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We hypothesized that COX contributes to both basal and hypoxic cerebral vasodilation, but COX-mediated vasodilation is greater in the posterior versus anterior cerebral circulation. CBF was measured in 9 healthy adults (28\u2009\u00b1\u20094 yr) during normoxia and isocapnic hypoxia (fraction of inspired oxygen\u2009=\u20090.11), with COX inhibition (oral indomethacin, 100mg) or placebo. Four-dimensional flow magnetic resonance imaging measured cross-sectional area (CSA) and blood velocity to quantify CBF in 11 cerebral arteries. Cerebrovascular conductance (CVC) was calculated (CVC\u2009=\u2009CBF \u00d7 100\/mean arterial blood pressure) and hypoxic reactivity was expressed as absolute and relative change in CVC [\u0394CVC\/\u0394 pulse oximetry oxygen saturation ([Formula: see text])]. At normoxic baseline, indomethacin reduced CVC by 44\u2009\u00b1\u20095% ( P &lt; 0.001) and artery CSA ( P &lt; 0.001), which was similar across arteries. Hypoxia ([Formula: see text] 80%\u201383%) increased CVC ( P &lt; 0.01), reflected as a similar relative increase in reactivity (% \u0394CVC\/\u2212\u0394[Formula: see text]) across arteries ( P &lt; 0.05), in part because of increases in CSA ( P &lt; 0.05). Indomethacin did not alter \u0394CVC or \u0394CVC\/\u0394[Formula: see text] to hypoxia. These findings indicate that 1) COX contributes, in a largely uniform fashion, to cerebrovascular tone during normoxia and 2) COX is not obligatory for hypoxic vasodilation in any regions supplied by large extracranial or intracranial arteries. <\/jats:p>","DOI":"10.1152\/ajpregu.00132.2019","type":"journal-article","created":{"date-parts":[[2019,12,23]],"date-time":"2019-12-23T10:39:58Z","timestamp":1577097598000},"page":"R468-R479","source":"Crossref","is-referenced-by-count":18,"title":["Differential contribution of cyclooxygenase to basal cerebral blood flow and hypoxic cerebral vasodilation"],"prefix":"10.1152","volume":"318","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7889-8146","authenticated-orcid":false,"given":"J. 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