{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T07:13:22Z","timestamp":1773299602260,"version":"3.50.1"},"reference-count":31,"publisher":"American Physiological Society","issue":"9","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Cell Physiology"],"published-print":{"date-parts":[[2012,11,1]]},"abstract":"<jats:p> H<jats:sub>2<\/jats:sub>S generated by the enzyme cystathionine-\u03b3-lyase (CSE) has been implicated in O<jats:sub>2<\/jats:sub> sensing by the carotid body. The objectives of the present study were to determine whether glomus cells, the primary site of hypoxic sensing in the carotid body, generate H<jats:sub>2<\/jats:sub>S in an O<jats:sub>2<\/jats:sub>-sensitive manner and whether endogenous H<jats:sub>2<\/jats:sub>S is required for O<jats:sub>2<\/jats:sub> sensing by glomus cells. Experiments were performed on glomus cells harvested from anesthetized adult rats as well as age and sex-matched CSE<jats:sup>+\/+<\/jats:sup> and CSE<jats:sup>\u2212\/\u2212<\/jats:sup> mice. Physiological levels of hypoxia (Po<jats:sub>2<\/jats:sub> \u223c30 mmHg) increased H<jats:sub>2<\/jats:sub>S levels in glomus cells, and dl-propargylglycine (PAG), a CSE inhibitor, prevented this response in a dose-dependent manner. Catecholamine (CA) secretion from glomus cells was monitored by carbon-fiber amperometry. Hypoxia increased CA secretion from rat and mouse glomus cells, and this response was markedly attenuated by PAG and in cells from CSE<jats:sup>\u2212\/\u2212<\/jats:sup> mice. CA secretion evoked by 40 mM KCl, however, was unaffected by PAG or CSE deletion. Exogenous application of a H<jats:sub>2<\/jats:sub>S donor (50 \u03bcM NaHS) increased cytosolic Ca<jats:sup>2+<\/jats:sup> concentration ([Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>) in glomus cells, with a time course and magnitude that are similar to that produced by hypoxia. [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> responses to NaHS and hypoxia were markedly attenuated in the presence of Ca<jats:sup>2+<\/jats:sup>-free medium or cadmium chloride, a pan voltage-gated Ca<jats:sup>2+<\/jats:sup> channel blocker, or nifedipine, an L-type Ca<jats:sup>2+<\/jats:sup> channel inhibitor, suggesting that both hypoxia and H<jats:sub>2<\/jats:sub>S share common Ca<jats:sup>2+<\/jats:sup>-activating mechanisms. These results demonstrate that H<jats:sub>2<\/jats:sub>S generated by CSE is a physiologic mediator of the glomus cell's response to hypoxia. <\/jats:p>","DOI":"10.1152\/ajpcell.00100.2012","type":"journal-article","created":{"date-parts":[[2012,6,29]],"date-time":"2012-06-29T00:20:37Z","timestamp":1340929237000},"page":"C916-C923","source":"Crossref","is-referenced-by-count":62,"title":["Endogenous H<sub>2<\/sub>S is required for hypoxic sensing by carotid body glomus cells"],"prefix":"10.1152","volume":"303","author":[{"given":"Vladislav V.","family":"Makarenko","sequence":"first","affiliation":[{"name":"Institute for Integrative Physiology and Center for Systems Biology of O2 Sensing, University of Chicago, Chicago, Illinois;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jayasri","family":"Nanduri","sequence":"additional","affiliation":[{"name":"Institute for Integrative Physiology and Center for Systems Biology of O2 Sensing, University of Chicago, Chicago, Illinois;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gayatri","family":"Raghuraman","sequence":"additional","affiliation":[{"name":"Institute for Integrative Physiology and Center for Systems Biology of O2 Sensing, University of Chicago, Chicago, Illinois;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Aaron P.","family":"Fox","sequence":"additional","affiliation":[{"name":"Institute for Integrative Physiology and Center for Systems Biology of O2 Sensing, University of Chicago, Chicago, Illinois;"},{"name":"Department of Neurobiology, Physiology, and Pharmacology, University of Chicago, Chicago, Illinois;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Moataz M.","family":"Gadalla","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland; and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ganesh K.","family":"Kumar","sequence":"additional","affiliation":[{"name":"Institute for Integrative Physiology and Center for Systems Biology of O2 Sensing, University of Chicago, Chicago, Illinois;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Solomon H.","family":"Snyder","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland; and"},{"name":"The Solomon H. 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