PT  - JOURNAL ARTICLE
AU  - T Yamashita
AU  - T Nakajima
AU  - E Hamada
AU  - H Hazama
AU  - M Omata
AU  - Y Kurachi
TI  - Flecainide inhibits the transient outward current in atrial myocytes isolated from the rabbit heart.
DP  - 1995 Jul 01
TA  - Journal of Pharmacology and Experimental Therapeutics
PG  - 315--321
VI  - 274
IP  - 1
4099  - http://jpet.aspetjournals.org/content/274/1/315.short
4100  - http://jpet.aspetjournals.org/content/274/1/315.full
SO  - J Pharmacol Exp Ther1995 Jul 01; 274
AB  - We examined the effects of flecainide, a class Ic antiarrhythmic agent, on membrane currents in single rabbit atrial myocytes, using the tight-seal whole cell voltage-clamp technique. Under the current-clamp condition, flecainide (1-100 microM) prolonged the action potential duration at both the early and the late phases of repolarization in a concentration-dependent manner without affecting the resting membrane potential. In the presence of 4-aminopyridine, however, the drug affected the atrial action potential duration differently than it did in the absence of 4-aminopyridine: it shortened the early phase and only slightly lengthened the late phase of the atrial action potential. Under the voltage-clamp condition, flecainide suppressed the 4-amino-pyridine-sensitive, Ca(++)-insensitive transient outward current in a concentration-dependent fashion (the concentration for the half-maximal effect was approximately 17 microM). The drug also slightly inhibited the voltage-dependent L-type Ca++ current and delayed outward K+ current. Flecainide apparently accelerated the inactivation time course of the transient outward current but did not affect the voltage-dependence of its steady-state inactivation. These actions of flecainide on the transient outward current could be described by a voltage-dependent first-order interaction of the drug with the channel.