6533b834fe1ef96bd129cdde

RESEARCH PRODUCT

Involvement of K+ channels in the relaxant effects of YC-1 in vascular smooth muscle

Rikuo OchiHermann NawrathSabine SeitzRolf GerhardAndreas JostJohanna RuppMakino WatanabeJörg W. WegenerAsher Shainberg

subject

MaleIndazolesPotassium ChannelsTime FactorsVascular smooth muscleCharybdotoxinMuscle RelaxationGuinea PigsAorta ThoracicIn Vitro TechniquesPharmacologyMuscle Smooth VascularMembrane PotentialsRats Sprague-DawleyGlibenclamidePhenylephrinechemistry.chemical_compoundmedicine.arterymedicineAnimalsDrug InteractionsPhenylephrinePharmacologyAortaTetraethylammoniumDose-Response Relationship DrugChemistryAnatomyIberiotoxinRatsVasodilationCarotid ArteriesPotassiumFemaleZaprinastmedicine.drug

description

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

yearjournalcountryeditionlanguage
1999-11-11European Journal of Pharmacology
https://doi.org/10.1016/s0014-2999(99)00574-9