Recent evidence has demonstrated SARS-CoV-2 uses ACE2 as an internalization receptor to enter the target cells. The spike (S) glycoprotein of SARS-CoV-2 recognizes and interacts with its target ACE2 receptor on the host cell surface, mediating viral entry during the infection cycle (Letko, Marzi, & Munster, 2020; Yan et al., 2020). Excessive binding of spike protein to ACE2 leads to downregulation of the ACE2 receptor (Jung et al., 2020). This finding is consistent with reports in the animal models infected with SARS-CoV (Crackower et al., 2002; Imai et al., 2005; Kuba et al., 2005). The reduction in ACE2 levels leads to excessive pro-inflammatory responses adversely affecting both lung and cardiovascular systems (Crackower et al., 2002; Imai et al., 2005; Kuba et al., 2005). These detrimental effects can be explained as the partial decrease in ACE2 function leads to dominant angiotensin II effects, including augmented cytokine storm, inflammation, vasoconstriction and susceptibility for thrombosis. These effects further increase the cardiovascular burden by worsening hypertension, HF and other cardiovascular disorders in predisposed patients (Liu, Blet, Smyth, & Li, 2020; Oudit et al., 2009). Importantly, the accumulation of Ang II was positively associated to viral load and lung injury (Liu et al., 2020). Moreover, reduction in the activity and/or number of ACE2 leads to deficiency of Ang-(1–7) production and consequently loss of its anti-inflammatory, vasodilatory, and cardiovascular protective effects (Lelis, Freitas, Machado, Crespo, & Santos, 2019; Patel et al., 2016). Therefore, it is hypothesized that inhibition of RAAS may be helpful to attenuate the inflammatory storm and ameliorate end-organ damage. Interestingly, recent data indicates individuals with COVID-19 who are being treated with ACE inhibitors or ARBs, for pre-existing conditions, are at lower risk of 28-day all-cause mortality than those not treated with ACE inhibitors or ARBs (Wang et al., 2020; Zhang et al., 2020). Although ARBs and ACE inhibitors do not directly impact ACE2, they indirectly elevate ACE2 activity and the beneficial Ang-(1–7) production and counter the excessive production of the harmful Ang II (Hanff, Harhay, Brown, Cohen, & Mohareb, 2020). Therefore, it was proposed that maintaining the levels of ACE2 and its downstream effector Ang-(1–7) may limit cardiovascular damage secondary to COVID-19 (Wang, Edin, et al., 2020).