individuals to lethal arrhythmias. In this review, we summarize recent studies of the biophysical and pharmacological properties of HERG and KvLQT1/minK K(+) channels.

Publication types

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

MeSH terms

  • Animals
  • Cation Transport Proteins*
  • DNA-Binding Proteins*
  • ERG1 Potassium Channel
  • Ether-A-Go-Go Potassium Channels
  • Heart / physiology*
  • Heart / physiopathology
  • Humans
  • Long QT Syndrome / physiopathology
  • Potassium Channels / chemistry
  • Potassium Channels / genetics
  • Potassium Channels / physiology*
  • Potassium Channels, Voltage-Gated*
  • Trans-Activators*
  • Transcriptional Regulator ERG

Substances

  • Cation Transport Proteins
  • DNA-Binding Proteins
  • ERG protein, human
  • ERG1 Potassium Channel
  • Ether-A-Go-Go Potassium Channels
  • KCNH2 protein, human
  • KCNH6 protein, human
  • Potassium Channels
  • Potassium Channels, Voltage-Gated
  • Trans-Activators
  • Transcriptional Regulator ERG