抄録
Objectives: Previous studies demonstrated that a class III antiarrhythmic agent amiodaraone inhibits K+ channels on cardiac myocytes, resulting in antiarrhythmic properties. However, it has not been determined that this agent may induce the inhibition of K+ channel activity in blood vessels. Therefore, the present study was designed to evaluate whether amiodarone modulates vasorelaxation mediated by adenosine triphosphate (ATP)-sensitive K+ channels in arteries from humans as well as rats. Methods: The ethical committee of our institute approved this study. Human omental arteries were obtained from surgical patients without hypertension, cardiac diseases, diabetes mellitus, hypercholesterolemia and smoking habit, under written informed consent. Aortas were taken from Wister rats under halothane anesthesia. Isometric force recordings were performed using human omental arterial or rat aortic rings without endothelium, under contraction with U46619 (3×10-8M) or phenylephrine (3×10-7M), respectively. Results: An ATP-sensitive K+ channel opener levcromakalim (10-8-10-5M) induced vasorelaxation in both human omental arterial and rat aortic rings in a concentration-dependent fashion, which is completely abolished by the treatment with a selective ATP-sensitive K+ channel antagonist glibenclamide (5×10-6M). Pretreatment with amiodarone (10-6-3×10-6M) did not alter the relaxation. Conclusions: These results suggest that clinically relevant concentrations of amiodarone do not affect vasodilation mediated by ATP-sensitive K+ channels in the vascular smooth muscle cells including those from humans.
