Renin-angiotensin-aldosterone axis, or renin-angiotensin aldosterone system (RAAS) is a vital one, for survival. This system maintains vascular tonicity by regulating extracellular fluid volume and arterial pressure. By this system, water, blood, plasma, lymph and interstitial fluid are controlled tightly for functioning of the pulsating organ heart and filtration organ kidney, without the onslaught of either extremes. Perturbation of this system can disturb blood pressure, leading to chronic or acute diseases, or even sudden death. Renin and angiotensin are two critical components forming the system. Renin (or angiotensinogenase), is secreted by the kidney granular cells.
 Angiotensinogen is a member of the serpin family (SERPINA8), so a potential enzyme inhibitor. The decapeptide angiotensin I further undergoes cleavage in the lungs capillaries, endothelial cells, and kidney epithelial cells by the endothelial-bound angiotensin-converting enzyme (ACE). This enzyme, a carboxypeptidase, also known as kininase II, peptidyl-dipeptidase A, or CD143, converts angiotensin I into the peptide angiotensin II. ACE is a common component of the RAAS, as well as kinin- kallikrein system (KKS). ACE interacts with Gprotein-coupled receptor (GPCR) AT1 by stimulating the Gq protein in vascular smooth muscle cells to activate phospholipase C, for increasing intracellular calcium. So, angiotensin II is a critical regulator of blood volume, pressure, and pH. Renin induced increment in TGF-b1 (transforming Growth Factor-b1) stimulates increment in PAI-1, fibronectin (FN) and collagen I, which indicates that renin plays part in renal fibrotic disease. A large number of factors can influence RAAS, some prominent of which include birth control pills, pregnancy, other hormones (estrogen, testosterone, thyroid, cortisol), diuretics, vasodilators, blood pressure drugs, also other medications.

References

1.Patel S, et al. Biomed Pharmacother. 2017;94:317–325.