ArticleNaunyn-Schmiedeberg's archives of pharmacology2018
Activation of NQO-1 mediates the augmented contractions of isolated arteries due to biased activity of soluble guanylyl cyclase in their smooth muscle.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 5 citations in OpenAlex.
- The Role of Hydrogen Sulfide in the Regulation of the Pulmonary Vasculature in Health and Disease.Antioxidants (Basel, Switzerland) · 2025Review
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3 authors at 2 institutions in 2 countries.
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Abstract
Earlier studies on isolated arteries demonstrated that the para-quinone thymoquinone, like acute hypoxia, induces augmentation of contractions, depending on biased activity of soluble guanylyl cyclase (sGC), generating inosine-3',5'-cyclic monophosphate (cyclic IMP) rather than guanosine-3',5'-cyclic monophosphate (cyclic GMP). NAD(P)H:quinone oxidoreductase 1 (NQO-1), the enzyme responsible for biotransformation of quinones into hydroquinones, was examined for its involvement in these endothelium-dependent augmentations, establishing a link between the metabolism of quinones by NQO-1 and biased sGC activity. Isolated arteries of Sprague-Dawley rats (aortae and mesenteric arteries) and farm pigs (coronary arteries) were studied for measurement of changes in tension and collected to measure NQO-1 activity or its protein level. β-lapachone, an ortho-quinone and hence substrate of NQO-1, increased the activity of the enzyme and augmented contractions in arteries with endothelium. This augmentation was inhibited by endothelium removal and inhibitors of endothelial NO synthase (eNOS), sGC, or NQO-1; in preparations without endothelium or treated with an eNOS inhibitor, it was restored by the NO donor DETA NONOate and by ITP and cyclic IMP, revealing biased sGC activity as the underlying mechanism, as with thymoquinone. Hydroquinone, the end product of quinone metabolism by NQO-1, augmented contractions depending on sGC activation but in an endothelium-independent manner. In coronary arteries, repeated acute hypoxia caused similar augmentations as those to quinones that were inhibited by the NQO-1 inhibitor dicoumarol. Augmentations of contraction observed with different naturally occurring quinones and with acute hypoxia are initiated by quinone metabolism by NQO-1, in turn interfering with the NO/biased sGC pathway, suggesting a possibly detrimental role of this enzyme in ischemic cardiovascular disorders.
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