Dandona P, Dhindsa S, Ghanim H, Chaudhuri A
Division of Endocrinology, Diabetes and Metabolism, State University of New York at Buffalo and Kaleida Health, Buffalo, NY 14209, USA.
J Hum Hypertens. 2007 Jan;21(1):20-7. doi: 10.1038/sj.jhh.1002101. Epub 2006 Nov 9.
Angiotensin II (Ang II) increases adhesion molecules, cytokines and chemokines and exerts a proinflammatory effect on leucocytes, endothelial cells and vascular smooth muscle cells. Acting via the type 1 receptor, Ang II initiates an inflammatory cascade of reduced nicotinamide-adenine dinucleotide phosphate oxidase, reactive oxygen species (ROS) and nuclear factor-kappaB, which mediates transcription and gene expression and increases adhesion molecules and chemokines. An excess of ROS decreases nitric oxide bioavailability, causes endothelial dysfunction, and promotes atherosclerosis. Moreover, Ang II interrupts the anti-inflammatory effects of insulin. Together, these effects promote a prothrombotic state as well as plaque rupture. Ang II receptor blockers suppress mediators of inflammation, including ROS and C-reactive protein, and they increase expression of inhibitory kappaB (an inhibitor of nuclear factor-kappaB). These anti-inflammatory and antioxidative effects, which are probably due in part to unopposed stimulation of the Ang II type 2 receptor, may be beneficial in acute coronary syndromes and may also contribute to the prevention of type II diabetes mellitus, as insulin resistance is mediated by inflammatory processes.
血管紧张素II（Ang II）可增加黏附分子、细胞因子和趋化因子，并对白细胞、内皮细胞和血管平滑肌细胞产生促炎作用。Ang II通过1型受体发挥作用，启动烟酰胺腺嘌呤二核苷酸磷酸氧化酶、活性氧（ROS）和核因子κB减少的炎症级联反应，该反应介导转录和基因表达，并增加黏附分子和趋化因子。过量的ROS会降低一氧化氮的生物利用度，导致内皮功能障碍，并促进动脉粥样硬化。此外，Ang II会阻断胰岛素的抗炎作用。这些作用共同促进了血栓形成状态以及斑块破裂。血管紧张素II受体阻滞剂可抑制包括ROS和C反应蛋白在内的炎症介质，并增加抑制性κB（核因子κB的抑制剂）的表达。这些抗炎和抗氧化作用可能部分归因于对血管紧张素II 2型受体的无对抗刺激，可能对急性冠状动脉综合征有益，也可能有助于预防II型糖尿病，因为胰岛素抵抗是由炎症过程介导的。
