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.

The influence of ATP-sensitive K+ channels (K(ATP) 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 K(ATP) blocker, impaired oxygenated force development in yellowtail flounder heart but was without effect on cod preparations. The mitochondrial K(ATP) (mK(ATP))-specific blocker 5-hydroxydecanoic acid (5HD) improved oxygenated force production in yellowtail flounder heart without influencing contractility during anoxia or reoxygenation. The specific mK(ATP) 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 K(ATP) channels can modulate contractility in yellowtail flounder heart and are potentially important in cardiac hypoxia survival in this species.