Key result
Quinidine (10 microM) decreased the open probability of ATP-sensitive potassium channels in rat ventricular cells by 67% at -50 mV and 28% at -130 mV.
Quinidine blocks ATP-sensitive potassium channels in a slow and voltage-dependent manner at clinically relevant concentrations, suggesting a potential mechanism for its effects in ischemic arrhythmias.
Voltage-dependent K-ATP blockade may underlie quinidine's antiarrhythmic effects in ischemia; leaves open human translation from this rat model.
The ATP-sensitive potassium channel current (IK-ATP) was studied in excised inside-out patches from rat ventricular cells at 20-23 degrees C. The bath solution contained 140 mM KF, and the pipette solution contained 140 mM KCl and 1.2 mM MgCl2. ATP (0.5 mM) in the bath inhibited IK-ATP. In the absence of ATP, 10 microM quinidine decreased open probability 67 +/- 1% (n = 6) at -50 mV and 28 +/- 12% at -130 mV (n = 5) without affecting single channel conductance (48-52 pS). The block increased with 25 and 50 microM quinidine and could be reversed on washing quinidine for several minutes. Interburst (closed) intervals were increased by quinidine, whereas open and closed time distributions within bursts were not changed. We conclude that quinidine blocks IK-ATP in a "slow" and voltage-dependent manner in clinically relevant concentrations. Because of the postulated role for IK-ATP in cardiac ischemia, quinidine block of this channel may play a role in ischemic arrhythmias.
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Undrovinas et al. (1990) studied this question. Quinidine vs. Baseline (absence of ATP) was evaluated on Open probability of ATP-sensitive potassium channel current (IK-ATP). Quinidine (10 microM) decreased the open probability of ATP-sensitive potassium channels in rat ventricular cells by 67% at -50 mV and 28% at -130 mV.
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