Abstract
The involvement of potassium channels in the venodilating capacity of the inodilator levosimendan in human saphenous vein preparations was investigated. Levosimendan caused relaxation with 50% effective concentration (EC50) of 0.32 +/- 0.04 microM in isolated veins contracted by 5-hydroxytryptamine. Fifteen microM glibenclamide, a blocker of the ATP-sensitive potassium channels (K(ATP)), partially inhibited the relaxing effect of the inodilator. In the presence of iberiotoxin, the selective blocker of large conductance calcium-activated potassium channels (BK(Ca)), levosimendan induced contraction with EC50 of 0.21 +/- 0.06 microM. We presume that levosimendan dilates human saphenous veins by interacting with hyperpolarizing potassium channels (K(ATP) and BK(Ca)).
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Drug Interactions
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Glyburide / pharmacology
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Humans
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Hydrazones / pharmacology*
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In Vitro Techniques
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Peptides / pharmacology
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Potassium Channel Blockers / pharmacology*
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Potassium Channels / drug effects*
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Potassium Channels / physiology
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Potassium Channels, Calcium-Activated / drug effects
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Potassium Channels, Calcium-Activated / physiology
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Pyridazines / pharmacology*
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Saphenous Vein / drug effects*
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Saphenous Vein / physiology
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Serotonin
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Simendan
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Vasodilation / drug effects*
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Vasodilation / physiology
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Vasodilator Agents / pharmacology*
Substances
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Hydrazones
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Peptides
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Potassium Channel Blockers
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Potassium Channels
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Potassium Channels, Calcium-Activated
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Pyridazines
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Vasodilator Agents
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Serotonin
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Simendan
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iberiotoxin
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Glyburide