- Pro-inflammatory processes in ARDS disrupt ACE function in the pulmonary endothelium. Thus, Ang-1 (angiotensin I) cannot be hydrolyzed to Ang-2.
- Excess Ang-1 contributes to hypotension via 4 physiological mechanisms: (1) decrease in smooth muscle contraction, (2) metabolism into Ang-(1-7) to agonize vasodilatory MAS and AT2 receptors (3) Activation of NO production (4) Impairs hydrolysis of bradykinin into bradykinin (1-7) and bradykinin (1-5)
- Exogenous Ang-2 decreases Ang-1 production and targets AT1 receptors to increase vascular tone.
- There is a strong physiological rationale for using exogenous Ang-II to treat COVID-19 associated vasodilatory shock compared to conventional vasopressors.
This information was taken from a physiological rationale paper on exogenous Ang-2 for the treatment of COVID-19-related shock. At this time, only a pre-print version of the paper is available. No trials of Ang-2 in COVID-19 cases are cited, but studies showing the effectiveness of Ang-2 in high-output shock are reported.
Chow et al. (March 23, 2020). Angiotensin II for the Treatment of COVID-19–Related Vasodilatory Shock. Anesthesia and Analgesia. DOI: 10.1213/ANE.0000000000004825