| Literature DB >> 11897764 |
Masaru Miyataka1, Kathryn A Rich, Marylou Ingram, Tadahiko Yamamoto, Richard J Bing.
Abstract
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. PGI2 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.Entities:
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Year: 2002 PMID: 11897764 DOI: 10.1161/hy0302.105689
Source DB: PubMed Journal: Hypertension ISSN: 0194-911X Impact factor: 10.190