Abstract: Aim The effects of midazolam on the whole-cell sodium currents in ratsympathetic neurons werestudied to explorethe mechanisms whereby midazolam mediates hypotension.Methods Whole-cell patch-clamprecordings wereperformed on enzymatically isolated ratsuperior cervical sympathetic neurons.Results Midazolam do se-dependent ly blocked the whole-cell sodiumcurrents evoked by a voltagestep to 0 mV from a holding potential of-80 mV with a mean drug concentration required toproduce 50 % currentinhibition (IC₅₀)values of 18.35 μmol·L^-1; Clinically relevant concentration of midazolam(0.3 μmol·L^-1)reduced sodium peak cur rents by 19.98%(P<0.05);3 μmol·L^-1 midazolam didn't affect the shape of I-V curves of sodium cur rents, butreduced the peak values by 21.75%.Similarly, 3 μmol·L^-1 midazolam didn't cause significantshif tin the voltage-dependence of activation curve either.However, 3 μmol·L^-1 midazolam caused a substantial hyperpolari zingshif t of the steady-state inactivation curve (7.75 mV, P<0.05), thatis the conditioning pulse potential at whih half-max imal channel is inactiva ted (V 1/2)was changed from-40.39 mV to-48.14 mV.Conclusion Clinically relevant concentration of midazolam has significantinhibition on sympathetic neurons.This inhibition is dose-dependent and relavant to the inactivation of sodium channel.The circulation depression of midazolam may berelevant to the di rectsuppresion of sympathetic neurons.

Key words: midazolam, sympathetic ganglion, sodium channel, patch-clamp