Nitric Oxide-Dependent Vasodilation Induced by Minoxidil in Isolated Rat Aorta

June 2021 in “ General physiology and biophysics ”

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 Hwag, Ju-Tae Sohn

minoxidil vasodilation endothelium L-NAME methylene blue ODQ glibenclamide lipid emulsion ATP-sensitive potassium channels nitric oxide guanylate cyclase Rogaine

Studysummary In this study, minoxidil-induced vasodilation in rat aorta was found to be mediated by ATP-sensitive potassium channels and nitric oxide pathways, but was not significantly altered by lipid emulsion pretreatment.

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The study investigated the vasodilatory effects of minoxidil at a toxic dose on isolated rat aorta, focusing on the role of the endothelium and lipid emulsion. It was found that minoxidil-induced vasodilation was more pronounced in endothelium-intact aorta compared to endothelium-denuded aorta. The vasodilation was significantly reduced by treatments with L-NAME, methylene blue, ODQ, and glibenclamide, and almost completely eliminated by the combination of L-NAME and glibenclamide. Lipid emulsion pretreatment did not significantly affect minoxidil-induced vasodilation, membrane hyperpolarization, or minoxidil concentration. The results suggest that minoxidil-induced vasodilation is mediated by ATP-sensitive potassium channels and pathways involving nitric oxide and guanylate cyclase.

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