Figure 3.

Schematic representation of the peptide flux involved in the RAAS highlighting the participation of the viral receptors ANPEP, DPP-IV, and ACE2. When hypotension is detected, the Angiotensinogen produced in the liver, is catalyzed by the enzyme renin synthetized in the juxtaglomerular cells in the kidney. The product Ang I is either cleaved by the ACE to produce Ang II, which activates any of the Ang II receptors (AT1R and AT2R). Ang I and Ang II can be also cleaved by ACE2 to produce Ang (1-9) and Ang (1-7), respectively. The additional cleavage of ACE to Ang (1-9) produces Ang (1-7) which finally activates the MasR. Additionally, Ang II can be further catalyzed twice by ANPEP producing Ang IV, which activates the AT4R. The effects every Ang II Receptor has, counteracts others so the accurate balance is necessary in order to control blood pressure, osmolarity and inflammation. Ang II is also necessary for aldosterone secretion, which reabsorbs sodium in the kidney, and the antidiuretic hormone release which retains water. The overall effect of the system is the increase of blood pressure. The blockage of the enzymes either with coronaviruses or with other molecules, alters the homeostasis of blood pressure and osmolarity.