PMC:7170368 / 9309-11999 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7170368","sourcedb":"PMC","sourceid":"7170368","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7170368","text":"Discussion\nIt was reported that the RAS plays a critical role in regulating hypertension and acute lung injury caused by viruses, such as SARS and H7N9 [5,7]. Changes in RAS activity are related to the pathogenesis of hypertension and inflammatory lung disease. Targeting RAS is an effective antihypertension therapeutic strategy. ACEIs and ARB, which inhibit the ACE/Ang II/AT1R system, are commonly used drugs for hypertensive patients. Recent evidence suggests that hypertensive COVID-19 patients are predisposed to develop severe cases [1]. Thus, it is important to determine the effect of RAS inhibitors on COVID-19 patients with hypertension.\nStudies have suggested that COVID-19 patients have increased Angiotensin II compared to healthy people [8]. The abnormal increase in Angiotensin II was related to hypertension and lung failure. In addition, RAS inhibitors have been shown to be associated with reduced mortality in patients with sepsis [9]. Angiotensin II positively regulates the expression of inflammatory cytokines through the activation of AT1R [10]. Excessively high levels of inflammatory cytokines are harmful to the outcomes of COVID-19 patients. Thus, it was suggested that it is beneficial for COVID-19 patients to use ACEIs/ARBs to inhibit the RAS. However, until now, no confirmed clinical evidence has been available. In this study, COVID-19 patients with hypertension were enrolled, and we found that ACEI/ARB therapy attenuated the inflammatory response, potentially through the inhibition of IL-6 levels, which is consistent with the findings that ACEI and ARB therapy alleviated LPS-induced pneumonic injury [11]. For patients with chronic heart failure, it has been proven that ACEI therapy was associated with decreased Th1/Th2 cytokine ratios and inflammatory cytokine production [12]. This study also suggests that ACEI/ARB therapy had a beneficial effect on the immune system by avoiding peripheral T cell depletion. Furthermore, the viral load was reported to be highly correlated with severe lung injury [8]. It was also observed that ACEI/ARB therapy decreased the viral load, but we hypothesize that RAS inhibitors do not directly inhibit viral replication; rather, they play an indirect antiviral role by regulating immune function and inhibiting inflammatory responses, and the mechanism needs to be clarified through in vitro and in vivostudies in the future.\nTaken together, this is the first clinical evidence demonstrating that RAS inhibitors improve the clinical outcomes of COVID-19 patients with hypertension, suggesting that these patients could benefit from the persistent or preferential usage of ACEI/ARB for antihypertensive 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