Azizi Michel
Bull Acad Natl Med. 2014 Feb;198(2):351-62; discussion 362.
Blockade of the renin-angiotensin system (RAS) with angiotensin-converting-enzyme (ACEI) inhibitors or angiotensin II receptor blockers (ARB) has become a major therapeutic tool. Due to internal counter-regulation, however, this system cannot be fully blocked by targeting only one of its components. Instead of increasing the doses of an ACEI, an ARB or a renin inhibitor, blocking RAS at two successive levels neutralizes the consequences of internal counter-regulation and thus provides a more complete blockade with more pronounced biological effects. Additive effects on blood pressure lowering and on renin secretion during combined administration of RAS blockers were first demonstrated in normotensive subjects and in various experimental models of hypertension, heart failure and renal failure. Although combined RAS blockade provided an additional hemodynamic response and more complete neutralization of the cellular effects of angiotensin II, no benefit was observed in terms of cardiovascular or renal protection in heart disease (heart failure, post-myocardial infarction, high vascular risk) or kidney disease (diabetic nephropathy). Moreover, more complete RAS blockade is risky in conditions where blood pressure and renal perfusion are renin-dependent (renal failure and hypotension) and also in hypoaldosteronism (hyperkalemia). The European, French and US. health agencies have contraindicated combined RAS blockade because of its unfavorable risk-benefit balance, especially in patients with diabetes or renal failure.
使用血管紧张素转换酶(ACEI)抑制剂或血管紧张素II受体阻滞剂(ARB)阻断肾素-血管紧张素系统(RAS)已成为一种主要的治疗手段。然而,由于体内的代偿调节,仅针对该系统的一个组成部分无法完全阻断它。与其增加ACEI、ARB或肾素抑制剂的剂量,在两个连续水平阻断RAS可抵消体内代偿调节的后果,从而实现更完全的阻断并产生更显著的生物学效应。RAS阻滞剂联合给药时对血压降低和肾素分泌的相加作用最初在血压正常的受试者以及高血压、心力衰竭和肾衰竭的各种实验模型中得到证实。尽管联合阻断RAS可提供额外的血流动力学反应,并更完全地中和血管紧张素II的细胞效应,但在心脏病(心力衰竭、心肌梗死后、高血管风险)或肾病(糖尿病肾病)的心血管或肾脏保护方面未观察到益处。此外,在血压和肾灌注依赖肾素的情况下(肾衰竭和低血压)以及在醛固酮减少症(高钾血症)中,更完全地阻断RAS存在风险。欧洲、法国和美国的卫生机构已对联合阻断RAS发出禁忌,因为其风险效益比不佳,尤其是在糖尿病或肾衰竭患者中。