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首页> 外文期刊>American Journal of Physiology >Role of 20-hydroxyeicosatetraenoic acid in the renal and vasoconstrictor actions of angiotensin II.
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Role of 20-hydroxyeicosatetraenoic acid in the renal and vasoconstrictor actions of angiotensin II.

机译：20-羟基二十碳四烯酸在血管紧张素II的肾脏和血管收缩作用中的作用。

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摘要

The present study examined the effects of ANG II on the renal synthesis of 20-hydroxyeicosatetraenoic acid (20-HETE) and its contribution to the renal vasoconstrictor and the acute and chronic pressor effects of ANG II in rats. ANG II (10(-11) to 10(-7) mol/l) reduced the diameter of renal interlobular arteries treated with inhibitors of nitric oxide synthase and cyclooxygenase, lipoxygenase, and epoxygenase by 81 +/- 8%. Subsequent blockade of the synthesis of 20-HETE with 17-octadecynoic acid (1 micromol/l) increased the ED(50) for ANG II-induced constriction by a factor of 15 and diminished the maximal response by 61%. Graded intravenous infusion of ANG II (5-200 ng/min) dose dependently increased mean arterial pressure (MAP) in thiobutylbarbitol-anesthetized rats by 35 mmHg. Acute blockade of the formation of 20-HETE with dibromododecenyl methylsulfimide (DDMS; 10 mg/kg) attenuated the pressor response to ANG II by 40%. An intravenous infusion of ANG II (50 ng. kg(-1). min(-1)) in rats for 5 days increased the formation of 20-HETE and epoxyeicosatrienoic acids (EETs) in renal cortical microsomes by 60 and 400%, respectively, and increased MAP by 78 mmHg. Chronic blockade of the synthesis of 20-HETE with intravenous infusion of DDMS (1 mg. kg(-1). h(-1)) or EETs and 20-HETE with 1-aminobenzotriazole (ABT; 2.2 mg. kg(-1). h(-1)) attenuated the ANG II-induced rise in MAP by 40%. Control urinary excretion of 20-HETE averaged 350 +/- 23 ng/day and increased to 1,020 +/- 105 ng/day in rats infused with ANG II (50 ng. kg(-1). min(-1)) for 5 days. In contrast, urinary excretion of 20-HETE only rose to 400 +/- 40 and 600 +/- 25 ng/day in rats chronically treated with ANG II and ABT or DDMS respectively. These results suggest that acute and chronic elevations in circulating ANG II levels increase the formation of 20-HETE in the kidney and peripheral vasculature and that 20-HETE contributes to the acute and chronic pressor effects of ANG II.
机译：本研究探讨了ANG II对大鼠20-羟基二十碳四烯酸（20-HETE）肾脏合成的影响及其对肾脏血管收缩的作用以及ANG II在大鼠中的急，慢性升压作用。 ANG II（10（-11）至10（-7）mol / l）使一氧化氮合酶和环氧合酶，脂氧合酶和环氧合酶抑制剂治疗的肾小叶动脉直径减少了81 +/- 8％。随后用17-十八碳烯酸（1 micromol / l）阻止20-HETE的合成，使ANG II诱导的收缩的ED（50）增加15倍，最大响应降低61％。 ANGII分级静脉输注（5-20​​0 ng / min）剂量依赖性地使硫丁基巴比妥麻醉的大鼠的平均动脉压（MAP）增加35 mmHg。用二溴十二碳烯基甲基硫酰亚胺（DDMS; 10 mg / kg）急性阻断20-HETE的形成使对ANG II的升压反应减弱40％。在大鼠中静脉输注ANG II（50 ng。kg（-1）.min（-1））5天使肾皮质微粒体中20-HETE和环氧二十碳三烯酸（EET）的形成增加了60％和400％，分别使MAP增加78 mmHg。静脉内注入DDMS（1 mg。kg（-1）.h（-1）。或EET）和20-HETE与1-氨基苯并三唑（ABT; 2.2 mg.kg（-1） ）.h（-1））使ANG II诱导的MAP升高降低了40％。注射ANG II（50 ng。kg（-1）。min（-1））的大鼠的20-HETE对照尿排泄平均为350 +/- 23 ng /天，并增加至1,020 +/- 105 ng /天。 5天。相比之下，在分别用ANG II和ABT或DDMS慢性治疗的大鼠中，20-HETE的尿排泄仅上升至400 +/- 40 ng /天和600 +/- 25 ng /天。这些结果表明循环中的ANG II水平的急性和慢性升高会增加肾脏和周围脉管系统中20-HETE的形成，并且20-HETE有助于ANG II的急性和慢性升压作用。

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