Carvedilol targets human K2P 3.1 (TASK1) K+ leak channels.

ABSTRACT:

Background and purpose

Human K(2P) 3.1 (TASK1) channels represent potential targets for pharmacological management of atrial fibrillation. K(2P) channels control excitability by stabilizing membrane potential and by expediting repolarization. In the heart, inhibition of K(2P) currents by class III antiarrhythmic drugs results in action potential prolongation and suppression of electrical automaticity. Carvedilol exerts antiarrhythmic activity and suppresses atrial fibrillation following cardiac surgery or cardioversion. The objective of this study was to investigate acute effects of carvedilol on human K(2P) 3.1 (hK(2P) 3.1) channels.

Experimental approach

Two-electrode voltage clamp and whole-cell patch clamp electrophysiology was used to record hK(2P) 3.1 currents from Xen

SUBMITTER: Staudacher K 

PROVIDER: S-EPMC3130955 | biostudies-literature | 2011 Jul

REPOSITORIES: biostudies-literature