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(Hypertension. 2002;39:785.)
© 2002 American Heart Association, Inc.

Scientific Contributions

Nitric Oxide, Anti-Inflammatory Drugs on Renal Prostaglandins and Cyclooxygenase-2

Masaru Miyataka; Kathryn A. Rich; Marylou Ingram; Tadahiko Yamamoto; Richard J. Bing

From the Huntington Medical Research Institutes, Department of Experimental Cardiology (M.M., K.A.R., M.I., R.J.B.), Pasadena, Cal; and Kinki University School of Medicine, First Department of Internal Medicine (T.Y.), Osaka, Japan.

Correspondence to Richard J. Bing, MD, Huntington Medical Research Institutes, 99 North El Molino Ave, Pasadena, CA 91101.

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.

Key Words: prostaglandins • kidney • aspirin • nitric oxide

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