Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the etiologic agent responsible for the global coronavirus disease 2019 (COVID-19) pandemic. Numerous studies have demonstrated that cardiovascular disease may affect COVID-19 progression. In the present study, we investigated the effect of hypertension on viral replication and COVID-19 progression using a hypertensive mouse model infected with SARS-CoV-2. Results revealed that SARS-CoV-2 replication was delayed in hypertensive mouse lungs. In contrast, SARS-CoV-2 replication in hypertensive mice treated with the antihypertensive drug captopril demonstrated similar virus replication as SARS-CoV-2-infected normotensive mice. Furthermore, antihypertensive treatment alleviated lung inflammation induced by SARS-CoV-2 replication (interleukin (IL)-1β up-regulation and increased immune cell infiltration). No differences in lung inflammation were observed between the SARS-CoV-2-infected normotensive mice and hypertensive mice. Our findings suggest that captopril treatment may alleviate COVID-19 progression but not affect viral replication.
严重急性呼吸系统综合症冠状病毒2型 (SARS-CoV-2) 是导致全球2019冠状病毒病 (COVID-19) 大流行的病原体。大量研究表明，心血管疾病可能会影响COVID-19的进展。在该研究中，我们使用感染了 SARS-CoV-2 的高血压小鼠模型研究了高血压对病毒复制和 COVID-19 进展的影响。结果显示，在高血压小鼠的肺中SARS-CoV-2的复制延迟。相比之下，用抗高血压药物卡托普利治疗的高血压小鼠的SARS-CoV-2 复制与感染了SARS-CoV-2 的正常血压小鼠的病毒复制相似。此外，抗高血压治疗减轻了由 SARS-CoV-2 复制引起的IL-1β上调和免疫细胞浸润增加。在感染 SARS-CoV-2 的血压正常小鼠和高血压小鼠之间没有观察到肺部炎症的差异。因此，我们的研究结果初步表明，卡托普利治疗可能会缓解COVID-19的进展，但不会影响病毒复制。.
Keywords: Animal model; Captopril; Hypertension; Inflammation; SARS-CoV-2.