Nitroxyl anion--the universal signalling partner of endogenously produced nitric oxide?
- PMID: 19630833
- PMCID: PMC2707965
- DOI: 10.1111/j.1476-5381.2009.00153.x
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.
Comment on
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A role for nitroxyl (HNO) as an endothelium-derived relaxing and hyperpolarizing factor in resistance arteries.Br J Pharmacol. 2009 Jun;157(4):540-50. doi: 10.1111/j.1476-5381.2009.00150.x. Epub 2009 Mar 26. Br J Pharmacol. 2009. PMID: 19338582 Free PMC article.
References
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- Dierks EA, Burstyn JN. Nitric oxide (NO.), the only nitrogen monoxide redox form capable of activating soluble guanylate cyclase. Biochem Pharmacol. 1996;51:1593–1600. - PubMed
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