A Review of the Mechanism of Action and Role of Bradykinin in Severity of COVID-19 Symptoms

Abstract

Over a year has passed since the diagnosis of the first coronavirus disease 2019 (COVID-19) case in Wuhan, China. After that, this disease spread worldwide and infected people with a spectrum of symptoms, the most important and fatal of which are respiratory symptoms. Kinins, particularly bradykinin, are responsible for many respiratory functions, including vasodilation, vasoconstriction, and regulating permeability in vessels and lung tissue. The present study aims to review the bradykinin synthesis and degradation process, its mechanism of action, and its contribution to pulmonary function. Also, we investigate the role of bradykinin in treating and reducing the severity of COVID-19 symptoms. Results indicate that engagement of angiotensin-converting enzyme 2 (ACE2), a factor contributing to vasomotion and vascular permeability, as a result of virus entrance and its failure to inactivate des-Arg9-bradykinin (DABK) along with infiltration of proinflammatory cytokines, leads to increased vascular permeability and pulmonary edema. Consequently, inhibition of DABK synthesis or activity through blockade of the type 2 bradykinin receptors can help manage pulmonary edema.