Key result
Antiarrhythmic drugs potently inhibited ATP-sensitive potassium channels in rat heart cells (e.g., quinidine IC50 2.7 microM, verapamil IC50 4.5 microM, amiodarone IC50 19.1 microM).
Population
Isolated adult rat heart cells
Comparison
Antiarrhythmic drugs and glyburide vs Untreated ATP-depleted cells (rotenone plus FCCP)
Design
Preclinical
Authors
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May support KATP inhibition as an antiarrhythmic mechanism in rat myocytes; hypothesis-generating and should not yet change practice.
Quinidine, verapamil, and amiodarone strongly inhibit ATP-sensitive potassium channels in adult rat heart cells, suggesting a potential mechanism for their antiarrhythmic effects.
Haworth et al. (1989) studied ATP-sensitive potassium channel activity. Antiarrhythmic drugs (glyburide, quinidine, verapamil, amiodarone) was evaluated on Rate of 86Rb uptake (measure of potassium conductance). Antiarrhythmic drugs potently inhibited ATP-sensitive potassium channels in rat heart cells (e.g., quinidine IC50 2.7 microM, verapamil IC50 4.5 microM, amiodarone IC50 19.1 microM).
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