From the Fondazione Umbra Cuore e Ipertensione-ONLUS, Division of Cardiology, Hospital S. Maria della Misericordia, Perugia, Italy (P.V., C.C.).
Department of Medicine and Surgery, and Chronic Disease Research Center (MACRO), University of Insubria, Varese, Italy (A.S., F.A.).
Hypertension. 2020 Aug;76(2):294-299. doi: 10.1161/HYPERTENSIONAHA.120.15353. Epub 2020 Jun 1.
Diffuse pulmonary inflammation, endothelial inflammation, and enhanced thrombosis are cardinal features of coronavirus disease 2019 (COVID-19), the disease caused by the severe acute respiratory syndrome coronavirus 2. These features are reminiscent of several adverse reactions triggered by angiotensin II and opposed by angiotensin, in many experimental models. Severe acute respiratory syndrome coronavirus 2 binds to ACE2 (angiotensin-converting enzyme 2) receptors and entries into the cell through the fusion of its membrane with that of the cell. Hence, it downregulates these receptors. The loss of ACE2 receptor activity from the external site of the membrane will lead to less angiotensin II inactivation and less generation of antiotensin. In various experimental models of lung injury, the imbalance between angiotensin II overactivity and of antiotensin deficiency triggered inflammation, thrombosis, and other adverse reactions. In COVID-19, such imbalance could play an important role in influencing the clinical picture and outcome of the disease. According to this line of thinking, some therapeutic approaches including recombinant ACE2, exogenous angiotensin, and angiotensin receptor blockers seem particularly promising and are being actively tested.
弥漫性肺部炎症、内皮炎症和增强的血栓形成是由严重急性呼吸综合征冠状病毒 2 引起的疾病 2019 冠状病毒病（COVID-19）的主要特征。这些特征让人联想到许多实验模型中由血管紧张素 II 引发并由血管紧张素拮抗的几种不良反应。严重急性呼吸综合征冠状病毒 2 通过其膜与细胞的融合结合 ACE2（血管紧张素转换酶 2）受体并进入细胞。因此，它会下调这些受体。膜外 ACE2 受体活性的丧失将导致血管紧张素 II 失活减少和抗高血压素生成减少。在肺损伤的各种实验模型中，血管紧张素 II 过度活跃与抗高血压素缺乏之间的失衡引发炎症、血栓形成和其他不良反应。在 COVID-19 中，这种失衡可能在影响疾病的临床特征和结果方面发挥重要作用。根据这一思路，一些治疗方法，包括重组 ACE2、外源性血管紧张素和血管紧张素受体阻滞剂，似乎特别有前途，并正在积极测试。
