Androulakis Emmanuel S, Tousoulis Dimitris, Papageorgiou Nikolaos, Tsioufis Costas, Kallikazaros Ioannis, Stefanadis Christodoulos
First Cardiology Unit, Hippokration Hospital, Athens University Medical School, Athens, Greece.
Cardiol Rev. 2009 Sep-Oct;17(5):216-21. doi: 10.1097/CRD.0b013e3181b18e03.
Inflammation is a key feature in the initiation, progression, and clinical implications of cardiovascular disorders, including essential hypertension. Increasing evidence shows that activation of renin-angiotensin-aldosterone system and enhanced local production of angiotensin II have been implicated in the pathophysiology of inflammation. Besides being a potent vasoactive peptide, angiotensin II regulates the inflammatory process. Specifically, it increases vascular permeability, participates in the recruitment of inflammatory cells and their adhesion to the activated endothelium, and regulates cell growth and fibrosis. Reactive oxygen species are implicated at every stage in inflammation and activate multiple intracellular signaling molecules and transcription factors associated with inflammatory responses, such as nuclear factor-kappa B and activator protein-1. Other components of the renin-angiotensin-aldosterone system, including aldosterone and/or mineralocorticoid receptor, induce the production of reactive oxygen species and participate in vascular inflammation. Several studies suggest a role of endothelin-1 as an important mediator of chronic inflammation and there is an increasing interest in the relationship between endothelin-1 and reactive oxygen species. These data may have great impact on future therapeutic strategies.
炎症是心血管疾病（包括原发性高血压）发生、发展及临床影响的关键特征。越来越多的证据表明，肾素 - 血管紧张素 - 醛固酮系统的激活以及局部血管紧张素II生成的增加与炎症的病理生理学有关。血管紧张素II除了是一种强效血管活性肽外，还调节炎症过程。具体而言，它增加血管通透性，参与炎症细胞的募集及其与活化内皮细胞的黏附，并调节细胞生长和纤维化。活性氧在炎症的各个阶段都有涉及，并激活与炎症反应相关的多种细胞内信号分子和转录因子，如核因子 - κB和活化蛋白 - 1。肾素 - 血管紧张素 - 醛固酮系统的其他成分，包括醛固酮和/或盐皮质激素受体，诱导活性氧的产生并参与血管炎症。多项研究表明内皮素 - 1作为慢性炎症的重要介质发挥作用，并且人们对内皮素 - 1与活性氧之间的关系越来越感兴趣。这些数据可能对未来的治疗策略产生重大影响。
