Nitrite as regulator of hypoxic signaling in mammalian physiology
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...
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| creator | 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. |
| description | 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. © 2009 Wiley Periodicals, Inc. Med Res Rev, 29, No. 5, 683–741, 2009 |
| doi_str_mv | 10.1002/med.20151 |
| format | Article |
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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. © 2009 Wiley Periodicals, Inc. Med Res Rev, 29, No. 5, 683–741, 2009</description><identifier>ISSN: 0198-6325</identifier><identifier>ISSN: 1098-1128</identifier><identifier>EISSN: 1098-1128</identifier><identifier>DOI: 10.1002/med.20151</identifier><identifier>PMID: 19219851</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Animals ; Humans ; hypoxia ; Hypoxia - metabolism ; ischemia/reperfusion ; Life Sciences ; Medicin och hälsovetenskap ; Nitrates - blood ; Nitrates - metabolism ; nitric oxide ; Nitric Oxide - metabolism ; Nitric Oxide Synthase Type III - metabolism ; nitrite ; Nitrites - blood ; Nitrites - metabolism ; Oxidation-Reduction ; Oxygen - blood ; Oxygen - metabolism ; Rats ; Reperfusion Injury - metabolism ; Signal Transduction ; vasodilation ; Vasodilation - physiology</subject><ispartof>Medicinal research reviews, 2009-09, Vol.29 (5), p.683-741</ispartof><rights>2009 Wiley Periodicals, Inc.</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c6391-d69949c8c6686073f43ef21c3ef68501220b45e02404048168da1df42ce7eb9b3</citedby><cites>FETCH-LOGICAL-c6391-d69949c8c6686073f43ef21c3ef68501220b45e02404048168da1df42ce7eb9b3</cites><orcidid>0000-0002-6686-1677 ; 0000-0003-0060-1052 ; 0000-0002-2703-9728</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fmed.20151$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fmed.20151$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,552,780,784,885,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19219851$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.inrae.fr/hal-02667191$$DView record in HAL$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:119232175$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>van Faassen, Ernst E.</creatorcontrib><creatorcontrib>Bahrami, Soheyl</creatorcontrib><creatorcontrib>Feelisch, Martin</creatorcontrib><creatorcontrib>Hogg, Neil</creatorcontrib><creatorcontrib>Kelm, Malte</creatorcontrib><creatorcontrib>Kim-Shapiro, Daniel B.</creatorcontrib><creatorcontrib>Kozlov, Andrey V.</creatorcontrib><creatorcontrib>Li, Haitao</creatorcontrib><creatorcontrib>Lundberg, Jon O.</creatorcontrib><creatorcontrib>Mason, Ron</creatorcontrib><creatorcontrib>Nohl, Hans</creatorcontrib><creatorcontrib>Rassaf, Tienush</creatorcontrib><creatorcontrib>Samouilov, Alexandre</creatorcontrib><creatorcontrib>Slama-Schwok, Anny</creatorcontrib><creatorcontrib>Shiva, Sruti</creatorcontrib><creatorcontrib>Vanin, Anatoly F.</creatorcontrib><creatorcontrib>Weitzberg, Eddie</creatorcontrib><creatorcontrib>Zweier, Jay</creatorcontrib><creatorcontrib>Gladwin, Mark T.