Disclaimer This article, including its tables, is intended to serve as a review of possible agents or biochemical warfare from a perspective of neurocritical care. It is in no way complete, nor is it intended to be complete. The appropriate agencies need to be consulted in case of a suspected attack or casualty. New Cardiovascular and Pulmonary Therapeutic Strategies Based on the Angiotensin-Converting Enzyme 2/Angiotensin-(1–7)/Mas Receptor Axis Angiotensin (Ang)-(1–7) is now recognized as a biologically active component of the renin-angiotensin system (RAS). The discovery of the angiotensin-converting enzyme homologue ACE2 revealed important metabolic pathways involved in the Ang-(1–7) synthesis. This enzyme can form Ang-(1–7) from Ang II or less efficiently through hydrolysis of Ang I to Ang-(1–9) with subsequent Ang-(1–7) formation. Additionally, it is well established that the G protein-coupled receptor Mas is a functional ligand site for Ang-(1–7). The axis formed by ACE2/Ang-(1–7)/Mas represents an endogenous counter regulatory pathway within the RAS whose actions are opposite to the vasoconstrictor/proliferative arm of the RAS constituted by ACE/Ang II/AT(1) receptor. In this review we will discuss recent findings concerning the biological role of the ACE2/Ang-(1–7)/Mas arm in the cardiovascular and pulmonary system. Also, we will highlight the initiatives to develop potential therapeutic strategies based on this axis. The renin-angiotensin system (RAS) plays a key role in several target organs, such as heart, blood vessels, and lungs, exerting a powerful control in the maintenance of the homeostasis [1] [2] [3] [4] . This system is activated by the conversion of the angiotensinogen to the inactive peptide angiotensin (Ang) I through the renin action [5] . Subsequently, Ang I is cleaved by the angiotensin-converting enzyme (ACE) generating Ang-(1-7) by ACE2 is important to regulate the RAS activity since Ang-(1-7) induces opposite effects to those elicited by Ang II [16] [17] [18] [19] [20] [21] [22] [23] [24] . Additionally, ACE2 can form Ang-(1-7) less efficiently through hydrolysis of Ang I to Ang-(1-9) with subsequent Ang-(1-7) formation [24] .