The vascular endothelium plays an essential role in the control of the blood flow. Pharmacological agents like quinone (menadione) at various doses modulate this process in a variety of ways. In this study,Q7, a 2-phenylamino-1,4-naphthoquinone derivative, significantly increased oxidative stress and induced vascular dysfunction at concentrations that were not cytotoxic to endothelial or vascular smooth muscle cells.Q7reduced nitric oxide (NO) levels and endothelial vasodilation to acetylcholine in rat aorta. It also blunted the calcium release from intracellular stores by increasing the phenylephrine-induced vasoconstriction when CaCl₂was added to a calcium-free medium but did not affect the influx of calcium from extracellular space.Q7increased the vasoconstriction to BaCl₂(10⁻³ M), an inward rectifying K⁺channels blocker, and blocked the vasodilation to KCl (10⁻² M) in aortic rings precontracted with BaCl₂. This was recovered with sodium nitroprusside (10⁻⁸ M), a NO donor. In conclusion,Q7induced vasoconstriction was through a modulation of cellular mechanisms involving calcium fluxes through K⁺channels, and oxidative stress induced endothelium damage. These findings contribute to the characterization of new quinone derivatives with low cytotoxicity able to pharmacologically modulate vasodilation.