Alexander R W
Division of Cardiology, Emory University School of Medicine, Atlanta, GA 30322.
Hypertension. 1995 Feb;25(2):155-61. doi: 10.1161/01.hyp.25.2.155.
Hypertension is a risk factor for the development of atherosclerosis, although the mechanisms have not been well elucidated. As the cellular and molecular mechanisms of the pathogenesis of atherosclerosis and the effects of hypertension are being more clearly defined, it becomes apparent that the two processes have certain common mechanisms. The endothelium is a likely central focus for the effect of both diseases. There is increasing evidence that atherosclerosis should be viewed fundamentally as an inflammatory disease. Atherogenic stimuli such as hyperlipidemia appear to active the inflammatory response by causing expression of mononuclear leukocyte recruiting mechanisms. The gene for one of these, the vascular cell adhesion molecule-1, is controlled at least in part by transcriptional factors regulated by oxidative stress, which modifies the redox state of the endothelial cell. Alterations in the redox state of the arterial wall also may contribute to vascular smooth muscle cell growth. In a somewhat parallel fashion, there is evidence that hypertension may also exert oxidative stress on the arterial wall. This article reviews evidence that leads to the postulate that hypertension predisposes to and accelerates atherosclerosis at least in part because of synergy between elevated blood pressure and other atherogenic stimuli to induce oxidative stress on the arterial wall.
高血压是动脉粥样硬化发生发展的一个危险因素，尽管其机制尚未完全阐明。随着动脉粥样硬化发病机制的细胞和分子机制以及高血压的影响越来越明确，很明显这两个过程有某些共同机制。内皮可能是这两种疾病作用的一个关键焦点。越来越多的证据表明，动脉粥样硬化应从根本上被视为一种炎症性疾病。诸如高脂血症等致动脉粥样硬化刺激似乎通过引发单核白细胞募集机制的表达来激活炎症反应。其中一种，即血管细胞黏附分子 -1 的基因，至少部分受氧化应激调节的转录因子控制，氧化应激会改变内皮细胞的氧化还原状态。动脉壁氧化还原状态的改变也可能促进血管平滑肌细胞生长。以一种 somewhat parallel fashion（此处原文有误，推测可能是“in a somewhat similar fashion”，意为“以一种有点相似的方式”），有证据表明高血压也可能对动脉壁施加氧化应激。本文综述了相关证据，这些证据支持这样一种假设，即高血压至少部分地易患并加速动脉粥样硬化，这是由于血压升高与其他致动脉粥样硬化刺激之间协同作用，从而在动脉壁上诱导氧化应激。
