RESUMO
BACKGROUND/PURPOSE: Inward rectifying potassium channel 6.2 (Kir6.2DelataC26 channel) is closely related to ATP-sensitive potassium channels. Whether sodium azide, barium ion, d-amphetamine or procaine acts directly on the Kir6.2DeltaC26 channel remains unclear. We studied the effects of these compounds on Kir6.2DeltaC26 channel expressed in Xenopus oocytes. METHODS: The coding sequence of a truncated form of mouse Kir6.2 (GenBank accession number NP_034732.1), Kir6.2(1-364) (i.e. Kir6.2DeltaC26), was subcloned into the pET20b(+) vector. Plasmid containing the correct T7 promoter-Kir6.2(1-364) cDNA fragment [Kir6.2/pET20b(+)] was then subject to NotI digestion to generate the templates for in vitro run-off transcriptions. The channel was expressed in Xenopus laevis oocytes. Two-electrode voltage clamping was used to measure the effects of sodium azide, barium ion, d-amphetamine and procaine on Kir6.2DeltaC26 channel current. RESULTS: Sodium azide activated and barium ion and d-amphetamine inhibited the Kir6.2DeltaC26 channel. Procaine did not have any significant effect on the Kir6.2DeltaC26 channel. CONCLUSION: Kir6.2DeltaC26 channel expressed in Xenopus oocytes can be used as a pharmacological tool for the study of inward rectifying potassium channels.
