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ANESTHETIC PHARMACOLOGY

Augmented Activity of Adenosine Triphosphate-Sensitive K⁺ Channels Induced by Droperidol in the Rat Aorta

Department of Anesthesiology, Wakayama Medical University, Wakayama, Wakayama, Japan

Address correspondence and reprint requests to Hiroyuki Kinoshita, MD, PhD, Department of Anesthesiology, Wakayama Medical University, 811-1 Kimiidera, Wakayama, Wakayama 641-0012, Japan. Address e-mail to hkinoshi{at}pd5.so-net.ne.jp.

Droperidol produces the inhibition of K⁺ channels in cardiac myocytes. However, the effects of droperidol on K⁺ channels have not been studied in blood vessels. Therefore, we designed the present study to determine whether droperidol modulates the activity of adenosine triphosphate (ATP)-sensitive K⁺ channels in vascular smooth muscle cells. Rat aortic rings without endothelium were suspended or used for isometric force and membrane potential recordings, respectively. Vasorelaxation and hyperpolarization induced by levcromakalim (10^–8 to 10^–5 M or 10^–5 M, respectively) were completely abolished by the ATP-sensitive K⁺ channel antagonist glibenclamide (10^–5 M). Droperidol (10^–7 M) and an -adrenergic receptor antagonist phentolamine (3 x 10^–9 M) caused a similar vasodilator effect (approximately 20% of vasorelaxation compared with maximal vasorelaxation induced by papaverine [3 x 10^–4 M]), whereas glibenclamide did not alter vasorelaxation induced by droperidol. Droperidol (3 x 10^–8 M to 10^–7 M) augmented vasorelaxation and hyperpolarization produced by levcromakalim, whereas phentolamine (3 x 10^–9 M) did not alter this vasorelaxation. Glibenclamide (10^–5 M) abolished the vasodilating and hyperpolarizing effects of levcromakalim in the aorta treated with droperidol (10^–7 M). These results suggest that droperidol augments vasodilator activity via ATP-sensitive K⁺ channels. However, it is unlikely that this augmentation is mediated by the inhibition of -adrenergic receptors in vascular smooth muscles.