{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T16:34:58Z","timestamp":1792773298043,"version":"4.5.0"},"reference-count":64,"publisher":"Wiley","license":[{"start":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T00:00:00Z","timestamp":1792713600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T00:00:00Z","timestamp":1792713600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100000024","name":"Canadian Institutes of Health Research","doi-asserted-by":"publisher","award":["RN291964\u2010366421"],"award-info":[{"award-number":["RN291964\u2010366421"]}],"id":[{"id":"10.13039\/501100000024","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000024","name":"Canadian Institutes of Health Research","doi-asserted-by":"publisher","award":["202210REH\u2010494703\u2010403917"],"award-info":[{"award-number":["202210REH\u2010494703\u2010403917"]}],"id":[{"id":"10.13039\/501100000024","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000038","name":"Natural Sciences and Engineering Research Council of Canada","doi-asserted-by":"publisher","award":["RGPIN\u20102026\u201005607"],"award-info":[{"award-number":["RGPIN\u20102026\u201005607"]}],"id":[{"id":"10.13039\/501100000038","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Physiology"],"abstract":"<jats:sec>\n                    <jats:title>Abstract<\/jats:title>\n                    <jats:p>\n                      Spinal sympathetic preganglionic neurons (SSPNs) are oxygen sensitive. These spinal oxygen sensors (SOS) increase sympathetic output when subjected to acute hypoxia, orchestrating cardiorespiratory responses to protect against the deleterious effects of oxygen deprivation. Most other oxygen\u2010sensing systems rely on mitochondrial mechanisms to detect and signal decreases in oxygen. Here, we apply pharmacological blockers of the mitochondrial respiratory chain and a mitochondrial\u2010targeted antioxidant to a rat perfused\n                      <jats:italic>in situ<\/jats:italic>\n                      spinal cord preparation to test the role of mitochondria in the SOS. We demonstrate that, unlike other oxygen\u2010sensitive cells, the mitochondrial respiratory chain is not essential for the SOS. Nonetheless, blockade of mitochondrial respiratory complexes augments SSPN activity. These results indicate that mitochondrial reactive oxygen species (ROS) can increase SSPN activity but do not appear to drive the SOS. We propose that, in chronic diseases prone to oxidative stress and\/or frequent hypoxic events, SSPN mitochondrial ROS directly contribute to sympathetic overactivity.\n                      <jats:boxed-text content-type=\"graphic\" position=\"anchor\">\n                        <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/tjp70853-gra-0001-m.png\">\n                          <jats:alt-text>image<\/jats:alt-text>\n                        <\/jats:graphic>\n                      <\/jats:boxed-text>\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key points<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>Decreases in oxygen concentration are detected by oxygen\u2010sensitive cells that orchestrate cardiorespiratory and vascular adjustments to avoid oxygen deprivation to vital tissues.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Recently discovered spinal oxygen sensors (SOS) increase sympathetic and respiratory activity in response to hypoxia.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Unlike other oxygen\u2010sensitive cells, here we report that the SOS do not rely on the mitochondrial electron transport chain for oxygen sensing.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Our findings show that pharmacological blockade of mitochondrial respiratory complexes can increase sympathetic activity but does not inhibit the hypoxic response.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>These results indicate that mitochondrial reactive oxygen species can affect sympathetic activity, but that mitochondria do not appear to play a key role in spinal oxygen sensing.<\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1113\/jp289341","type":"journal-article","created":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T14:46:43Z","timestamp":1792766803000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Mitochondrial electron transport chain activity is not essential for the acute hypoxic response of spinal oxygen sensors"],"prefix":"10.1113","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3793-2955","authenticated-orcid":false,"given":"Marina R.","family":"Sartori","sequence":"first","affiliation":[{"name":"Department of Physiology and Pharmacology, Cumming School of Medicine Hotchkiss Brain Institute and Alberta Children's Hospital Research Institute, University of Calgary  Calgary Alberta Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0003-0751-0126","authenticated-orcid":false,"given":"Amna","family":"Amir","sequence":"additional","affiliation":[{"name":"School of Nursing and Midwifery Mount Royal University  Calgary Alberta Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9942-4775","authenticated-orcid":false,"given":"Richard J. A.","family":"Wilson","sequence":"additional","affiliation":[{"name":"Department of Physiology and Pharmacology, Cumming School of Medicine Hotchkiss Brain Institute and Alberta Children's Hospital Research Institute, University of Calgary  Calgary Alberta Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,10,23]]},"reference":[{"issue":"29","key":"e_1_2_5_2_1","doi-asserted-by":"crossref","first-page":"10460","DOI":"10.1523\/JNEUROSCI.0045-15.2015","article-title":"Functional oxygen sensitivity of astrocytes","volume":"35","author":"Angelova P. R.","year":"2015","journal-title":"Journal of Neuroscience"},{"issue":"12","key":"e_1_2_5_3_1","first-page":"1273","article-title":"Mitochondria\u2010targeted plastoquinone derivatives as tools to interrupt execution of the aging program. 1. Cationic plastoquinone derivatives: Synthesis and in vitro studies","volume":"73","author":"Antonenko Y. 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