Renin Related Peptides
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Introduction
Renin Substrates (RS), also known as Angiotensinogen, is a relatively abundant serum globulin in plasma, mainly synthesized in the liver, and is the only known natural renin substrate. After the amino acid fragment is cleaved by renin, a descending peptide precursor, angiotensin I (ATI), is formed. ATI is further converted to a biologically active octapeptide substance, ATII, under the action of angiotensin-converting enzyme. Although RS is not biologically active, its extracellular reserve as an angiotensin peptide may depend on its concentration to limit the rate of transformation of the renin-angiotensin system (RAS) and play an important role in RAS. Therefore, RS plays an important role in the normal development of the cardiovascular system, the maintenance of cardiovascular function, the maintenance of electrolyte and fluid balance, and the regulation of blood pressure.
Mechanism of action
Renin Substrates is hydrolyzed by the action of renin to produce a decapeptide (1-10), which is Ang I. In plasma and tissues, especially in the vascular endothelium of the pulmonary circulation, ACE is present. Under the action of ACE, ATI hydrolyzes 2 amino acid residues by C-terminal hydrolysis to produce an octapeptide (l-8), which is Ang II. In addition, ATI is hydrolyzed by various enzymes to produce a variety of polypeptides. Among them, the role of ATII is the most important. ATII exerts its cardiovascular function mainly through the ATII receptor, which can cause blood vessels to contract and raise blood pressure. Promote the secretion of aldosterone from the adrenal cortex. The action of aldosterone on the renal tubules can play the role of sodium retention, water retention, and potassium release, resulting in increased blood volume.
Application of Renin Substrates
The renin-angiotensin system (RAS) plays an important role in maintaining water and salt balance and regulating cardiovascular activity. Renin Substrates is the only precursor substance of angiotensin, and its concentration changes limit the rate of transformation in RAS. Therefore, controlling RS can prevent cardiovascular diseases such as cerebral infarction.
References
- McKinley, M. J., Albiston, A. L., Allen, A. M., Mathai, M. L., May, C. N., McAllen, R. M., ... & Chai, S. Y. (2003). The brain renin–angiotensin system: location and physiological roles. The international journal of biochemistry & cell biology, 35(6), 901-918.
- Reynier-Rebuffel, A. M., Pinard, E., Aubineau, P. F., Meric, P., & Seylaz, J. (1983). Generalized cerebral vasoconstriction induced by intracarotid infusion of angiotensin II in the rabbit. Brain research, 269(1), 91-101.
