Hypertension is a risk factor for erectile dysfunction (ED) and both conditions are associated with oxidative stress. Given that nitrite is described to display antioxidant effects, we hypothesized that treatment with nitrite would exert antioxidant effects attenuating both reactive oxygen species (ROS) generation in the corpora cavernosa (CC) and ED induced by hypertension. Two kidney, one clip (2K1C) hypertension was induced in male Wistar rats. Treatment with sodium nitrite (15 mg/kg/day, p.o., gavage) was initiated two weeks after surgery to induce hypertension and maintained for four weeks. Nitrite abrogated both the decrease in intracavernosal pressure and endothelial dysfunction of the CC induced by hypertension. Treatment with nitrite decreased hypertension-induced ROS generation in the CC assessed in situ using the fluorescent dye dihidroethidium (DHE) and with the lucigenin assay. Western immunoblotting analysis revealed that nitrite prevented the increase in Nox1 expression in the CC from 2K1C rats. Decreased concentrations of hydrogen peroxide (H2O2) were found in the CC from hypertensive rats and treatment with nitrite prevented this response. Treatment with nitrite increased the fluorescence of DAF-2DA in the CC from sham-operated rats and restored nitric oxide (NO) levels in the CC from 2K1C rats. In summary, we found novel evidence that nitrite reversed the decrease in intracavernosal pressure induced by 2K1C hypertension. This response was partially attributed to the antioxidant effect of nitrite that blunted ROS generation and endothelial dysfunction in the CC. In addition, nitrite-derived NO may have promoted direct protective actions against hypertension-induced CC dysfunction.

中文翻译：

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亚硝酸盐处理可防止海绵体中活性氧的产生，并恢复高血压大鼠的海绵体内压力。

高血压是勃起功能障碍（ED）的危险因素，两种情况都与氧化应激有关。鉴于描述了亚硝酸盐显示出抗氧化作用，我们假设亚硝酸盐处理将发挥抗氧化作用，从而减弱海绵体（CC）和高血压诱发的ED中的活性氧（ROS）生成。在雄性Wistar大鼠中诱发了两个肾脏，一个夹子（2K1C）高血压。手术后两周开始用亚硝酸钠（15 mg / kg /天，口服，管饲法）治疗以诱发高血压，并维持四周。亚硝酸盐消除了高血压引起的海绵体内胆囊压降低和CC的内皮功能障碍。亚硝酸盐治疗可降低使用CC荧光染料（DHE）和荧光素原测定法评估的CC中高血压引起的ROS生成。Western免疫印迹分析表明，亚硝酸盐阻止了2K1C大鼠CC中Nox1表达的增加。在高血压大鼠的CC中发现过氧化氢（H2O2）浓度降低，而亚硝酸盐治疗阻止了这种反应。亚硝酸盐处理增加了假手术大鼠CC中DAF-2DA的荧光，并恢复了2K1C大鼠CC中一氧化氮（NO）的水平。总之，我们发现了新的证据，亚硝酸盐逆转了由2K1C高血压引起的海绵体腔内压力的降低。该反应部分归因于亚硝酸盐的抗氧化作用，后者抑制了CC中ROS的产生和内皮功能障碍。此外，亚硝酸盐衍生的NO可能已经促进了针对高血压引起的CC功能障碍的直接保护作用。