Angeli Fabio, Reboldi Gianpaolo, Trapasso Monica, Verdecchia Paolo
Dipartimento di Medicina e Chirurgia, Università degli Studi dell'Insubria di Varese e Dipartimento di Medicina e Riabilitazione Cardiopolmonare, IRCCS Maugeri di Tradate.
Dipartimento di Medicina e Centro di Ricerca Clinica e Traslazionale (CERICLET), Università di Perugia.
G Ital Cardiol (Rome). 2022 Jan;23(1):10-14. doi: 10.1714/3715.37055.
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) rapidly spread across the world, killing more than 4 million individuals globally, with 240 million individuals being confirmed by laboratory tests. Among different therapeutic strategies to prevent SARS-CoV-2 infection, vaccines are the most promising approach for curbing the pandemic. They elicit an immune neutralizing response and thus offer protection against coronavirus disease 2019 (COVID-19). However, some questions regarding the safety of COVID-19 vaccines have been raised and based on sparse reports of severe systemic reactions after vaccination. Among these, evidences on the potential effect of vaccination on the acute rise in blood pressure have been recently accrued. Approved vaccines in Europe increase the endogenous synthesis of SARS-CoV-2 Spike proteins from a variety of cells. Once synthetized in the cells reached by the vaccine, the Spike proteins first assemble in the cytoplasm and then migrate to the cell surface to protrude with a native-like conformation. Spike proteins are recognized by the immune system which rapidly develops an immune response. Furthermore, the Spike proteins assembled in the cells which are eventually destroyed by the immune response circulate in the blood as free-floating forms. Free-floating Spike proteins may interact with angiotensin-converting enzyme 2 (ACE2) receptors leading to internalization, degradation, and dysregulation of the catalytic activities of these receptors. The consequent loss of ACE2 receptor activity leads to a rapid drop in the generation of angiotensin1,7 resulting from inactivation of angiotensin II. The imbalance between angiotensin II (overactivity) and of angiotensin1,7 (deficiency) might play a role in the genesis of acute elevation in blood pressure.
严重急性呼吸综合征冠状病毒2(SARS-CoV-2)在全球迅速传播,导致全球超过400万人死亡,2.4亿人经实验室检测确诊感染。在预防SARS-CoV-2感染的不同治疗策略中,疫苗是遏制这一疫情最有前景的方法。它们引发免疫中和反应,从而提供针对2019冠状病毒病(COVID-19)的保护。然而,基于接种疫苗后严重全身反应的稀少报告,人们对COVID-19疫苗的安全性提出了一些问题。其中,最近积累了关于接种疫苗对血压急性升高潜在影响的证据。欧洲批准的疫苗可增加多种细胞中SARS-CoV-2刺突蛋白的内源性合成。一旦在疫苗到达的细胞中合成,刺突蛋白首先在细胞质中组装,然后迁移到细胞表面以天然样构象突出。刺突蛋白被免疫系统识别,免疫系统会迅速产生免疫反应。此外,在最终被免疫反应破坏的细胞中组装的刺突蛋白以游离形式在血液中循环。游离的刺突蛋白可能与血管紧张素转换酶2(ACE2)受体相互作用,导致这些受体的内化、降解和催化活性失调。ACE2受体活性的丧失导致血管紧张素II失活后血管紧张素1,7生成迅速下降。血管紧张素II(活性过高)和血管紧张素1,7(缺乏)之间的失衡可能在血压急性升高的发生中起作用。