Basic & Clinical Pharmacology & Toxicology · 2004 · 54 citations · 11 references
MedicinePharmacologyPhysiologyIon Channel BiophysicsNeuropharmacologyPharmacodynamicsHemodynamic PharmacologyIon Channel PharmacologyIon Channel PhysiologyIon Channel RegulationPotassium Channel BiophysicsVasoactive MedicationsAtp DependenceCalcium-activated Potassium ChannelsLevosimendan TherapyPotassium Channel BlockadePotassium Channel BlockersPotassium Channel FunctionPotassium Channel PharmacologyPotassium Channel Physiology
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)).
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