Ghanem Firas A, Movahed Assad
Section of Cardiology, Department of Medicine, The Brody School of Medicine, East Carolina University, Greenville, North Carolina, USA.
J Am Soc Hypertens. 2007 Mar-Apr;1(2):113-9. doi: 10.1016/j.jash.2007.01.004.
Hypertension is one of the most important contributors to atherosclerosis. A possible link between inflammation and elevated blood pressure has been suggested by several cross-sectional and longitudinal studies. Possible mechanisms include an imbalance between vasoconstrictors and vasodilators, amplified thrombogenesis and platelet activation, and perhaps a direct effect of inflammatory mediators. C-reactive protein (CRP), an inflammatory cytokine, may play an essential role in vascular inflammation and can directly decrease the production of nitric oxide, a vasocodilator. Angiotensin II (Ang II) up-regulates several inflammatory cytokines, leukocyte adhesion molecules, and chemokines through the activation of the nuclear factor-kappa B leading to a decrease in the bioavailability of vasodilators. The increase in oxidative stress and endothelin-1 production through Ang II may further contribute to vasoconstriction. Adipose tissue can add to the production of CRP and creates a prothrombotic state. The presence of low-grade inflammation, especially elevations of CRP, can help predict the risk of future cardiovascular events and is associated with target organ damage in hypertensive individuals. Angiotensin converting enzyme inhibitors, angiotensin receptor blockers, beta-adrenoreceptor antagonists, and, to a lesser degree calcium channel antagonists, have shown efficacy in reducing CRP. Lifestyle changes such as exercise, weight loss, and tobacco cessation have also shown a similar efficacy. Whether targeting inflammation in the treatment of uncomplicated hypertension can alter the natural history of the disease or lead to improved outcome has yet to be determined.
高血压是动脉粥样硬化最重要的促成因素之一。多项横断面研究和纵向研究表明炎症与血压升高之间可能存在联系。可能的机制包括血管收缩剂与血管舒张剂之间的失衡、血栓形成和血小板活化加剧，以及炎症介质可能产生的直接作用。炎症细胞因子C反应蛋白（CRP）可能在血管炎症中起关键作用，并且可直接减少血管舒张剂一氧化氮的生成。血管紧张素II（Ang II）通过激活核因子-κB上调多种炎症细胞因子、白细胞粘附分子和趋化因子，导致血管舒张剂的生物利用度降低。通过Ang II增加氧化应激和内皮素-1的生成可能进一步导致血管收缩。脂肪组织可增加CRP的产生并形成促血栓状态。低度炎症的存在，尤其是CRP升高，有助于预测未来心血管事件的风险，并且与高血压患者的靶器官损害相关。血管紧张素转换酶抑制剂、血管紧张素受体阻滞剂、β肾上腺素能受体拮抗剂以及在较小程度上的钙通道拮抗剂，已显示出降低CRP的疗效。运动、减肥和戒烟等生活方式改变也显示出类似的疗效。在单纯性高血压治疗中针对炎症是否可以改变疾病的自然病程或带来更好的结局，还有待确定。