</creatorcontrib><title>Nitrite as regulator of hypoxic signaling in mammalian physiology</title><title>Medicinal research reviews</title><addtitle>Med. Res. Rev</addtitle><description>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. © 2009 Wiley Periodicals, Inc. Med Res Rev, 29, No. 5, 683–741, 2009</description><subject>Animals</subject><subject>Humans</subject><subject>hypoxia</subject><subject>Hypoxia - metabolism</subject><subject>ischemia/reperfusion</subject><subject>Life Sciences</subject><subject>Medicin och hälsovetenskap</subject><subject>Nitrates - blood</subject><subject>Nitrates - metabolism</subject><subject>nitric oxide</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric Oxide Synthase Type III - metabolism</subject><subject>nitrite</subject><subject>Nitrites - blood</subject><subject>Nitrites - metabolism</subject><subject>Oxidation-Reduction</subject><subject>Oxygen - blood</subject><subject>Oxygen - metabolism</subject><subject>Rats</subject><subject>Reperfusion Injury - metabolism</subject><subject>Signal Transduction</subject><subject>vasodilation</subject><subject>Vasodilation - physiology</subject><issn>0198-6325</issn><issn>1098-1128</issn><issn>1098-1128</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>D8T</sourceid><recordid>eNp1Uk1v3CAQRVWrZpv20D9Q-VQpBycMGGwulVZpkq20TasqUY6IxdhLYxsXvEn878t2na9KERIMM-89hplB6CPgQ8CYHLWmPCQYGLxCM8CiSAFI8RrNMESbU8L20LsQfmMMEUPfoj0QJIYYzND83A7eDiZRIfGm3jRqcD5xVbIee3dndRJs3anGdnViu6RVbRsvqkv69Risa1w9vkdvKtUE82E699Hl6cnF8SJd_jj7djxfpppTAWnJhciELjTnBcc5rTJqKgI67rxgGAjBq4wZTDIcVwG8KBWUVUa0yc1KrOg-Sne64db0m5XsvW2VH6VTVk6u62gZyZjgHCJevIjvvSsfSfdEiGWhBHIWuV923AiIxdWmG7xqnks8i3R2LWt3I0lOGIEsChzsBNb_0Rbzpdz6MOE8BwE320Q_T49592djwiBbG7RpGtUZtwmS5yzPgD8R1d6F4E31oAxYbgdBxozkv0GI2E9Pf_CInDofAUc7wK1tzPiykvx-8vVecmqADYO5e2Aofx1TpDmTV-dnUuDlz_ziF5EL-hcv2cyp</recordid><startdate>200909</startdate><enddate>200909</enddate><creator>van Faassen, Ernst E.</creator><creator>Bahrami, Soheyl</creator><creator>Feelisch, Martin</creator><creator>Hogg, Neil</creator><creator>Kelm, Malte</creator><creator>Kim-Shapiro, Daniel B.</creator><creator>Kozlov, Andrey V.</creator><creator>Li, Haitao</creator><creator>Lundberg, Jon O.</creator><creator>Mason, Ron</creator><creator>Nohl, Hans</creator><creator>Rassaf, Tienush</creator><creator>Samouilov, Alexandre</creator><creator>Slama-Schwok, Anny</creator><creator>Shiva, Sruti</creator><creator>Vanin, Anatoly F.</creator><creator>Weitzberg, Eddie</creator><creator>Zweier, Jay</creator><creator>Gladwin, Mark T.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>1XC</scope><scope>5PM</scope><scope>ADTPV</scope><scope>AOWAS</scope><scope>D8T</scope><scope>ZZAVC</scope><orcidid>https://orcid.org/0000-0002-6686-1677</orcidid><orcidid>https://orcid.org/0000-0003-0060-1052</orcidid><orcidid>https://orcid.org/0000-0002-2703-9728</orcidid></search><sort><creationdate>200909</creationdate><title>Nitrite as regulator of hypoxic signaling in mammalian physiology</title><author>van Faassen, Ernst E. ; 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| subjects | Animals Humans hypoxia Hypoxia - metabolism ischemia/reperfusion Life Sciences Medicin och hälsovetenskap Nitrates - blood Nitrates - metabolism nitric oxide Nitric Oxide - metabolism Nitric Oxide Synthase Type III - metabolism nitrite Nitrites - blood Nitrites - metabolism Oxidation-Reduction Oxygen - blood Oxygen - metabolism Rats Reperfusion Injury - metabolism Signal Transduction vasodilation Vasodilation - physiology |
| title | Nitrite as regulator of hypoxic signaling in mammalian physiology |
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