title: Nitroxyl anion--the universal signalling partner of endogenously produced nitric oxide?
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.
authors.affiliation: Integrative & Systems Biology, Faculty of Biomedical & Life Sciences, University of Glasgow, Glasgow, UK. W.Martin@bio.gla.ac.uk
authors.forename: William
authors.initials: W
authors.lastname: Martin
mesh_terms: D000818:Animals; D000838:Anions / Q000378:metabolism*; D016232:Endothelins / Q000502:physiology; D045462:Endothelium-Dependent Relaxing Factors / Q000502:physiology; D008638:Mesenteric Arteries / Q000378:metabolism / Q000502:physiology; D051379:Mice; D009569:Nitric Oxide / Q000502:physiology*; D009589:Nitrogen Oxides / Q000378:metabolism*; D051381:Rats; D015398:Signal Transduction / Q000502:physiology; D014664:Vasodilation / Q000502:physiology
chemical_list: D000838:Anions; D016232:Endothelins; D045462:Endothelium-Dependent Relaxing Factors; D009589:Nitrogen Oxides; D009569:Nitric Oxide; C039900:nitroxyl