{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,19]],"date-time":"2026-09-19T16:28:10Z","timestamp":1789835290006,"version":"4.0.1"},"reference-count":54,"publisher":"Wiley","issue":"16","license":[{"start":{"date-parts":[[2020,6,12]],"date-time":"2020-06-12T00:00:00Z","timestamp":1591920000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2020,8]]},"abstract":"Key points<\/jats:title>\nATP\u2010sensitive K+<\/jats:sup> (KATP<\/jats:sub>) channels mediate hypoxia\u2010induced cerebral vasodilatation and hyperperfusion in animals.<\/jats:p><\/jats:list-item>\nWe tested whether KATP<\/jats:sub> channels blockade affects the increase in human cerebral blood flow (CBF) and the maintenance of oxygen delivery (CDO2<\/jats:sub>) during hypoxia.<\/jats:p><\/jats:list-item>\nHypoxia\u2010induced increases in the anterior circulation and total cerebral perfusion were attenuated under KATP<\/jats:sub> channels blockade affecting the relative changes of brain oxygen delivery.<\/jats:p><\/jats:list-item>\nTherefore, in humans, KATP<\/jats:sub> channels activation modulates the vascular tone in the anterior circulation of the brain, contributing to CBF and CDO2<\/jats:sub> responses to hypoxia.<\/jats:p><\/jats:list-item>\n<\/jats:list><\/jats:p><\/jats:sec>Abstract<\/jats:title>ATP\u2010sensitive K+<\/jats:sup> (KATP<\/jats:sub>) channels mediate hypoxia\u2010induced cerebral vasodilatation and hyperperfusion in animals. We tested whether KATP<\/jats:sub> channels blockade affects the increase in cerebral blood flow (CBF) and the maintenance of oxygen delivery (CDO2<\/jats:sub>) during hypoxia in humans. Nine healthy men were exposed to 5\u2010min trials of normoxia and isocapnic hypoxia (IHX, 10% O2<\/jats:sub>) before (BGB) and 3\u00a0h after glibenclamide ingestion (AGB). Mean arterial pressure (MAP), arterial saturation (), partial pressure of oxygen () and carbon dioxide (), internal carotid artery blood flow (ICABF), vertebral artery blood flow (VABF), total (t)CBF (Doppler ultrasound) and CDO2<\/jats:sub> were quantified during the trials. IHX provoked similar reductions in and , while MAP was not affected by oxygen desaturation or KATP<\/jats:sub> blockade. A smaller increase in ICABF (\u0394BGB: 36\u00a0\u00b1\u00a023 vs<\/jats:italic>. \u0394AGB 11\u00a0\u00b1\u00a018%, p<\/jats:italic>\u00a0=\u00a00.019) but not in VABF (\u2206BGB 26\u00a0\u00b1\u00a021 vs<\/jats:italic>. \u2206AGB 27\u00a0\u00b1\u00a027%, p<\/jats:italic>\u00a0=\u00a00.893) was observed during the hypoxic trial under KATP<\/jats:sub> channels blockade. Thus, IHX\u2010induced increases in tCBF (\u2206BGB 32\u00a0\u00b1\u00a019 vs<\/jats:italic>. \u2206AGB 14\u00a0\u00b1\u00a013%, p<\/jats:italic>\u00a0=\u00a00.012) and CDO2<\/jats:sub> relative changes (\u2206BGB 7\u00a0\u00b1\u00a013 vs<\/jats:italic>. \u2206AGB \u22126\u00a0\u00b1\u00a014%, p<\/jats:italic>\u00a0=\u00a00.048) were attenuated during the AGB hypoxic trial. In a separate protocol, 6 healthy men (5 from protocol 1) underwent a 5\u2010min exposure to normoxia and IHX before and 3\u00a0h after placebo (5\u00a0mg of cornstarch) ingestion. IHX reduced and , but placebo did not affect the ICABF, VABF, tCBF, or CDO2<\/jats:sub> responses. Therefore, in humans, KATP<\/jats:sub> channels activation modulates vascular tone in the anterior rather than the posterior circulation of the brain, contributing to tCBF and CDO2<\/jats:sub> responses to hypoxia.<\/jats:p><\/jats:sec>","DOI":"10.1113\/jp279751","type":"journal-article","created":{"date-parts":[[2020,5,28]],"date-time":"2020-05-28T09:05:10Z","timestamp":1590656710000},"page":"3343-3356","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":22,"title":["KATP<\/sub> channels modulate cerebral blood flow and oxygen delivery during isocapnic hypoxia in humans"],"prefix":"10.1113","volume":"598","author":[{"given":"Marcos P.","family":"Rocha","sequence":"first","affiliation":[{"name":"Laboratory of Exercise Sciences Department of Physiology and Pharmacology Fluminense Federal University RJ Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Monique O.","family":"Campos","sequence":"additional","affiliation":[{"name":"Laboratory of Exercise Sciences Department of Physiology and Pharmacology Fluminense Federal University RJ Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jo\u00e3o D.","family":"Mattos","sequence":"additional","affiliation":[{"name":"Laboratory of Exercise Sciences Department of Physiology and Pharmacology Fluminense Federal University RJ Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3441-9910","authenticated-orcid":false,"given":"Daniel E.","family":"Mansur","sequence":"additional","affiliation":[{"name":"Laboratory of Exercise Sciences Department of Physiology and Pharmacology Fluminense Federal University RJ Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Helena N. 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