{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,28]],"date-time":"2026-10-28T21:37:09Z","timestamp":1793223429772,"version":"4.5.0"},"reference-count":30,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Regulatory, Integrative and Comparative Physiology"],"published-print":{"date-parts":[[2010,4]]},"abstract":"<jats:p> Inhibitors of cyclooxygenase (COX)-2 prevent suppression of aquaporin-2 and reduce polyuria in the acute phase after release of bilateral ureteral obstruction (BUO). We hypothesized that BUO leads to COX-2-mediated local accumulation of prostanoids in inner medulla (IM) tissue. To test this, rats were subjected to BUO and treated with selective COX-1 or COX-2 inhibitors. Tissue was examined at 2, 6, 12, and 24 h after BUO. COX-2 protein abundance increased in IM 12 and 24 h after onset of BUO but did not change in cortex. COX-1 did not change at any time points in any region. A full profile of all five primary prostanoids was obtained by mass spectrometric determination of PGE<jats:sub>2<\/jats:sub>, PGF<jats:sub>2\u03b1<\/jats:sub>, 6-keto-PGF<jats:sub>1\u03b1<\/jats:sub>, PGD<jats:sub>2<\/jats:sub>, and thromboxane (Tx) B<jats:sub>2<\/jats:sub> concentrations in kidney cortex\/outer medulla and IM fractions. IM concentration of PGE<jats:sub>2<\/jats:sub>, 6-keto-PGF<jats:sub>1\u03b1<\/jats:sub>, and PGF<jats:sub>2\u03b1<\/jats:sub> was increased at 6 h BUO, and PGE<jats:sub>2<\/jats:sub> and PGF<jats:sub>2\u03b1<\/jats:sub> increased further at 12 h BUO. TxB<jats:sub>2<\/jats:sub> increased after 12 h BUO. 6-keto-PGF<jats:sub>1\u03b1<\/jats:sub> remained significantly increased after 24 h BUO. The COX-2 inhibitor parecoxib lowered IM PGE<jats:sub>2,<\/jats:sub> TxB<jats:sub>2<\/jats:sub>, 6-keto-PGF<jats:sub>1\u03b1<\/jats:sub>, and PGF<jats:sub>2\u03b1<\/jats:sub> below vehicle-treated BUO and sham rats at 6, 12 and, 24 h BUO. The COX-1 inhibitor SC-560 lowered PGE<jats:sub>2<\/jats:sub>, PGF<jats:sub>2\u03b1<\/jats:sub>, and PGD<jats:sub>2<\/jats:sub> in IM compared with untreated 12 h BUO, but levels remained significantly above sham. In cortex tissue, PGE<jats:sub>2<\/jats:sub> and 6-keto-PGF<jats:sub>1\u03b1<\/jats:sub> concentrations were elevated at 6 h only. In conclusion, COX-2 activity contributes to the transient increase in prostacyclin metabolite 6-keto-PGF<jats:sub>1\u03b1<\/jats:sub> and TxB<jats:sub>2<\/jats:sub> concentration in the kidney IM, and COX-2 is the predominant isoform that is responsible for accumulation of PGE<jats:sub>2<\/jats:sub> and PGF<jats:sub>2\u03b1<\/jats:sub> with minor, but significant, contributions from COX-1. PGD<jats:sub>2<\/jats:sub> synthesis is mediated exclusively by COX-1. In BUO, therapeutic interventions aimed at the COX-prostanoid pathway should target primarily COX-2. <\/jats:p>","DOI":"10.1152\/ajpregu.00336.2009","type":"journal-article","created":{"date-parts":[[2010,2,11]],"date-time":"2010-02-11T00:24:03Z","timestamp":1265847843000},"page":"R1017-R1025","source":"Crossref","is-referenced-by-count":29,"title":["Urinary tract obstruction induces transient accumulation of COX-2-derived prostanoids in kidney tissue"],"prefix":"10.1152","volume":"298","author":[{"given":"Rikke","family":"N\u00f8rregaard","sequence":"first","affiliation":[{"name":"The Water and Salt Research Center,"},{"name":"Institute of Clinical Medicine and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Boye L","family":"Jensen","sequence":"additional","affiliation":[{"name":"Department of Physiology and Pharmacology, University of Southern Denmark, Odense;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sukru Oguzkan","family":"Topcu","sequence":"additional","affiliation":[{"name":"The Water and Salt Research Center,"},{"name":"Institute of Clinical Medicine and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guixian","family":"Wang","sequence":"additional","affiliation":[{"name":"The Water and Salt Research Center,"},{"name":"Institute of Clinical Medicine and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Horst","family":"Schweer","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Philipps University Marburg, Marburg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S\u00f8ren","family":"Nielsen","sequence":"additional","affiliation":[{"name":"The Water and Salt Research Center,"},{"name":"Institute of Anatomy, University of Aarhus, Aarhus;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J\u00f8rgen","family":"Fr\u00f8ki\u00e6r","sequence":"additional","affiliation":[{"name":"The Water and Salt Research Center,"},{"name":"Institute of Clinical Medicine and"},{"name":"Department of Clinical Physiology and Nuclear Medicine, Aarhus University Hospital-Skejby, Aarhus, Denmark; 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