During the spread of the severe acute respiratory syndrome coronavirus-2, some reports of data still emerging and in need of full analysis indicate that certain groups of patients are at risk of COVID-19. This includes patients with hypertension, heart disease, diabetes mellitus, and clearly the elderly. Many of those patients are treated with renin-angiotensin system blockers. Because the ACE2 (angiotensin-converting enzyme 2) protein is the receptor that facilitates coronavirus entry into cells, the notion has been popularized that treatment with renin-angiotensin system blockers might increase the risk of developing a severe and fatal severe acute respiratory syndrome coronavirus-2 infection. The present article discusses this concept. ACE2 in its full-length form is a membrane-bound enzyme, whereas its shorter (soluble) form circulates in blood at very low levels. As a mono-carboxypeptidase, ACE2 contributes to the degradation of several substrates including angiotensins I and II. ACE (angiotensin-converting enzyme) inhibitors do not inhibit ACE2 because ACE and ACE2 are different enzymes. Although angiotensin II type 1 receptor blockers have been shown to upregulate ACE2 in experimental animals, the evidence is not always consistent and differs among the diverse angiotensin II type 1 receptor blockers and differing organs. Moreover, there are no data to support the notion that ACE inhibitor or angiotensin II type 1 receptor blocker administration facilitates coronavirus entry by increasing ACE2 expression in either animals or humans. Indeed, animal data support elevated ACE2 expression as conferring potential protective pulmonary and cardiovascular effects. In summary, based on the currently available evidence, treatment with renin-angiotensin system blockers should not be discontinued because of concerns with coronavirus infection.

中文翻译：

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肾素-血管紧张素系统阻滞剂和 COVID-19 大流行

在严重急性呼吸系统综合症冠状病毒-2 传播期间，一些仍在出现且需要全面分析的数据报告表明，某些患者群体面临着 COVID-19 的风险。这包括高血压、心脏病、糖尿病患者，当然还有老年人。其中许多患者接受肾素-血管紧张素系统阻滞剂治疗。由于 ACE2（血管紧张素转换酶 2）蛋白是促进冠状病毒进入细胞的受体，因此人们普遍认为，使用肾素-血管紧张素系统阻滞剂治疗可能会增加患上严重且致命的严重急性呼吸综合征冠状病毒的风险。 2感染。本文讨论这个概念。全长形式的 ACE2 是一种膜结合酶，而其较短（可溶）形式在血液中循环的水平非常低。作为一种单羧肽酶，ACE2 有助于多种底物的降解，包括血管紧张素 I 和 II。ACE（血管紧张素转换酶）抑制剂不会抑制 ACE2，因为 ACE 和 ACE2 是不同的酶。尽管血管紧张素 II 1 型受体阻滞剂已被证明可以在实验动物中上调 ACE2，但证据并不总是一致，并且在不同的血管紧张素 II 1 型受体阻滞剂和不同器官之间存在差异。此外，没有数据支持以下观点：ACE 抑制剂或血管紧张素 II 1 型受体阻滞剂给药可通过增加动物或人类中 ACE2 的表达来促进冠状病毒进入。事实上，动物数据支持 ACE2 表达升高具有潜在的肺部和心血管保护作用。总之，根据目前现有的证据，不应因为担心冠状病毒感染而停止肾素-血管紧张素系统阻滞剂的治疗。