Infection by β-coronavirus SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus-
2) alters the homeostasis of the vascular endothelium, promoting an inflammatory state
which causes damage and favors the prothrombotic state. The direct viral cytotoxicity induced by
the SARS-CoV-2 leads to endothelial cell death; thus, altering the vessel functions. Moreover,
SARS-CoV infection induces endothelial dysfunction (ED) and reduces the levels of nitric oxide
(NO); thus, aggravating the vascular injuries, which promotes thrombotic events due to an alteration
in the homeostasis. NO is a pleiotropic molecule that induces vasodilation, regulates the immune
response, inhibits platelet aggregation, and decreases the cellular adhesion to vascular endothelium.
Moreover, NO acts directly against invasive agents, exhibiting antibacterial, antiviral,
and antifungal activity. High levels of NO result in an increase in the ED, causing an inflammatory
amplification that aggravates the disease through undesirable positive feedback. The objective of
this review was to present and discuss the involvement of NO on ED in SARS-CoV-2 infections.
This review may also highlight new perspectives for therapeutic interventions through the supplementation
of exogenous NO. The maintenance of homeostatic NO levels could represent a useful
approach in the prevention of coronavirus-induced ED.