About REN / Renin:
Renin is a protein that converts angiotensinogen into angiotensin I.
Renin refers to an enzyme that is formed in the kidney.
Renin produces angiotensin II, which, when produced, increases blood pressure and renal sodium retention.
It also inhibits aldosterone secretion from the adrenal cortex to control levels of potassium, phosphate, calcium, magnesium, and hydrogen ions in body fluids.
The kidneys release the renin hormone into your bloodstream as it detects salt concentration changes, which helps regulate blood flow through the kidneys.
The mechanism of renin is still not completely understood, but it involves two main steps. Step one is the cleavage of angiotensinogen into angiotensin I by a protease (angiotensin-converting enzyme or ACE). The second step occurs when this protein converts to Ang II with an amidohydrolase and has some other processes that happen before finally producing aldosterone. This conversion process happens in cells like those found in kidney tubules, blood vessels, and tissues from the lungs, heart, brain, stomach wall, and pancreas.
The protein has a molecular weight of 67.000 g/mol and consists of about 1000 amino acids. A significant part of the enzyme comprises alpha-helices or coils formed by neighbouring loops that form beta-sheets. The molecule also contains two lobes consisting primarily of beta strands: one lobe with an N-terminal DNA binding domain and another lobe with a reactive site containing three cysteine residues (Cys) close to each other known as Cys 33 Glu 34 His 35.
There is no clear consensus yet concerning how this hydrogen bond network stabilizes the active state. Still, for example, it could be hypothesized that these interactions may help stabilize the catalytic triad to attack the substrate better, which is, in turn, held more securely by the H-bonds formed between its protein and ligand.
Renin helps to regulate blood pressure by interacting with other proteins called protease-activated receptors (PARs). PARs are found on the walls of blood vessels and detect certain substances made from damaged cells to initiate an inflammatory response. When renin is released, it binds to these same PARs.
In addition, it has a synergistic effect when combined with another protein called plasminogen activator inhibitor type-III (PAI-III) which can inhibit PAI-II and tPA that would also destroy fibrin clots. This means that not only does renin help remove low-density lipoproteins or cholesterol from the bloodstream, but it can promote clotting at the site of injury while inhibiting hemorrhaging.