1. Nitric oxide-dependent vasodilation induced by minoxidil in isolated rat aorta
- Author
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Sung Il Bae, Soo Hee Lee, Dawon Kang, Ji Yoon Kim, Seong-Ho Ok, Sun Min Kim, Hyun Jin Kim, Eun Jin Kim, Ju-Tae Sohn, Seung Hyun Ahn, and Yeran Hwag
- Subjects
Nitric Oxide Synthase Type III ,Endothelium ,Physiology ,Biophysics ,Vasodilation ,Pharmacology ,Nitric Oxide ,Nitric oxide ,Glibenclamide ,chemistry.chemical_compound ,medicine.artery ,medicine ,Animals ,Aorta ,General Medicine ,Membrane hyperpolarization ,Rats ,NG-Nitroarginine Methyl Ester ,medicine.anatomical_structure ,chemistry ,Minoxidil ,cardiovascular system ,Endothelium, Vascular ,Methylene blue ,medicine.drug - 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.
- Published
- 2021