Modulatory effect of 2-(4-hydroxyphenyl)amino-1,4-naphthoquinone on endothelial vasodilation in rat aorta

Palacios, Javier, Cifuentes, Fredi, Valderrama, Jaime A., Benites, Julio, Rios, David, Gonzalez, Constanza, Chiong, Mario, Cartes-Saavedra, Benjamin, Lafourcade, Carlos, Wyneken, Ursula, Gonzalez, Pamela, Owen, Gareth I., Pardo, Fabian, Sobrevia, Luis and Calderon, Pedro Buc (2016) Modulatory effect of 2-(4-hydroxyphenyl)amino-1,4-naphthoquinone on endothelial vasodilation in rat aorta. Oxidative Medicine and Cellular Longevity, 2016 . doi:10.1155/2016/3939540


Author Palacios, Javier
Cifuentes, Fredi
Valderrama, Jaime A.
Benites, Julio
Rios, David
Gonzalez, Constanza
Chiong, Mario
Cartes-Saavedra, Benjamin
Lafourcade, Carlos
Wyneken, Ursula
Gonzalez, Pamela
Owen, Gareth I.
Pardo, Fabian
Sobrevia, Luis
Calderon, Pedro Buc
Title Modulatory effect of 2-(4-hydroxyphenyl)amino-1,4-naphthoquinone on endothelial vasodilation in rat aorta
Journal name Oxidative Medicine and Cellular Longevity   Check publisher's open access policy
ISSN 1942-0994
1942-0900
Publication date 2016-01-01
Sub-type Article (original research)
DOI 10.1155/2016/3939540
Open Access Status DOI
Volume 2016
Total pages 12
Place of publication New York, NY, United States
Publisher Hindawi Publishing Corporation
Language eng
Formatted abstract
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. 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.
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: UQ Centre for Clinical Research Publications
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