Aprindine (3 μM) inhibits the delayed rectifier K+ current (IK) with little influence on the inward rectifier K+ current (IK1) or the Ca2+ current[2].
The muscarinic acetylcholine receptor-operated K+ current (IK.ACh) was activated by the extracellular application of carbachol (1 μM) or by the intracellular loading of GTPγS. Aprindine inhibits the carbachol- and GTPγS-induced IK.ACh with the IC50 values of 0.4 μM and 2.5 μM, respectively[2].
References:
[1]. M L De Bruin, et al . Anti-HERG activity and the risk of drug-induced arrhythmias and sudden death. Eur Heart J. 2005 Mar;26(6):590-7.
[2]. Y Ohmoto-Sekine, et al. Inhibitory effects of aprindine on the delayed rectifier K+ current and the muscarinic acetylcholine receptor-operated K+ current in guinea-pig atrial cells. Br J Pharmacol. 1999 Feb;126(3):751-61.
















