Involvement of mitochondrial ATP-sensitive potassium channels in etomidate preconditioning-induced protection in human myeloid HL-60 cells.

Exposure of HL-60 cells, a human myeloid cell line, to 500μM etomidate for 24h reduced cell viability and increased nitric oxide production and mitochondrial permeability transition pore (mPTP) opening. Preconditioning (1h) with 1μM etomidate 4h before exposure to the 500μM dose of etomidate attenuated those detrimental effects. The mitochondrial ATP-sensitive potassium channel (mitoK(ATP) channel) inhibitor 5-hydroxydecanoic acid reduced the etomidate preconditioning effects. The mitoK(ATP) channel opener diazoxide attenuated the mPTP opening caused by the large dose of etomidate. Our results suggest that etomidate can induce a preconditioning effect that may involve mitoK(ATP) channel activation.