Modulatory Effect of 2-(4-Hydroxyphenyl)amino-1,4-naphthoquinone on Endothelial Vasodilation in Rat Aorta
Author
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Palacios, Javier
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Cifuentes, Fredi
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Valderrama, Jaime A.
Author
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Benites, Julio
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Ríos, David
Author
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González, Constanza
Author
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Chiong Lay, Mario
Author
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Cartes Saavedra, Benjamín
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Lafourcade, Carlos
Author
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Wyneken, Úrsula
Admission date
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2017-03-01T20:44:15Z
Available date
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2017-03-01T20:44:15Z
Publication date
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2016
Cita de ítem
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Oxidative Medicine and Cellular Longevity. Número de artículo: 3939540
es_ES
Identifier
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10.1155/2016/3939540
Identifier
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https://repositorio.uchile.cl/handle/2250/142898
Abstract
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The vascular endotheliumplays 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. Q7 reduced 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 CaCl2 was added to a calcium-free medium but did not affect the influx of calcium from extracellular space. Q7 increased 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, Q7 induced 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.