Vaziri Nosratola D
Department of Medicine, University of California, Irvine, California, USA.
Iran J Kidney Dis. 2008 Jan;2(1):1-10.
Hypertension (HTN) is a major cause of stroke, left ventricular hypertrophy, congestive heart failure, arteriosclerosis, end-stage renal disease, and peripheral vascular disease. Oxidative stress and its constant companion, inflammation, play a critical part in the pathogenesis of many acute and chronic illnesses including HTN and its long-term complications. There is compelling evidence that oxidative stress, inflammation, and HTN are involved in a self-perpetuating vicious cycle which, if not interrupted, culminates in progressive target organ injury and dysfunction. This article is intended to review the available evidence for the role of oxidative stress and inflammation in the pathogenesis of HTN. In addition, evidence will be presented to demonstrate the role of HTN in the pathogenesis of oxidative stress and inflammation. Finally, evidence for participation of tissue angiotensin system in the vicious cycle of oxidative stress, inflammation, and HTN will be presented, and the approach to treatment of HTN-associated oxidative stress will be discussed.
高血压（HTN）是导致中风、左心室肥厚、充血性心力衰竭、动脉硬化、终末期肾病和外周血管疾病的主要原因。氧化应激及其相伴的炎症在包括高血压及其长期并发症在内的许多急慢性疾病的发病机制中起着关键作用。有令人信服的证据表明，氧化应激、炎症和高血压参与了一个自我延续的恶性循环，如果不加以阻断，最终会导致进行性靶器官损伤和功能障碍。本文旨在综述氧化应激和炎症在高血压发病机制中作用的现有证据。此外，还将展示证据以证明高血压在氧化应激和炎症发病机制中的作用。最后，将展示组织血管紧张素系统参与氧化应激、炎症和高血压恶性循环的证据，并讨论治疗与高血压相关氧化应激的方法。
