Abstract
This study addresses the question whether K + channels are involved in the vasorelaxant effects of 3-(5′-hydroxymethyl-2′-furyl)-1-benzyl-indazole (YC-1 ). In rat aorta, guinea pig aorta, and guinea pig a. carotis, YC-1 inhibited contractions induced by phenylephrine (3 μM) more potently than those induced by K +(48 mM). In rat aorta, tetraethylammonium (10 mM), charybdotoxin (0.2 μM), and iberiotoxin (0.1 μM), but not glibenclamide (10 μM), attenuated the relaxant effects of YC-1. In guinea pig a. carotis, YC-1 (30 μM) induced a hyperpolarisation which was antagonised by 1 H-[1,2,4]oxadiazolo[4,3- a]quinoxalin-1-one (ODQ; 50 μM). In rat aorta, YC-1 (30 μM) increased the rate constant of 86Rb-efflux. The effect of YC-1 was potentiated by zaprinast (10 μM), but inhibited by ODQ (50 μM) or charybdotoxin (0.2 μM). In smooth muscle cells from rat aorta, YC-1 (10 μM) increased BK Ca channel activity. It is suggested that YC-1-induced vasorelaxation is partially mediated by the activation of K + channels.
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