ArticleBritish journal of pharmacology2009
Nitroxyl anion--the universal signalling partner of endogenously produced nitric oxide?
Article in British journal of pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Angeli's Salt, a nitroxyl anion donor, reverses endothelin-1 mediated vascular dysfunction in murine aorta.European journal of pharmacology · 2017Article
- Role of reactive oxygen and nitrogen species in the vascular responses to inflammation.Free radical biology & medicine · 2012Review
- Endothelium-derived hyperpolarising factors and associated pathways: a synopsis.Pflugers Archiv : European journal of physiology · 2010Review
- Robert F. Furchgott, Nobel laureate (1916-2009)--a personal reflection.British journal of pharmacology · 2009Article
- Endothelium in pharmacology: 30 years on.British journal of pharmacology · 2009Article
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Abstract
Although it is generally assumed that the primary product of the three isoforms of NO synthase is the nitric oxide radical (NO(*)), growing evidence suggests that the one-electron reduced form of nitrogen monoxide, nitroxyl anion (NO(-)), may be a natural co-product. Thus, evidence from conduit and resistance arteries and nitrergically innervated tissues indicates that NO(-) exerts widespread signalling functions alongside NO(*) in the cardiovascular and autonomic nervous systems, and perhaps beyond. In this issue of the BJP Andrews et al. add to this debate by providing strong evidence that NO(*) and HNO both contribute to the EDRF-mediated component of in mouse (MMA) and rat (RMA) mesenteric resistance arteries.
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