Background: The blockade of cardiac transmembrane potassium channels, which is commonly seen with various antiarrhythmic drugs, plays an important role in their mechanism of action. We studied and compared the less-explored effects of three Class IA antiarrhythmics on the transient outward current (Ito) and on the inward rectifier (Ikl), ATP sensitive (KATP, and delayed rectifier (IK) potassium currents in rabbit ventricular myocytes. Methods and Results: Transmembrane currents were measured by applying the whole-cell configuration of the patch-clamp technique at 37°C in myocytes enzymatically isolated from rabbit ventricular preparations. Quinidine (10 μM), disopyramide (10 μM), and procainamide (50 μM) were studied at concentrations close to or exceeding the therapeutic plasma level. All studied drugs significantly decreased the amplitude of IKATP (activated by 50 μM pinacidil) and IK currents. None of them influenced significantly Ikl. The amplitude of Iω was decreased by quinidine and disopyramide but was not considerably altered by procainamide. The fast inactivation of Ito was not changed by procainamide and was significantly accelerated by quinidine and disopyramide. Conclusion: Although quinidine, disopyramide, and procainamide are all classified as Class IA antiarrhythmics, these drugs had different effects on various potassium currents, which may partially explain their distinct effect on repolarization in various cardiac tissues and on cardiac arrhythmias in clinical settings.
|Number of pages||11|
|Journal||Journal of Cardiovascular Pharmacology and Therapeutics|
|Publication status||Published - Mar 1 2003|
- Antiarrhythmic drugs
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Pharmacology (medical)