{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,19]],"date-time":"2026-05-19T12:45:59Z","timestamp":1779194759495,"version":"3.51.4"},"reference-count":27,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Hypertension"],"published-print":{"date-parts":[[2002,3]]},"abstract":"<jats:p>\n            Nonsteroidal anti-inflammatory drugs (NSAIDs) are frequently used as analgesics. They inhibit cyclooxygenases (COX), preventing the formation of prostaglandins, including prostacyclin and thromboxane. A serious side effect of COX-1 and COX-2 is renal damage. We report here that both a nonselective NSAID (aspirin, acetylsalicylic acid) and COX-2 selective NSAIDs (celecoxib and NS-398) diminished renal prostacyclin and thromboxane concentration in the renal medulla. NSAIDs failed to change COX-2 and iNOS (the inducible form of NO synthase) expression. A NO donor, B-NOD, preserved renal prostacyclin and thromboxane after administration of aspirin. PGI\n            <jats:sub>2<\/jats:sub>\n            and COX-2 protein were mainly expressed in the renal medulla, whereas iNOS expression was greater in the cortex. B-NOD preserved renal prostacyclin levels after administration of NSAIDs.\n          <\/jats:p>","DOI":"10.1161\/hy0302.105689","type":"journal-article","created":{"date-parts":[[2002,7,28]],"date-time":"2002-07-28T23:16:47Z","timestamp":1027898207000},"page":"785-789","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":25,"title":["Nitric Oxide, Anti-Inflammatory Drugs on Renal Prostaglandins and Cyclooxygenase-2"],"prefix":"10.1161","volume":"39","author":[{"given":"Masaru","family":"Miyataka","sequence":"first","affiliation":[{"name":"From the Huntington Medical Research Institutes, Department of Experimental Cardiology (M.M., K.A.R., M.I., R.J.B.), Pasadena, Cal; and \u2020 Kinki University School of Medicine, First Department of Internal Medicine (T.Y.), Osaka, Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kathryn A.","family":"Rich","sequence":"additional","affiliation":[{"name":"From the Huntington Medical Research Institutes, Department of Experimental Cardiology (M.M., K.A.R., M.I., R.J.B.), Pasadena, Cal; and \u2020 Kinki University School of Medicine, First Department of Internal Medicine (T.Y.), Osaka, Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marylou","family":"Ingram","sequence":"additional","affiliation":[{"name":"From the Huntington Medical Research Institutes, Department of Experimental Cardiology (M.M., K.A.R., M.I., R.J.B.), Pasadena, Cal; and \u2020 Kinki University School of Medicine, First Department of Internal Medicine (T.Y.), Osaka, Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tadahiko","family":"Yamamoto","sequence":"additional","affiliation":[{"name":"From the Huntington Medical Research Institutes, Department of Experimental Cardiology (M.M., K.A.R., M.I., R.J.B.), Pasadena, Cal; and \u2020 Kinki University School of Medicine, First Department of Internal Medicine (T.Y.), Osaka, Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Richard J.","family":"Bing","sequence":"additional","affiliation":[{"name":"From the Huntington Medical Research Institutes, Department of Experimental Cardiology (M.M., K.A.R., M.I., R.J.B.), Pasadena, Cal; and \u2020 Kinki University School of Medicine, First Department of Internal Medicine (T.Y.), Osaka, Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","unstructured":"Insel PA. 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