Please use this identifier to cite or link to this item: http://hdl.handle.net/20.500.12779/4407
Title: 2,5-Di-t-butyl-1,4-benzohydroquinone induces endothelium-dependent relaxation of rat thoracic aorta
Authors: Fusi, Fabio 
Valoti, Massimo
Frosini, Maria
Sgaragli, GIAN PIETRO
Keywords: Antioxidant activity; Smooth Muscle
Issue Date: 1999
Project: None 
Journal: EUROPEAN JOURNAL OF PHARMACOLOGY
Abstract: 
The aim of this work was to clarify the mechanism by which 2,5-di-t-butyl-1,4-benzohydroquinone (BHQ) induces relaxation of rat thoracic aorta. In particular, the role of endothelium-derived nitric oxide (NO) was investigated. BHQ concentration dependently (0.1-10 microM) relaxed rat aorta rings precontracted with phenylephrine. This effect was dependent on the intactness of the endothelium, suppressed by preincubation with 100 microM N(omega)-nitro-L-arginine methyl ester and antagonised by 3-30 microM methylene blue. The 10 microM BHQ-induced relaxation, however, was followed by the gradual and slow return to phenylephrine-induced tone. Superoxide dismutase (250 U/ml) increased the BHQ-induced relaxation, while preincubation with 3 mM diethyldithiocarbamate inhibited it in a time-dependent fashion. BHQ gave rise to superoxide anion formation which was markedly inhibited by the addition of superoxide dismutase (250 U/ml), either in the presence or in the absence of aorta rings. The non-specific blocker of Ca2+ channels, Ni2+, concentration dependently attenuated the BHQ relaxing effect. BHQ did not modify the relaxation induced by the NO donor 3-morpholino-sydnonimine in endothelium-deprived rings. In conclusion, BHQ induces endothelium-dependent relaxation and gives rise, by auto-oxidation, to the formation of superoxide anion. The former effect results from the enhanced synthesis of NO rather than from its enhanced biological activity; NO synthase is presumed to be stimulated by BHQ-induced activation of Ca2+ influx through Ni2+-sensitive Ca2+ channels
Description: 
37070
URI: http://hdl.handle.net/20.500.12779/4407
ISSN: 0014-2999
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