Difference between revisions of "Debska 2002 Biochim Biophys Acta"
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|abstract=We have investigated the presence of diazoxide- and nicorandil-activated K<sup>+</sup> 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<sub>atp</sub> 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<sub>atp</sub> channel) in rat skeletal muscle which can modulate mitochondrial oxidative phosphorylation. | |abstract=We have investigated the presence of diazoxide- and nicorandil-activated K<sup>+</sup> 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<sub>atp</sub> 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<sub>atp</sub> channel) in rat skeletal muscle which can modulate mitochondrial oxidative phosphorylation. | ||
|keywords=Skeletal muscle, Mitochondrial ATP-regulated potassium channel, Potassium channel opener, Oxidative phosphorylation | |keywords=Skeletal muscle, Mitochondrial ATP-regulated potassium channel, Potassium channel opener, Oxidative phosphorylation | ||
|discipline=Mitochondrial Physiology | |||
}} | }} | ||
{{Labeling | {{Labeling | ||
| | |instruments=Oxygraph-2k | ||
|organism=Rat | |organism=Rat | ||
|tissues=Skeletal Muscle | |tissues=Skeletal Muscle | ||
|preparations=Permeabilized Cell or Tissue; Homogenate | |preparations=Isolated Mitochondria, Permeabilized Cell or Tissue; Homogenate | ||
| | |discipline=Mitochondrial Physiology | ||
}} | }} | ||
Revision as of 11:14, 9 September 2011
| 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. |
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. • Keywords: Skeletal muscle, Mitochondrial ATP-regulated potassium channel, Potassium channel opener, Oxidative phosphorylation
Labels:
Organism: Rat
Tissue;cell: Skeletal Muscle"Skeletal Muscle" is not in the list (Heart, Skeletal muscle, Nervous system, Liver, Kidney, Lung;gill, Islet cell;pancreas;thymus, Endothelial;epithelial;mesothelial cell, Blood cells, Fat, ...) of allowed values for the "Tissue and cell" property.
Preparation: Isolated Mitochondria"Isolated Mitochondria" is not in the list (Intact organism, Intact organ, Permeabilized cells, Permeabilized tissue, Homogenate, Isolated mitochondria, SMP, Chloroplasts, Enzyme, Oxidase;biochemical oxidation, ...) of allowed values for the "Preparation" property., Permeabilized Cell or Tissue; Homogenate"Permeabilized Cell or Tissue; Homogenate" is not in the list (Intact organism, Intact organ, Permeabilized cells, Permeabilized tissue, Homogenate, Isolated mitochondria, SMP, Chloroplasts, Enzyme, Oxidase;biochemical oxidation, ...) of allowed values for the "Preparation" property.
HRR: Oxygraph-2k
