内过氧化物在花生四烯酸诱导的大鼠离体灌注肾血管收缩中的作用。
Role of endoperoxides in arachidonic acid-induced vasoconstriction in the isolated perfused kidney of the rat.
作者信息
Quilley J, McGiff J C, Nasjletti A
机构信息
Department of Pharmacology, New York Medical College, Valhalla.
出版信息
Br J Pharmacol. 1989 Jan;96(1):111-6. doi: 10.1111/j.1476-5381.1989.tb11790.x.
Abstract
- Administration of arachidonic acid caused dose-dependent vasoconstriction in the isolated rat kidney perfused in situ with Krebs-Henseleit solution. 2. Inhibition of cyclo-oxygenase with indomethacin or meclofenamate reduced the renal vasoconstrictor effect of arachidonic acid. 3. The renal vasoconstrictor effect of arachidonic acid was unaffected by CGS-13080 at concentrations that effectively reduced thromboxane A2 (TxA2) synthesis by platelets and the kidney. 4. The endoperoxide/TxA2 receptor antagonist, SQ 29,548, abolished the renal vasoconstrictor effect of arachidonic acid and of U46619, an endoperoxide analogue. In contrast, SQ 29,548 did not affect the renal vasoconstrictor response to angiotensin II, prostaglandin E2 or F2 alpha. 5. These data suggest that the vasoconstrictor effect of arachidonic acid in the isolated kidney of the rat is mediated by its metabolites, including the prostaglandin endoperoxides.
摘要
- 在用Krebs-Henseleit溶液原位灌注的离体大鼠肾脏中，给予花生四烯酸会引起剂量依赖性血管收缩。2. 用吲哚美辛或甲氯芬那酸抑制环氧化酶可降低花生四烯酸的肾血管收缩作用。3. 在有效降低血小板和肾脏血栓素A2（TxA2）合成的浓度下，CGS-13080对花生四烯酸的肾血管收缩作用没有影响。4. 内过氧化物/TxA2受体拮抗剂SQ 29,548消除了花生四烯酸和内过氧化物类似物U46619的肾血管收缩作用。相比之下，SQ 29,548不影响对血管紧张素II、前列腺素E2或F2α的肾血管收缩反应。5. 这些数据表明，花生四烯酸在大鼠离体肾脏中的血管收缩作用是由其代谢产物介导的，包括前列腺素内过氧化物。
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