Ferrario Carlos M, Richmond Renee S, Smith Ronald, Levy Pavel, Strawn William B, Kivlighn Salah
The Hypertension and Vascular Disease Center, Wake Forest University School of Medicine, Medical School Boulevard, Winston-Salem, NC 27157, USA.
Am J Ther. 2004 Jan-Feb;11(1):44-53. doi: 10.1097/00045391-200401000-00010.
Clinical and experimental evidence suggests that the pathways by which hypertension and dyslipidemia lead to vascular disease may overlap and that angiotensin II (Ang II) is involved in restructuring of the arterial wall in both atherosclerosis and hypertension. Ang II represents a potent proinflammatory agent promoting recruitment of monocytes into the vascular intima. Ang II also indirectly facilitates transformation of macrophages and smooth muscle cells into foam cells by promoting superoxide radical formation (via NADP/NADPH oxidase stimulation). The oxidative stress produced by Ang II leads to enhanced low-density lipoprotein oxidation and degradation of nitric oxide, an important vascular protective molecule capable of retarding atherosclerosis progression. The importance of the renin-angiotensin system (RAS) in atherogenesis is highlighted by studies in animal models as well as human beings indicating that inhibition of angiotensin-converting enzyme or blockade of type 1 Ang II receptors retards the development of atherosclerotic lesions. In light of a causal and central role of Ang II in atherogenesis, blockade of the RAS represents an important therapeutic consideration in the prevention and treatment of atherosclerotic disease.
临床和实验证据表明，高血压和血脂异常导致血管疾病的途径可能重叠，并且血管紧张素II（Ang II）参与动脉粥样硬化和高血压中的动脉壁重塑。Ang II是一种强大的促炎剂，可促进单核细胞募集到血管内膜。Ang II还通过促进超氧自由基形成（通过刺激NADP/NADPH氧化酶）间接促进巨噬细胞和平滑肌细胞向泡沫细胞的转化。Ang II产生的氧化应激导致低密度脂蛋白氧化增强和一氧化氮降解，一氧化氮是一种重要的血管保护分子，能够延缓动脉粥样硬化进展。动物模型和人类研究均表明，抑制血管紧张素转换酶或阻断1型Ang II受体可延缓动脉粥样硬化病变的发展，这突出了肾素-血管紧张素系统（RAS）在动脉粥样硬化发生中的重要性。鉴于Ang II在动脉粥样硬化发生中具有因果关系和核心作用，阻断RAS是预防和治疗动脉粥样硬化疾病的重要治疗考虑因素。
