Role of angiotensin and oxidative stress in essential hypertension
Role of angiotensin and oxidative stress in essential hypertension
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DOI：
10.1161/01.hyp.34.4.943
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发表时间：
1999-10-01
期刊：
影响因子：
8.3
通讯作者：
Reckelhoff, JF
中科院分区：
文献类型：
--
作者：
Romero, JC;Reckelhoff, JF
在这篇综述中，我们研究了血管紧张素 II 的小幅增加通过刺激氧化应激导致血压升高和维持高血压的可能性。低剂量的血管紧张素 II（2 至 10 ng.kg(-1).min(-1)，不会立即引起加压反应），连续静脉输注 7 至 30 天时，可使平均动脉压增加 30 至 40 mm Hg。这种对血管紧张素的缓慢加压反应伴随着氧化应激的刺激，通过 8-异前列腺素 F-2 α（F-2-异前列腺素）水平的显着增加来衡量。超氧自由基和一氧化氮可以化学结合形成过氧亚硝酸盐，然后氧化花生四烯酸形成F-2-异前列腺素。 F-2-异前列腺素具有有效的血管收缩和抗尿钠作用。此外，血管紧张素 II 可以刺激内皮素的产生，这也被证明可以刺激氧化应激。通过这种方式，一氧化氮浓度的降低（被超氧化物猝灭）以及 F-2-异前列腺素和内皮素的形成可以增强血管紧张素 II 的血管收缩作用。我们推测，这些机制是血管紧张素 II 缓慢加压反应发展的基础，当循环血管紧张素 II 水平正常时，也参与高血压的产生，正如许多原发性高血压和肾血管性高血压病例中发生的那样。
In this review, we examine the possibility that small increments in angiotensin II are responsible for an increase in blood pressure and maintenance of hypertension through the stimulation of oxidative stress. A low dose of angiotensin II (2 to 10 ng . kg(-1) . min(-1), which does not elicit an immediate presser response), when given for 7 to 30 days by continuous intravenous infusion, can increase mean arterial pressure by 30 to 40 mm Hg. This slow presser response to angiotensin is accompanied by the stimulation of oxidative stress, as measured by a significant increase in levels of 8-iso-prostaglandin F-2 alpha (F-2-isoprostane). Superoxide radicals and nitric oxide can combine chemically to form peroxynitrite, which can then oxidize arachidonic acid to form F-2-isoprostanes. F-2-isoprostanes exert potent vasoconstrictor and antinatriuretic effects. Furthermore, angiotensin II can stimulate endothelin production, which also has been shown to stimulate oxidative stress. In this way, a reduction in the concentration of nitric oxide (which is quenched by superoxide) along with the formation of F-2-isoprostanes and endothelin could potentiate the vasoconstrictor effects of angiotensin II. We hypothesize that these mechanisms, which underlie the development of the slow presser response to angiotensin II, also participate in the production of hypertension when circulating angiotensin II levels appear normal, as occurs in many cases of essential and renovascular hypertension.