Effects of 7-bromoethoxybenzene-tetrahydropalmatine on voltage-dependent currents in guinea pig ventricular myocytes
Abstract
AIM: To study the anti-arrhythmic mechanism of 7-bromoethoxybenzene-tetrahydropalmatine (EBP).
METHODS: Whole-cell current and voltage clamp on isolated guinea pig ventricular cells.
RESULTS: EBP 30 mumol.L-1 prolonged APD90 from 430 +/- 47 ms to 514 +/- 61 ms (n = 5, P < 0.05) without effects on the action potential amplitude and resting potential. Delayed outward K+ current and its tail current were blocked by EBP in a concentration-dependent fashion, while EBP did not change the amplitudes of the sodium current, the L type calcium current, and the inwardly rectifying potassium current.
CONCLUSION: The mechanism of anti-arrhythmic action of EBP was to prolong the APD through inhibiting the delayed rectified potassium current.
Keywords:
METHODS: Whole-cell current and voltage clamp on isolated guinea pig ventricular cells.
RESULTS: EBP 30 mumol.L-1 prolonged APD90 from 430 +/- 47 ms to 514 +/- 61 ms (n = 5, P < 0.05) without effects on the action potential amplitude and resting potential. Delayed outward K+ current and its tail current were blocked by EBP in a concentration-dependent fashion, while EBP did not change the amplitudes of the sodium current, the L type calcium current, and the inwardly rectifying potassium current.
CONCLUSION: The mechanism of anti-arrhythmic action of EBP was to prolong the APD through inhibiting the delayed rectified potassium current.