U.O.C. Medicina Vascolare, Dipartimento Biomedico di Medicina Interna e Specialistica, Università degli Studi di Palermo, Italy.
Curr Pharm Des. 2012;18(28):4385-413. doi: 10.2174/138161212802481282.
The role of inflammation in cardiovascular disease and in hypertensive disease above all, is complex. Several studies confirm that activation of renin-angiotensin-aldosterone system (RAAS), through increase in the production of angiotensin II (Ang II), is closely related to local vascular inflammation. Over the BP lowering effects of anti-hypertensive treatments, several ancillary effects for every class may be found, distinguishing the various drugs from one another. Given the pro-inflammatory effects of Ang II and aldosterone, agents that interfere with the components of RAAS, such as ACE inhibitors, Angiotensin Receptor Blockers (ARBs), and mineralocorticoid receptor antagonists (spironolactone or the more selective eplerenone), represent logical therapeutic tools to reduce vascular inflammation and cardiovascular risk, as suggested in large clinical trials in patients with hypertension and diabetes. Regarding ACE inhibitors, actually there is no convincing evidence indicating that ACEi's reduce plasma levels of major inflammatory markers in hypertension models. Lack of evidence concerns especially these inflammation markers, such as fibrinogen of CRP, which are less closely related to atherosclerotic disease and vascular damage and conversely are affected by several more aspecific factors. Results obtained by trials accomplished using ARBs seem to be more univocal to confirm, although to great extent, these is an anti-inflammatory effect of drugs blocking AT1 receptor. In order to strictly study the effects of blockage of RAAS on inflammation, future studies may explore different strategies by, for example, simultaneously acting on the ACE and the AT1 angiotensin receptors.
炎症在心血管疾病和高血压疾病中的作用非常复杂。多项研究证实，肾素-血管紧张素-醛固酮系统（RAAS）的激活，通过增加血管紧张素 II（Ang II）的产生，与局部血管炎症密切相关。在降压治疗的作用之外，每类药物可能都有一些辅助作用，这使得不同药物之间有所区别。鉴于 Ang II 和醛固酮的促炎作用，干扰 RAAS 成分的药物，如血管紧张素转换酶抑制剂（ACEI）、血管紧张素受体阻滞剂（ARB）和盐皮质激素受体拮抗剂（螺内酯或更具选择性的依普利酮），是减少血管炎症和心血管风险的合理治疗工具，这在高血压和糖尿病患者的大型临床试验中得到了证实。关于 ACEI，实际上没有令人信服的证据表明 ACEI 可以降低高血压模型中主要炎症标志物的血浆水平。缺乏证据主要涉及这些炎症标志物，如纤维蛋白原和 CRP，它们与动脉粥样硬化疾病和血管损伤的关系不太密切，而与其他更非特异性的因素有关。使用 ARB 完成的试验结果似乎更能明确证实，尽管在很大程度上，这些药物阻断 AT1 受体具有抗炎作用。为了严格研究 RAAS 阻断对炎症的影响，未来的研究可能会探索不同的策略，例如同时作用于 ACE 和 AT1 血管紧张素受体。
