Sinha Nakshi, Dabla Pradeep Kumar
Department of Biochemistry, Chacha Nehru Bal Chikitsalya, Associated to Maulana Azad Medical College, Geeta Colony, New Delhi -110031, India.
Curr Hypertens Rev. 2015;11(2):132-42. doi: 10.2174/1573402111666150529130922.
Free radicals or reactive oxygen species (ROS) are generated by oxygen metabolism which is balanced by the rate of oxidant formation and the rate of oxidant elimination. Oxidative stress is a result of imbalance between the generation of reactive oxygen species (ROS) and the antioxidant defence systems. Hypertension is one of the major risk factors for cardiovascular diseases and is considered as a leading cause of mortality and morbidity. These diseases affect more than 600 million people and it has been estimated that 29% of the world population will be suffering from hypertension by 2025. It has been indicated by experimental evidence that reactive oxygen species (ROS) play an important role in the pathophysiology of hypertension. The vasculature is a rich source of NADPH oxidase which produces most of the reactive oxygen species and plays an important role in renal dysfunction and vascular damage. Recent studies indicate that increased oxidative stress is the important mediator of endothelial injury in the pathology of hypertension associated to increased production of pro oxidants such as superoxideanion hydrogen peroxide, reduced nitric oxide synthesis and decreased bioavailability of antioxidants. Oxidative stress is found to be associated with endothelial dysfunction, inflammation, hypertrophy, apoptosis, cell migration, fibrosis, and angiogenesis in relation to vascular remodelling of hypertension. Results in humans are still less conclusive inspite of data available that involve oxidative stress as a causative factor of essential hypertension. The aim of this review is to present a novel focus on the role of oxidative stress in the pathophysiology of hypertension and recent biomarkers which are found to be associated with reactive oxygen species and the role of antioxidants as therapy of hypertension.
自由基或活性氧（ROS）由氧代谢产生，其通过氧化剂形成速率和氧化剂消除速率达到平衡。氧化应激是活性氧（ROS）生成与抗氧化防御系统之间失衡的结果。高血压是心血管疾病的主要危险因素之一，被认为是导致死亡和发病的主要原因。这些疾病影响着超过6亿人，据估计，到2025年全球29%的人口将患有高血压。实验证据表明，活性氧（ROS）在高血压的病理生理学中起重要作用。脉管系统是NADPH氧化酶的丰富来源，该酶产生大部分活性氧，并在肾功能障碍和血管损伤中起重要作用。最近的研究表明，氧化应激增加是高血压病理中内皮损伤的重要介质，与超氧阴离子、过氧化氢等促氧化剂生成增加、一氧化氮合成减少以及抗氧化剂生物利用度降低有关。氧化应激被发现与高血压血管重塑相关的内皮功能障碍、炎症、肥大、细胞凋亡、细胞迁移、纤维化和血管生成有关。尽管有数据表明氧化应激是原发性高血压的致病因素，但人类研究结果仍不太确凿。本综述的目的是聚焦氧化应激在高血压病理生理学中的作用以及最近发现的与活性氧相关的生物标志物，还有抗氧化剂作为高血压治疗手段的作用。
