We have investigated the presence of diazoxide- and nicorandil-activated K+ 
channels in rat skeletal muscle. Activation of potassium transport in the rat 
skeletal muscle myoblast cell line L6 caused a stimulation of cellular oxygen 
consumption, implying a mitochondrial effect. Working with isolated rat skeletal 
muscle mitochondria, both potassium channel openers (KCOs) stimulate 
respiration, depolarize the mitochondrial inner membrane and lead to oxidation 
of the mitochondrial NAD-system in a strict potassium-dependent manner. This is 
a strong indication for KCO-mediated stimulation of potassium transport at the 
mitochondrial inner membrane. Moreover, the potassium-specific effects of both 
diazoxide and nicorandil on oxidative phosphorylation in skeletal muscle 
mitochondria were completely abolished by the antidiabetic sulfonylurea 
derivative glibenclamide, a well-known inhibitor of ATP-regulated potassium 
channels (K(ATP) channels). Since both diazoxide and nicorandil facilitated 
swelling of de-energised mitochondria in KSCN buffer at the same concentrations, 
our results implicate the presence of a mitochondrial ATP-regulated potassium 
channel (mitoK(ATP) channel) in rat skeletal muscle which can modulate 
mitochondrial oxidative phosphorylation.