Abstract

Hydrogen sulfide (H2S), known for decades as toxic gas, was found as an endogenously produced biological gas in the 1980s. It was recently reported that the H2S generation pathway exists in rat skeletal muscle, and that H2S modulates ion channel activity in many cellular systems. However, the effects of H2S on K+ channels have not been described in skeletal muscle. Therefore, we examined the effects of H2S on K+ currents in L6 skeletal myotubes using NaHS as an H2S donor. A single L6 myotube was used to record membrane current by the whole cell patch-clamp technique. Depolarizing voltage pulses of 400-ms duration and 10-mV steps were given every 10 s from the holding potential of −40 mV over the range between −30 and 80 mV. Our results show that L6 myotube has an E-4031 sensitive current, which may be the ERG K+ current (IKERG), which was inhibited by NaHS in a concentration-dependent manner. The blocking effect reached a steady state at about 5 min of NaHS perfusion and the 50% concentration of NaHS was about 10 μM. Meanwhile, there was another type of membrane current in the L6 myotubes, which was decreased by apamin. NaHS increased this apamin-sensitive K current in a concentration-dependent manner. We conclude that NaHS decreases the ERG K+ current and increases the apamin-sensitive K+ current in L6 myotubes. These effects may be involved in the physiological or toxic effects of NaHS.

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