Intracellular Nucleotide-Mediated Gatings of the SUR/Kir6.0 Complex Potassium Channels and Their Modification by Pinacidil

We examined the properties of intracellular nucleotide-mediated gatings and their modification by pinacidil in the HEK293T cells co-transfected with SUR2B and either Kir6.l or Kir6.2, using the patch clamp technique. In the cell-attached form, both types of K^+ channels were activated by pinacidil,...

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Bibliographic Details
Published in:Japanese Journal of Pharmacology 1998, Vol.76 (suppl.1), p.112-112
Main Authors: Eisaku Satoh, Mitsuhiko Yamada, Chikako Kondo, Yuji Okuyama, Shojiro Isomoto, Yoshiyuki Horio, Yoshihisa Kurachi
Format: Article
Language:Japanese
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Summary:We examined the properties of intracellular nucleotide-mediated gatings and their modification by pinacidil in the HEK293T cells co-transfected with SUR2B and either Kir6.l or Kir6.2, using the patch clamp technique. In the cell-attached form, both types of K^+ channels were activated by pinacidil, a K^+ channel opening agent (KCO). In inside-out (I-O) patches, SUR2B/Kir6.2 channels opened spontaneously and was inhibited by intracellular ATP (ATP_i ). Pinacidil attenuated the ATP_i -mediated channel inhibition in a concentration-dependent manner. In contrast, SUR2B/Kir6.l opened in I-O patches not spontaneously but only in the presence of intracellular nucleotides, such as UDP or ATP. High concentrations of ATP but not UDP, inhibited the channel openings. Pinacidil enhanced the potencies of the nucleotides in activating the channel, but did not attenuate the inhibitory effects of ATP_i . These results indicate that Kir subunits crucially determine the nucleotide-mediated gating behavior of SUR/Kir6.0 channels and thereby the mode of action of KCOs on these SUR/Kir6.0 complex channels.
ISSN:0021-5198