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Debska 2002 Biochim Biophys Acta

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Debska G, Kicinska A, Skalska J, Szewczyk A, May R, Elger CE, Kunz WS (2002) Opening of potassium channels modulates mitochondrial function in rat skeletal muscle. Biochim Biophys Acta 1556:97-105.

Β» PMID: 12460666

Debska G, Kicinska A, Skalska J, Szewczyk A, May R, Elger CE, Kunz WS (2002) Biochim Biophys Acta

Abstract: 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 (Katp 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 (mitoKatp channel) in rat skeletal muscle which can modulate mitochondrial oxidative phosphorylation. β€’ Keywords: Skeletal muscle, Mitochondrial ATP-regulated potassium channel, Potassium channel opener, Oxidative phosphorylation

β€’ O2k-Network Lab: PL Warsaw Szewczyk A


Organism: Rat  Tissue;cell: Skeletal muscle  Preparation: Isolated mitochondria 

HRR: Oxygraph-2k