Renin-angiotensin-system, a potential pharmacological candidate, in acute respiratory distress syndrome during mechanical ventilation

Highlights

• This review highlights a dual role of renin-angiotensin system in the pathogenesis of acute respiratory distress syndrome, as well as ventilator-induced lung injury.

• This review also highlights the evidence, from both of experimental and clinical studies, of targeting renin-angiotensin system with pharmacological tools to improve outcomes in acute respiratory distress syndrome.

• This review not only focuses the traditional view about ACE/Ang-II/AT1R axis and ACE2/Ang-(1–7)/MasR axis, but also mentions AT2R which increasingly be a promising target in ARDS, as well as VILI.

Abstract

While effective treatments for acute respiratory distress syndrome (ARDS) are lacking, mechanical lung ventilation can sustain adequate gas exchange in critically ill patients with respiratory failure due to ARDS. However, as a result of the phenomenon of ventilator-induced lung injury (VILI), there is an increasing need to seek beneficial pharmacological therapies for ARDS. Recent studies have suggested the renin-angiotensin system (RAS), which consists of the ACE/Ang-II/AT1R axis and ACE2/Ang-(1–7)/MasR axis, plays a dual role in the pathogenesis of ARDS and VILI. This review highlights the deleterious action of ACE/Ang-II/AT1R axis and the beneficial role of ACE2/Ang-(1–7)/MasR axis, as well as AT2R, in VILI and ARDS, and also discusses the possibility of targeting RAS components with pharmacological interventions to improve outcomes in ARDS.