Na(+)-activated K+ current in cardiac cells: rectification, open probability, block and role in digitalis toxicity

Pflugers Arch. 1990 Aug;416(6):766-8. doi: 10.1007/BF00370627.

Abstract

The Na(+)-activated K+ current was studied in inside-out patches and in whole cells isolated from the guinea-pig cardiac ventricle. The single channel conductance showed inward rectification for K+i less than K+e, but outward rectification for K+i greater than K+e. The open probability was dependent on Na+i and Na+,K(+)-pump activity. In the presence of pump blockade the channel remained active at low Na+i. Similar results were obtained in whole cells. These results suggest the existence of Na+ gradients depending on Na+,K(+)-pump activity and passive inward leak of Na+. The channel and whole cell current were blocked by R56865. The drug did not change the single channel conductance but markedly reduced open probability by shortening burst duration. The current may play an important role in action potential shortening during pump blockade.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Benzothiazoles
  • Biological Transport / drug effects
  • Biological Transport / physiology
  • Carrier Proteins / physiology
  • Digitalis Glycosides / toxicity
  • Electric Conductivity / drug effects
  • Electric Conductivity / physiology
  • Guinea Pigs
  • Heart / drug effects
  • Heart / physiology*
  • Myocardium / cytology*
  • Myocardium / ultrastructure
  • Piperidines
  • Potassium / pharmacokinetics*
  • Potassium Channels / drug effects
  • Potassium Channels / physiology
  • Sodium / pharmacology*
  • Sodium-Potassium-Chloride Symporters
  • Thiazoles

Substances

  • Benzothiazoles
  • Carrier Proteins
  • Digitalis Glycosides
  • Piperidines
  • Potassium Channels
  • Sodium-Potassium-Chloride Symporters
  • Thiazoles
  • R 56865
  • Sodium
  • Potassium