Hydroxylamine-induced relaxation inhibited by K+ channel blockers in rat aortic rings.
Hydroxylamine, a putative endogenous nitric oxide donor, relaxed rat aorta in a concentration-dependent manner (0.01-30 microM). Removal of endothelium or pretreatment of aortic tissue with N(G)-nitro-L-arginine (L-NOARG, 100 microM) did not affect the relaxant effect of hydroxylamine but L-NOARG at 100 microM abolished the acetylcholine-induced relaxation. Methylene blue (10 microM) significantly reduced the relaxant effect of hydroxylamine in endothelium-denuded arteries. Tetrapentylammonium ions (0.3-3 microM), tetraethylammonium ions (1-3 mM) and charybdotoxin (100 nM) reduced the relaxant effect of hydroxylamine in the endothelium-denuded arteries while glibenclamide (3 microM) had no effect. Neither tetrapentylammonium nor tetraethylammonium ions affected relaxations induced by forskolin and verapamil. The effects of tetrapentylammonium ions (3 microM) and charybdotoxin (100 nM) were additive. Tetrapentylammonium ions (3 microM), tetraethylammonium ions (3 mM) and charybdotoxin (100 nM) decreased the relaxation induced by sodium nitroprusside in the endothelium-denuded arteries while glibenclamide (3 microM) had no effect. The concentration-relaxation curve for the relaxant effect of hydroxylamine was shifted to the right in the presence of high extracellular K+ (15-60 mM). Neither tetrapentylammonium ions (3 microM) nor charybdotoxin (100 nM) affected hydroxylamine-induced relaxation of the endothelium-denuded aorta precontracted with 60 mM K+. These results indicate that hydroxylamine relaxes the rat aorta partially through activation of tetrapentylammonium-, tetraethylammonium- and charybdotoxin-sensitive K+ channels and its action is comparable with that of sodium nitroprusside, an exogenous nitric oxide donor. The endothelium is not involved in the aortic response to hydroxylamine.
Huang
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Y
Department of Physiology, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, NT, China. yu-huang@cuhk.edu.hk
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects / Q000502:physiology; D002118:Calcium / Q000378:metabolism; D005576:Colforsin / Q000494:pharmacology; D004730:Endothelium, Vascular / Q000502:physiology; D005110:Extracellular Space / Q000378:metabolism; D019811:Hydroxylamine / Q000494:pharmacology*; D066298:In Vitro Techniques; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000187:drug effects* / Q000502:physiology; D009569:Nitric Oxide / Q000378:metabolism / Q000502:physiology; D009599:Nitroprusside / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism; D026902:Potassium Channel Blockers; D051381:Rats; D017207:Rats, Sprague-Dawley; D014664:Vasodilation / Q000187:drug effects*; D014665:Vasodilator Agents / Q000494:pharmacology*; D014700:Verapamil / Q000494:pharmacology
D026902:Potassium Channel Blockers; D014665:Vasodilator Agents; D009599:Nitroprusside; D005576:Colforsin; D019811:Hydroxylamine; D009569:Nitric Oxide; D000255:Adenosine Triphosphate; D014700:Verapamil; D011188:Potassium; D002118:Calcium