Nitric oxide-dependent vasodilation induced by minoxidil in isolated rat aortaopen access
- Lee, Soo Hee; Ok, Seong-Ho; Kang, Dawon; Kim, Hyun-Jin; Ahn, Seung Hyun; Bae, Sung Il; Kim, Ji-Yoon; Kim, Eun-Jin; Kim, Sunmin; Hwag, Yeran; Sohn, Ju-Tae
- Issue Date
- GENERAL PHYSIOL AND BIOPHYSICS
- Minoxidil; Lipid emulsion; Vasodilation; Nitric oxide; Toxic dose
- GENERAL PHYSIOLOGY AND BIOPHYSICS, v.40, no.3, pp.197 - 206
- Journal Title
- GENERAL PHYSIOLOGY AND BIOPHYSICS
- Start Page
- End Page
- 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, N-W-nitro-L-arginine methyl ester (L-NAME), methylene blue, 1H-[1,24 ]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. lIowever, 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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- College of Medicine > Department of Medicine > Journal Articles
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