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Mitochondrial ATP-sensitive K+ channels influence force development and anoxic contractility in a flatfish, yellowtail flounder Limanda ferruginea, but not Atlantic cod Gadus morhua heart
Ocean Sciences Centre, Memorial University of Newfoundland, St John's, Newfoundland, Canada AlC 5S7
* Author for correspndence (e-mail: wdriedzic{at}mun.ca
Accepted 25 February 2002
The influence of ATP-sensitive K+ channels (KATP channels) on cardiac performance during anoxia and reoxygenation was investigated in two species of fish showing different cardiac responses to anoxia. Force production in isometrically contracting ventricular muscle preparations from yellowtail flounder is potentiated at the onset of anoxia, while force immediately declines in Atlantic cod preparations. Glibenclamide, a general KATP blocker, impaired oxygenated force development in yellowtail flounder heart but was without effect on cod preparations. The mitochondrial KATP (mKATP)-specific blocker 5-hydroxydecanoic acid (5HD) improved oxygenated force production in yellowtail flounder heart without influencing contractility during anoxia or reoxygenation. The specific mKATP agonist diazoxide preserved resting tension and eliminated anoxic force potentiation in yellowtail flounder heart preparations. Neither 5HD nor diazoxide affected contractility in cod ventricle preparations. Results indicate that KATP channels can modulate contractility in yellowtail flounder heart and are potentially important in cardiac hypoxia survival in this species.
Key words: adenosine 5'-triphosphate-sensitive potassium channel, fish heart, hypoxia, mitochondria, calcium, yellowtail flounder, Limanda ferruginea, Atlantic cod, Gadus morhua
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