Miyataka Masaru, Rich Kathryn A, Ingram Marylou, Yamamoto Tadahiko, Bing Richard J
Huntington Medical Research Institutes, Department of Experimental Cardiology, Pasadena, Cal 91101, USA.
Hypertension. 2002 Mar 1;39(3):785-9. doi: 10.1161/hy0302.105689.
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.
非甾体抗炎药（NSAIDs）常被用作镇痛药。它们抑制环氧化酶（COX），阻止前列腺素的形成，包括前列环素和血栓素。COX - 1和COX - 2的一个严重副作用是肾损伤。我们在此报告，一种非选择性NSAID（阿司匹林，乙酰水杨酸）和COX - 2选择性NSAIDs（塞来昔布和NS - 398）均降低了肾髓质中肾前列腺素和血栓素的浓度。NSAIDs未能改变COX - 2和诱导型一氧化氮合酶（iNOS）的表达。一种一氧化氮供体B - NOD在给予阿司匹林后可维持肾前列腺素和血栓素水平。前列环素（PGI2）和COX - 2蛋白主要在肾髓质表达，而iNOS在皮质中的表达更高。B - NOD在给予NSAIDs后可维持肾前列腺素水平。
