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The renin–angiotensin–aldosterone system (RAAS) has been recognized as a key player in the complex scenario of cardiovascular regulation. Aside from its role in the cardiovascular diseases, RAAS dysregulation has emerged as a central pathomechanism in the severe acute respiratory syndrome coronavirus 1 (SARS-CoV1) epidemic, dating back to 2002–2004, and the current COVID-19 pandemic with SARS-CoV2, with the latter involving the interaction with angiotensin-converting enzyme 2 (ACE2). ACE2 is the enzyme responsible for Ang 1-7 production that partly counteracts the RAAS effects and promotes nitric oxide synthase activation; moreover, it has also been reported to act as a receptor for both SARS viruses. In the setting of the ongoing COVID-19 pandemic, the SARS–ACE2 interaction is highly debated with respect to both viral infectivity and usage/discontinuation of RAAS medication—ACE inhibitors (ACEi) and angiotensin-receptor blockers (ARBs)—in diagnosed or suspected SARS-CoV2 patients. Since ACE inhibitors and ARBs are largely prescribed in cardiovascular pathology, a better understanding of the interaction between SARS-CoV2 and RAAS is urgently needed. In this review, we will briefly discuss the SARS-CoV2 and ACE2 interaction and why the discontinuation of RAAS medication is unsafe for either diagnosed or suspected SARS-CoV2 patients.

Keywords: angiotensin-converting-enzyme 2; SARS-Cov2; COVID-19 pandemic