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Symptoms of COVID-19 range from asymptomatic/mild symptoms to severe illness and death, consequence of an excessive inflammatory process triggered by SARS-CoV-2 infection. The diffuse inflammation leads to endothelium dysfunction in pulmonary blood vessels, uncoupling eNOS activity, lowering NO production, causing pulmonary physiological alterations and coagulopathy. On the other hand, iNOS activity is increased, which may be advantageous for host defense, once NO plays antiviral effects. However, overproduction of NO may be deleterious, generating a pro-inflammatory effect. In this review, we discussed the role of endogenous NO as a protective or deleterious agent of the respiratory and vascular systems, the most affected in COVID-19 patients, focusing on eNOS and iNOS roles. We also reviewed the currently available NO therapies and pointed out possible alternative treatments targeting NO metabolism, which could help mitigate health crises in the present and future CoV's spillovers. [Display omitted] • Pathophysiological alterations due to SARS-CoV-2 infection lead to an imbalance NO production. • Reduction of eNOS-derived NO production causes endothelial dysfunction, which represents a risk factor for sever COVID-19. • Excessive iNOS-mediated NO production promotes peroxynitrite formation, which generates several cellular damages. • Therapies that regulate NO bioavailability and production could be the answer for dealing with the present and futures CoV's spillovers. [ABSTRACT FROM AUTHOR]