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Overview
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Background
Quinidine is a clinical antiarrhythmic drug, which is used to treat abnormal heart rhythms and malaria[1].
The application of quinidine in the bath results in a dose-dependent decrease in the peak amplitude of Ik. Kd for Ik block at 0 mV is estimated to be 41 μM[1].
In rats, quinidine inhibits metabolism of amphetamine. Quinidine pretreatment significantly reduces excretion of p-hydroxyamphetamine at 24 and 48 hours, to 7.2% and 24.1% of vehicle control levels, and significantly increases excretion of amphetamine between 24 and 48 hours to 542%[2].
Reference:
[1]. Kehl S J, et al. Quinidine-induced inhibition of the fast transient outward K+ current in rat melanotrophs. Br J Pharmacol, 1991, 103(3): 1807-13.
[2]. Moody D E, et al. Quinidine inhibits in vivo metabolism of amphetamine in rats: impact upon correlation between GC/MS and immunoassay findings in rat urine. J Anal Toxicol, 1990, 14(5): 311-7.
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Overview