Neves Mario Fritsch, Cunha Ana Rosa, Cunha Michelle Rabello, Gismondi Ronaldo Altenburg, Oigman Wille
Departamento de Clinica Medica, Universidade do Estado do Rio de Janeiro, Ave. 28 de Setembro, 77 sala 329, Rio De Janeiro, 20551-030, Brazil.
Centro de Ciências Médicas, Universidade Federal Fluminense, Hospital Universitário Antônio Pedro, Niterói, RJ, 24033-900, Brazil.
High Blood Press Cardiovasc Prev. 2018 Jun;25(2):137-145. doi: 10.1007/s40292-018-0252-5. Epub 2018 Feb 23.
Many cardiovascular diseases present renin-angiotensin-aldosterone system (RAAS) hyperactivity as an important pathophysiological mechanism to be target in the therapeutic approaches. Moreover, arterial stiffness is currently considered as a new independent risk factor for cardiovascular disease in different clinical conditions, including hypertension and chronic kidney disease. In fact, excessive stimulation of angiotensin type 1 (AT1) receptors, as well as mineralocorticoid receptors, results in cellular growth, oxidative stress and vascular inflammation, which may lead to arterial stiffness and accelerate the process of vascular aging. In the last decades, a vasoprotective axis of the RAAS has been discovered, and now it is well established that new components with antioxidant and anti-inflammatory properties play important roles promoting vasodilation, natriuresis and reducing collagen deposition, thus attenuating arterial stiffness and improving endothelial function. In this review, we will focus on these pathophysiological mechanisms and the relevance of RAAS inhibition by different strategies to increase arterial compliance and to decelerate vascular aging.
许多心血管疾病表现出肾素-血管紧张素-醛固酮系统（RAAS）的过度活跃，这是治疗方法中一个重要的病理生理机制靶点。此外，动脉僵硬度目前被认为是包括高血压和慢性肾病在内的不同临床情况下心血管疾病的一个新的独立危险因素。事实上，血管紧张素1型（AT1）受体以及盐皮质激素受体的过度刺激会导致细胞生长、氧化应激和血管炎症，这可能会导致动脉僵硬度增加并加速血管老化过程。在过去几十年中，已经发现了RAAS的一个血管保护轴，现在已经明确，具有抗氧化和抗炎特性的新成分在促进血管舒张、利钠和减少胶原蛋白沉积方面发挥着重要作用，从而减轻动脉僵硬度并改善内皮功能。在这篇综述中，我们将聚焦于这些病理生理机制以及通过不同策略抑制RAAS对增加动脉顺应性和减缓血管老化的相关性。
