Department of Physiological Sciences State University of Londrina, Londrina, PR;
Department of Pathological Sciences State University of Londrina, Londrina, PR;
Am J Physiol Heart Circ Physiol. 2014 May 15;306(10):H1472-80. doi: 10.1152/ajpheart.00520.2013. Epub 2014 Mar 14.
We investigated the involvement of nitric oxide (NO) and reactive oxygen species (ROS) on autonomic cardiovascular parameters, vascular reactivity, and endothelial cells isolated from aorta of monosodium glutamate (MSG) obese rats. Obesity was induced by administration of 4 mg/g body wt of MSG or equimolar saline [control (CTR)] to newborn rats. At the 60th day, the treatment was started with N(G)-nitro-L-arginine methyl ester (L-NAME, 20 mg/kg) or 0.9% saline. At the 90th day, after artery catheterization, mean arterial pressure (MAP) and heart rate were recorded. Plasma was collected to assess lipid peroxidation. Endothelial cells isolated from aorta were evaluated by flow cytometry and fluorescence intensity (FI) emitted by NO-sensitive dye [4,5-diaminofluoresceindiacetate (DAF-2DA)] and by ROS-sensitive dye [dihydroethidium (DHE)]. Vascular reactivity was made by concentration-response curves of acetylcholine. MSG showed hypertension compared with CTR. Treatment with L-NAME increased MAP only in CTR. The MSG induced an increase in the low-frequency (LF) band and a decrease in the high-frequency band of pulse interval. L-NAME treatment increased the LF band of systolic arterial pressure only in CTR without changes in MSG. Lipid peroxidation levels were higher in MSG and were attenuated after L-NAME. In endothelial cells, basal FI to DAF was higher in CTR than in MSG. In both groups, acetylcholine increased FI for DAF from basal. The FI baseline to DHE was higher in MSG than in CTR. Acetylcholine increased FI to DHE in the CTR group, but decreased in MSG animals. We suggest that reduced NO production and increased production of ROS may contribute to hypertension in obese MSG animals.
我们研究了一氧化氮（NO）和活性氧（ROS）在谷氨酸钠（MSG）肥胖大鼠自主心血管参数、血管反应性和主动脉内皮细胞中的作用。肥胖是通过给新生大鼠施用 4mg/g 体重的 MSG 或等摩尔盐水[对照（CTR）]来诱导的。在第 60 天，开始用 N(G)-硝基-L-精氨酸甲酯（L-NAME，20mg/kg）或 0.9%盐水进行治疗。在第 90 天，在动脉导管插入术后，记录平均动脉压（MAP）和心率。收集血浆以评估脂质过氧化。从主动脉分离的内皮细胞通过流式细胞术和一氧化氮敏感染料[4,5-二氨基荧光素二乙酸酯（DAF-2DA）]和 ROS 敏感染料[二氢乙啶（DHE）]发射的荧光强度（FI）进行评估。血管反应性通过乙酰胆碱的浓度-反应曲线来确定。MSG 显示与 CTR 相比有高血压。在 CTR 中，L-NAME 治疗仅增加了 MAP。MSG 诱导脉搏间隔的低频（LF）带增加和高频带减少。在 CTR 中，L-NAME 治疗增加了收缩压的 LF 带，但在 MSG 中没有变化。MSG 中的脂质过氧化水平较高，经 L-NAME 治疗后降低。在内皮细胞中，与 MSG 相比，对照组的 DAF 的基础 FI 较高。在两组中，乙酰胆碱均增加了 DAF 的 FI 从基础值。MSG 的 DHE 的基础 FI 比 CTR 高。乙酰胆碱增加了 CTR 组的 DHE 的 FI，但在 MSG 动物中减少了。我们认为，NO 生成减少和 ROS 生成增加可能导致肥胖 MSG 动物的高血压。
