Frequency and Voltage-dependent Inhibition of Delayed Outward Potassium Current by Flecainide in Iso

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Effects of flecanide on membrane currents were studied using an isolated single atrial cell from guinea pig hearts. The tightseal cell clamp technique was used. In the current clamp condition, flecainide prol(?)nged significantly the atrial action potential (APD) with frequency dependence.Delayed outward K current (I_k) and outward tail current were specifically inhibited by flecainide in a frequency and concentration fashion. Flecainide inhibit(?)d I_k more strongly as the membrane potential become more positive from+10mV to+60mV.The value of I_k was attenuated to 0.973 nA from 1.105 nA of control and the value of tail current was reduced to 0.113 nA from 0.288 nA of control at 60 mV. The drug did not affect on the holding current.The effects of flecainide on the action potential and transmembrane ionic currents strongly suggest that the main mechanism of action of this agent is to inhibit Voltage-dependent potassium current. In the Voltage clamp condition, flecainide affected neither the conventional L type Ca~(2+) current nor the I~(k1) current significantly. Our research proved that F1e was not completely consistent with class Ic agents, because F1e could markedly increase the APD in the experiment. Effects of flecanide on membrane currents were studied using an isolated single atrial cell from guinea pig hearts. The tightseal cell clamp technique was used. In the current clamp condition, flecainide prol (?) Nged significantly the atrial action potential (APD) with frequency dependence .Delayed outward K current (I_k) and outward tail current were specifically inhibited by flecainide in a frequency and concentration fashion. Flecainide inhibit (?) D I_k more strongly as the membrane potential became more positive from +10 mV to +60 mV.The value of I_k was attenuated to 0.973 nA from 1.105 nA of control and the value of tail current was reduced to 0.113 nA from 0.288 nA of control at 60 mV. The drug did not affect on holding current. The effects of flecainide on the action potential and transmembrane ionic currents strongly suggest that the main mechanism of action of this agent is to inhibit voltage-dependent potassium current. In the Voltage clamp condition, flecain late affected neither the conventional L type Ca ~ (2+) current nor the I ~ (k1) current significantly. Our research proved that F1e was not completely consistent with class Ic agents, F1e could markedly increase the APD in the experiment.
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