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Because K\n                    <jats:sub>2P<\/jats:sub>\n                    3\/9 activity is sensitive to cytosolic ATP concentration ([ATP]\n                    <jats:sub>cyt<\/jats:sub>\n                    , K\n                    <jats:sub>1\/2<\/jats:sub>\n                    \u2009\u2248\u20092.5\u2009mM), it has been proposed that hypoxia suppresses mitochondrial ATP production and thereby reduces [ATP]\n                    <jats:sub>cyt<\/jats:sub>\n                    to inhibit K\n                    <jats:sub>2P<\/jats:sub>\n                    3\/9 activity. To test this hypothesis, we developed a K\n                    <jats:sub>ATP<\/jats:sub>\n                    channel\u2010based bioassay using a patch\u2010cramming approach to measure [ATP]\n                    <jats:sub>cyt<\/jats:sub>\n                    in living cells. Co\u2010expression of Kir6.2(\u0394C36\u2010R50G) and SUR1(G1485D) in HEK293 cells formed a functional K\n                    <jats:sub>ATP<\/jats:sub>\n                    channel (designated R50G*) with markedly reduced ATP sensitivity. In inside\u2010out patches, normalized R50G* () activity showed ~100\u2010fold lower ATP sensitivity (K\n                    <jats:sub>1\/2<\/jats:sub>\n                    \u2009\u2248\u20092.0\u2009mM) than that of the wild\u2010type K\n                    <jats:sub>ATP<\/jats:sub>\n                    (K\n                    <jats:sub>1\/2<\/jats:sub>\n                    \u2009\u2248\u200920\u2009\u03bcM). Inside\u2010out patches from HEK293 cells containing R50G* were crammed into CB cells under normoxia (21% O\n                    <jats:sub>2<\/jats:sub>\n                    ), exposing the patch to the CB cell cytoplasm. Based on  activity in crammed CB cells, [ATP]\n                    <jats:sub>cyt<\/jats:sub>\n                    was estimated to be ~4.9\u2009mM in normoxia. In CB cells, hypoxia (1% O\n                    <jats:sub>2<\/jats:sub>\n                    , 15\u2009s) did not affect  activity, indicating that [ATP]\n                    <jats:sub>cyt<\/jats:sub>\n                    remained stable during hypoxia. FCCP (1\u2009\u03bcM), a mitochondrial uncoupler, increased  activity, which corresponded to [ATP]\n                    <jats:sub>cyt<\/jats:sub>\n                    of ~3.7\u2009mM. As hypoxia (~1% O\n                    <jats:sub>2<\/jats:sub>\n                    ) inhibited K\n                    <jats:sub>2P<\/jats:sub>\n                    3\/9 activity by 65% within 5\u2009s, our result demonstrates that inhibition of K\n                    <jats:sub>2P<\/jats:sub>\n                    3\/9 by hypoxia is independent of [ATP]\n                    <jats:sub>cyt<\/jats:sub>\n                    and that ATP depletion is unlikely to be the initiating signal for hypoxia\u2010induced excitation of CB cells.\n                  <\/jats:p>","DOI":"10.1111\/apha.70294","type":"journal-article","created":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T05:35:59Z","timestamp":1787031359000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Acute Hypoxia Inhibits\n                    <scp>\n                      K\n                      <sub>2P<\/sub>\n                      3\n                    <\/scp>\n                    \/9 (\n                    <scp>TASK1<\/scp>\n                    \/3) Independently of Cytosolic\n                    <scp>ATP<\/scp>\n                    in Carotid Body Type 1 Cells"],"prefix":"10.1111","volume":"242","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7402-7298","authenticated-orcid":false,"given":"Dawon","family":"Kang","sequence":"first","affiliation":[{"name":"Department of Physiology, College of Medicine Gyeongsang National University  Jinju Korea"},{"name":"Institute of Medical Science Gyeongsang National University  Jinju Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiaju","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics Chicago Medical School, Rosalind Franklin University of Medicine and Science  North Chicago Illinois USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Donghee","family":"Kim","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics Chicago Medical School, Rosalind Franklin University of Medicine and Science  North Chicago Illinois 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