Nitrite as Regulator of Hypoxic Signaling in Mammalian Physiology
2009
van Faassen, Ernst E. | Bahrami, Soheyl | Feelisch, Martin | Hogg, Neil | Kelm, Malte | Kim-Shapiro, Daniel B. | Kozlov, Andrey V. | Li, Haitao | Lundberg, Jon O. | Mason, Ron | Nohl, Hans | Rassaf, Tienush | Samouilov, Alexandre | Slama-Schwok, Anny | Shiva, Sruti | Vanin, Anatoly F. | Weitzberg, Eddie | Zweier, Jay | Gladwin, Mark T. | Universiteit Utrecht / Utrecht University [Utrecht] | AUVA Research Center ; Partenaires INRAE | University of Warwick [Coventry] | Medical College of Wisconsin | RWTH Aachen University = Rheinisch-Westfälische Technische Hochschule Aachen (RWTH Aachen) | Wake Forest University | The Ohio State University [Columbus] (OSU) | Karolinska Institutet [Stockholm] | Research Triangle Park | University of Veterinary Medicine [Vienna] (Vetmeduni) | Unité de recherche Virologie et Immunologie Moléculaires (VIM (UR 0892)) ; Institut National de la Recherche Agronomique (INRA) | National Institutes of Health [Bethesda, MD, USA] (NIH) | Russian Academy of Sciences [Moscow] (RAS) | University of Pittsburgh School of Medicine ; Pennsylvania Commonwealth System of Higher Education (PCSHE)
International audience
Mostrar más [+] Menos [-]Inglés. In this review we consider the effects of endogenous and pharmacological levels of nitrite under conditions of hypoxia. In humans, the nitrite anion has long been considered as metastable intermediate in the oxidation of nitric oxide radicals to the stable metabolite nitrate. This oxidation cascade was thought to be irreversible under physiological conditions. However, a growing body of experimental observations attests that the presence of endogenous nitrite regulates a number of signaling events along the physiological and pathophysiological oxygen gradient. Hypoxic signaling events include vasodilation, modulation of mitochondrial respiration, and cytoprotection following ischemic insult. These phenomena are attributed to the reduction of nitrite anions to nitric oxide if local oxygen levels in tissues decrease. Recent research identified a growing list of enzymatic and nonenzymatic pathways for this endogenous reduction of nitrite. Additional direct signaling events not involving free nitric oxide are proposed. We here discuss the mechanisms and properties of these various pathways and the role played by the local concentration of free oxygen in the affected tissue.
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