Angiotensin is a peptide that can narrow down the blood vessels and lift up the blood pressure. Renin-angiotensin system is a group of peptides that act as receptors for drugs that take part in lowering the blood pressure. Angiotensin peptide also aids in secretion of aldosterone from the cortical region of the adrenal gland. Aldosterone helps in retaining the sodium in the distal part of the Nephron of the kidney. This will raise the blood pressure. Angiotensin has originated from its precursor angiotensinogen. Angiotensinogen is a globulin molecule produced in the liver. The angiotensinogen in human has a length of 452 amino acids while its length in other species might be different. The part of the peptide which is mostly involved in its function is the first twelve amino acids which are Asp-Arg-Val-Tyr-Ile-His-Pro-Phe-His-Leu-Val-Ile.
Angiotensin-I is found to regulate the mechanism of Angiotensin II. Angiotensin-II is responsible for many complications related to vascular system due to Diabetes mellitus. According to the studies conducted in Malaysia and Singapore, pretreatment of rats with Angiotensin-I (10-7M) decreased the effects of Angiotensin -I in normoglycemic rats and not in diabetic rats. Human Angiotensin-I has the molecular weight of 1296.5 with the polypeptide sequence of DRVYIHPFHL. The three letter code of Angiotensin-I sequence is H-Asp-Arg-Val-Tyr-Ile-His-Pro-Phe-His-Leu-OH. Angiotensin-II results from the cleavage of Angiotensin-I by the enzyme called Angiotensin-converting enzyme. It is found from the studies that non-Angiotensin converting enzyme also is involved in conversion of Angiotensin-I to Angiotensin-II. It is proved that Chymase in humans effectively converted decapeptide Angiotensin-I to octapeptide Angiotensin-II by breaking the bond in Angiotensin-I at Phe-His9 position.
This N-terminal decapeptide Angiotensin-I is observed to have resulted from angiotensinogen in the liver when rennin acts on it. Renin is released from the kidneys due to the activity of renal sympaticus, reduced blood pressure in the kidney interior near the juxtaglomerular cells or due to the reduced supply of Na+ and Cl- to Macula densa. If the Macula densa does not sense much of Na+, then it says that the delivery of renin by the juxtaglomerular cells has increased. Renin will break the peptide bond that exists between the Leucine and Valine amino acid residues of angiotensinogen. The resultant peptide is made of of 10 amino acids called as Angiotensin-I. Angiotensin I has no physiologic role as such; instead acts as precursor for Angiotensin II. Angiotensin II is found to be involved in vasoconstriction and hence enhances blood pressure. Temocapril (30 micromole/L) is one of the drugs that can prevent the vasoconstriction due to Angiotensin-I.