Department of Physiology, College of Medicine, Nanchang University, Nanchang 330006, China.
Department of Experimental Teaching Center, Nanchang University, Nanchang 330031, China.
Biomed Pharmacother. 2018 Jan;97:423-428. doi: 10.1016/j.biopha.2017.10.122. Epub 2017 Nov 6.
The pathological characteristics of atherosclerosis (AS) include lipid accumulation, fibrosis formation and atherosclerotic plaque produced in artery intima, which leads to vascular sclerosis, lumen stenosis and irritates the ischemic changes of corresponding organs. Endothelial dysfunction was closely associated with AS. Nitric oxide (NO) is a multifunctional signaling molecule involved in the maintenance of metabolic and cardiovascular homeostasis. NO is also a potent endogenous vasodilator and enters for the key processes that suppresses the formation vascular lesion even AS. NO bioavailability indicates the production and utilization of endothelial NO in organisms, its decrease is related to oxidative stress, lipid infiltration, the expressions of some inflammatory factors and the alteration of vascular tone, which plays an important role in endothelial dysfunction. The enhancement of arginase activity and the increase in asymmetric dimethylarginine and hyperhomocysteinemia levels all contribute to AS by intervening NO bioavailability in human beings. Diabetes mellitus, obesity, chronic kidney disease and smoking, etc., also participate in AS by influencing NO bioavailability and NO level. Here, we reviewed the relationship between NO bioavailability and AS according the newest literatures.
动脉粥样硬化（AS）的病理特征包括脂质积聚、纤维化形成和动脉内膜中的粥样斑块形成，导致血管硬化、管腔狭窄，并刺激相应器官的缺血性变化。内皮功能障碍与 AS 密切相关。一氧化氮（NO）是一种多功能信号分子，参与维持代谢和心血管稳态。NO 也是一种有效的内源性血管舒张剂，参与抑制血管病变形成甚至 AS 的关键过程。NO 的生物利用度表示生物体中内皮型一氧化氮的产生和利用，其减少与氧化应激、脂质浸润、某些炎症因子的表达以及血管张力的改变有关，在内皮功能障碍中发挥重要作用。精氨酸酶活性的增强以及不对称二甲基精氨酸和高同型半胱氨酸血症水平的增加都通过干预人类的 NO 生物利用度来促进 AS 的发生。糖尿病、肥胖、慢性肾脏病和吸烟等也通过影响 NO 生物利用度和 NO 水平参与 AS 的发生。在这里，我们根据最新的文献综述了 NO 生物利用度与 AS 之间的关系。
