• Hiroyuki Kinoshita, Toshiharu Azma, Katsutoshi Nakahata, Hiroshi Iranami, Yoshiki Kimoto, Mayuko Dojo, Osafumi Yuge, and Yoshio Hatano.
• Department of Anesthesia, Japanese Red Cross Society, Wakayama Medical Center, Japan. hkinoshi@pd5.so-net.ne.jp
• Arterioscler. Thromb. Vasc. Biol. 2004 Dec 1;24(12):2290-5.

ObjectiveThe present study was designed to examine in the human omental artery whether high concentrations of D-glucose inhibit the activity of ATP-sensitive K+ channels in the vascular smooth muscle and whether this inhibitory effect is mediated by the production of superoxide.Methods And ResultsHuman omental arteries without endothelium were suspended for isometric force recording. Changes in membrane potentials were recorded and production of superoxide was evaluated. Glibenclamide abolished vasorelaxation and hyperpolarization in response to levcromakalim. D-glucose (10 to 20 mmol/L) but not l-glucose (20 mmol/L) reduced these vasorelaxation and hyperpolarization. Tiron and diphenyleneiodonium, but not catalase, restored vasorelaxation and hyperpolarization in response to levcromakalim in arteries treated with D-glucose. Calphostin C and Gö6976 simultaneously recovered these vasorelaxation and hyperpolarization in arteries treated with D-glucose. Phorbol 12-myristate 13 acetate (PMA) inhibited the vasorelaxation and hyperpolarization, which are recovered by calphostin C as well as Gö6976. D-glucose and PMA, but not l-glucose, significantly increased superoxide production from the arteries, whereas such increased production was reversed by Tiron.ConclusionsThese results suggest that in the human visceral artery, acute hyperglycemia modulates vasodilation mediated by ATP-sensitive K+ channels via the production of superoxide possibly mediated by the activation of protein kinase C.

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