Thiopental inhibits function of different inward rectifying potassium channel isoforms by a similar mechanism
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Thiopental is a well-known intravenous barbiturate anesthetic with important cardiac side effects. The actions of thiopental on the transmembrane ionic currents that determine the resting potential and action potential duration in cardiomyocytes have been studied widely. We aimed at elucidating the characteristics and mechanism of inhibition by thiopental on members of the subfamily of inward rectifying Kir2.x (Kir2.1, 2.2 and 2.3), Kir1.1 and Kir6.2/SUR2A channels. These inward rectifier potassium channels were transfected in HEK-293 cells and macroscopic currents were recorded in the whole-cell and inside-out configurations of the patch-clamp technique. Thiopental inhibited Kir2.1, Kir2.2, Kir2.3, Kir1.1 and Kir6.2/SUR2A currents with similar potency; in whole-cell experiments 30μM thiopental decreased Kir2.1, Kir2.2, Kir2.3 and Kir1.1 currents to 55±6, 39±8, 42±5 and 49±5%25 at -120mV, respectively. Point mutations on Kir2.3 (I213L) or Kir2.1 (L222I) did not modify the potency of block. Thiopental inhibited all Kir channels in a concentration-dependent and voltage-independent manner. Also, the time course of thiopental inhibition was slow (T1/2-4min) and independent of external or internal drug application. However, in the presence of PIP2, inhibition by thiopental on Kir2.1 was significantly decreased. Thiopental at clinically relevant concentrations significantly inhibited all Kir channels evaluated in this work. The reduction of thiopental effects during PIP2 treatment suggests that thiopental inhibition on Kir2.1 channels is related to channel-PIP2 interaction. © 2010 Elsevier B.V.
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Inward rectifier potassium channel; PIP2; Thiopental inwardly rectifying potassium channel; inwardly rectifying potassium channel subunit Kir2.1; inwardly rectifying potassium channel subunit Kir6.2; phosphatidylinositol 4,5 bisphosphate; thiopental; inwardly rectifying potassium channel; isoprotein; phosphatidylinositol 4,5 bisphosphate; thiopental; article; cell strain HEK293; concentration response; controlled study; inhibition kinetics; patch clamp; point mutation; priority journal; whole cell; antagonists and inhibitors; dose response; drug effects; drug interaction; genetics; human; membrane potential; patch clamp technique; transformed cell line; Cell Line, Transformed; Dose-Response Relationship, Drug; Drug Interactions; Humans; Membrane Potentials; Patch-Clamp Techniques; Phosphatidylinositol 4,5-Diphosphate; Point Mutation; Potassium Channels, Inwardly Rectifying; Protein Isoforms; Thiopental; Cell Line, Transformed; Dose-Response Relationship, Drug; Drug Interactions; Humans; Membrane Potentials; Patch-Clamp Techniques; Phosphatidylinositol 4,5-Diphosphate; Point Mutation; Potassium Channels, Inwardly Rectifying; Protein Isoforms; Thiopental
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