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Life Sci. 2012 Feb 13;90(7-8):272-7. doi: 10.1016/j.lfs.2011.11.009. Epub 2011 Dec 1.

Dexmedetomidine directly inhibits vascular ATP-sensitive potassium channels.

Author information

1
Department of Anesthesiology and Critical Care Medicine, Kochi Medical School, Kochi, Japan. takashika@kochi-u.ac.jp

Abstract

AIMS:

Dexmedetomidine is reported to have an effect on peripheral vasoconstriction; however, the exact mechanisms underlying this process are unclear. In this study, we hypothesized that dexmedetomidine-induced inhibition of vascular ATP-sensitive K(+) (K(ATP)) channels may be associated with this vasoconstriction. To test this hypothesis, we investigated the effects of dexmedetomidine on vascular K(ATP)-channel activity at the single-channel level.

MAIN METHODS:

We used cell-attached and inside-out patch-clamp configurations to examine the effects of dexmedetomidine on the activities of native rat vascular K(ATP) channels, recombinant K(ATP) channels with different combinations of various inwardly rectifying potassium channels (Kir6.0 family: Kir6.1, 6.2) and sulfonylurea receptor subunits (SUR1, 2A, 2B), and SUR-deficient channels derived from a truncated isoform of Kir6.2 subunit, namely, Kir6.2ΔC36 channels.

KEY FINDINGS:

Dexmedetomidine was observed to inhibit the native rat vascular K(ATP) channels in both cell-attached and inside-out configurations. This drug also inhibited the activity of all types of recombinant SUR/Kir6.0 K(ATP) channels as well as Kir6.2ΔC36 channels with equivalent potency.

SIGNIFICANCE:

These results indicate that dexmedetomidine directly inhibits K(ATP) channels through the Kir6.0 subunit.

PMID:
22155038
DOI:
10.1016/j.lfs.2011.11.009
[Indexed for MEDLINE]

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