Nitric oxide-dependent vasodilation induced by minoxidil in isolated rat aorta

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, N W -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.

Endocrine Disruptor Bisphenol a Affects the Neurochemical Profile of Nerve Fibers in the Aortic Arch Wall in the Domestic Pig

“…The next group of fibers, in which the number clearly changed after administration of BPA at a dosage of 0.5 mg/kg b.w./day, included the fibers containing nNOS, which is a marker of nitrergic nerves [5]. Nitric oxide (NO) in the arteries (similar to CGRP) shows relaxant activity, and, therefore, it is considered to be one of the most important vasodilators [65,66]. Thus, the increase in the number of nerves containing nNOS may result from the influence of BPA on the aortic muscles.…”