on October 14, 2004
Published online before print October 14, 2004, doi: 10.1161/01.ATV.0000148006.78179.c7
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Submitted on August 8, 2004
Accepted on September 28, 2004
Inhibitory Effect of High Concentration of Glucose on Relaxations to Activation of ATP-Sensitive K+ Channels in Human Omental Artery
Hiroyuki Kinoshita *;
From the Department of Anesthesia (H.K., K.N., H.I.), Japanese Red Cross Society, Wakayama Medical Center, and the Department of Anesthesiology (Y.K., M.D., Y.H.), Wakayama Medical University, Wakayama; and the Department of Anesthesia (T.A.), Hiroshima General Hospital, and the Department of Anesthesiology (O.Y.), Hiroshima University School of Medicine, Hiroshima, Japan.
* To whom correspondence should be addressed. E-mail: hkinoshi{at}pd5.so-net.ne.jp.
Objective--The 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 Results--Human 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.
Conclusions--These 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.
Key words: ATP-sensitive K+ channels • high glucose • human artery • protein kinase C • superoxide
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