General Physiology and Biophysics Vol.40, No.3, p.197–206, 2021
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Title: Nitric oxide-dependent vasodilation induced by minoxidil in isolated rat aorta |
Author: Soo Hee Lee, Seong-Ho Ok, Dawon Kang, Hyun-Jin Kim, Seung Hyun Ahn, Sung Il Bae, Ji-Yoon Kim, Eun-Jin Kim, Sunmin Kim, Yeran Hwang, Ju-Tae Sohn |
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Abstract: We examined the effect of endothelium and lipid emulsion on vasodilation induced by minoxidil at a toxic dose and determined the underlying mechanism. The effects of endothelial denudation, NW-nitro-L-arginine methyl ester (L-NAME), methylene blue, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), and glibenclamide, alone or in combination, on minoxidil-induced vasodilation in endothelium-intact rat aorta were examined. Additionally, the effects of lipid emulsion on minoxidil-induced membrane hyperpolarization and minoxidil concentration were examined. The vasodilatory effects of minoxidil at the toxic dose were higher in endothelium-intact aorta than in endothelium-denuded aorta. L-NAME, methylene blue, ODQ, and glibenclamide attenuated minoxidil-induced vasodilation of endothelium-intact rat aorta. Combined treatment with L-NAME and glibenclamide almost eliminated minoxidil-induced vasodilation. However, lipid emulsion pretreatment did not significantly alter minoxidil-induced vasodilation. Lipid emulsion did not significantly alter minoxidil-induced membrane hyperpolarization and minoxidil concentration. Overall, minoxidil-induced vasodilation is mediated by ATP-sensitive potassium channels and pathways involving nitric oxide and guanylate cyclase.
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Keywords: Minoxidil — Lipid emulsion — Vasodilation — Nitric oxide — Toxic dose |
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Published online: 09-Jun-2021
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Year: 2021, Volume: 40, Issue: 3 |
Page From: 197, Page To: 206 |
doi:10.4149/gpb_2021012
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