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Journal|[J]Journal of Ideas in HealthVolume 4, Issue Special2. 2021. PP 389-394
MT肾素-血管紧张素-醛固酮系统抑制剂——COVID-19中的一个混乱领域
Renin-angiotensin-aldosterone system inhibitors – a realm of confusion in COVID-19
摘要 / Abstract
MT
目前,关于肾素-血管紧张素-醛固酮系统( RAAS )抑制剂在COVID-19大流行中的使用安全性存在持续争议。一方面,RAAS抑制剂似乎决定了SARS-CoV-2受体ACE2的过度表达。因此,它们可增加SARS-CoV-2感染的危险性及其严重程度。另一方面,RAAS的停用导致心血管失代偿,各大医学会的劝阻。此外,大队列研究报告了对COVID - 19患者RAAS抑制剂有益或至少中性作用。在全世界,数百万患者接受RAAS抑制剂治疗高血压和其他重要的合并症。在这种情况下,了解这些药物的确切效果就变得至关重要。本文旨在填补当前知识的空白,提出一个推定的机制,借此更好地解释RAAS抑制剂给药的有益结果。RAAS抑制剂可以是有益的,因为它们抵消了经典血管紧张素转换酶( ACE )轴的过度有害激活,使血管紧张素Ⅱ水平下降。血管紧张素受体阻滞剂( ARBs )增加血管紧张素Ⅱ水平,血管紧张素转换酶抑制剂( ACEI )增加血管紧张素Ⅰ水平;这些底物将与SARS - CoV - 2竞争ACE2结合,降低病毒感染性。此外,经RAAS抑制剂治疗后,上调的ACE2会裂解这些底物( 血管紧张素Ⅰ和Ⅱ ),特别是对血管紧张素1 - 7具有扩血管、保护作用。
原文
Currently, there is a persisting dispute regarding the renin-angiotensin-aldosterone-system (RAAS) inhibitors' safety of use in COVID-19 pandemics. On one side, RAAS inhibitors appear to determine an overexpression of ACE2, the receptor of SARS-CoV-2. Therefore, they could increase the risk of SARS-CoV-2 infection and its degree of severity. On the other side, the discontinuation of RAAS leads to cardiovascular decompensation and has been discouraged by the major medical societies. Also, large-cohort studies report beneficial or at least neutral effects for the RAAS inhibitors in COVID-19 patients. Worldwide, millions of patients receive RAAS inhibitors for the treatment of hypertension and other important comorbidities. In this context, knowledge of the exact effect of these medications becomes of crucial significance. This paper aims to fill in a gap in the current knowledge and presents a putative mechanism by which RAAS inhibitor administration's beneficial results can be explained better. RAAS inhibitors can be beneficial, as they counteract the excessive detrimental activation of the classical angiotensin-converting enzyme (ACE) axis, decreasing the angiotensin II levels. The angiotensin receptor blockers (ARBs) increase the angiotensin II levels, while the angiotensin-converting enzyme inhibitors (ACEI) increase the angiotensin I levels; these substrates will compete with the SARS-CoV-2 for the ACE2 binding, decreasing the viral infectivity. In addition, following the RAAS inhibitors treatment, the up-regulated ACE2 will cleave these substrates (angiotensin I and II), particularly to angiotensin 1-7 that possesses vasodilator, protective effects.
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