title: Nitrite, NO and hypoxic vasodilation.
abstract: The ability to deliver oxygen and other nutrients to working tissues at a rate acutely matched to demand is the quintessential function of the cardiovascular system. Thus, an understanding of the biochemical mechanisms involved in hypoxic vasodilation remains a major goal in vascular biology. Nitric oxide, its metabolites, and oxidation status are recognized as playing important roles in this process. Previous work examining how nitrite can be converted to bioactive nitric oxide (NO) under hypoxic conditions has focused on the role of the red blood cell and haemoglobin. In a recent issue of the British Journal of Pharmacology, Pinder et al. demonstrate that plasma nitrite, in the absence of haemoglobin, is capable of increasing the maximal dilation of rabbit aortic rings under hypoxic conditions. Furthermore, they demonstrate that this relaxation can occur with or without the endothelium. This observation, even if it is only a small proportion of the relaxant activity of nitrite, highlights how NO metabolites may be involved in a variety of mechanisms of vessel control.
authors.affiliation: Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA. j.d.allen@duke.edu
authors.forename: Jason D
authors.initials: JD
authors.lastname: Allen
authors.forename: Andrew J
authors.initials: AJ
authors.lastname: Gow
mesh_terms: D000818:Animals; D001013:Aorta, Thoracic / Q000378:metabolism; D015687:Cell Hypoxia; D004730:Endothelium, Vascular / Q000378:metabolism; D006801:Humans; D009569:Nitric Oxide / Q000378:metabolism*; D009573:Nitrites / Q000378:metabolism*; D010100:Oxygen / Q000378:metabolism; D011817:Rabbits; D014664:Vasodilation
chemical_list: D009573:Nitrites; D009569:Nitric Oxide; D010100:Oxygen