renin-angiotensin system

Sevelamer carbonate is a non-absorbed phosphate binding crosslinked polymer, with the same polymeric structure as sevelamer hydrochloride, in which carbonate replaces chloride as the counterion.

Diammonium Glycyrrhizinate (Glycyrrhizin) , an extensively used anti-inflammatory agent, is isolated from the licorice root. It is metabolized to glycyrrhetinic acid, which inhibits 11-β-hydroxysteroid dehydrogenase and other enzymes involved in the metabolism of corticosteroids. Therefore, glycyrrhizic acid, the main and sweet component of licorice, has been studied for its ability to cause hypermineralocorticoidism with potassium loss and sodium retention, edema, increased blood pressure, as well as inhibited the renin-angiotensin-aldosterone system.

Angiotensin II human acetate is a key vasoconstrictor peptide in the renin-angiotensin system. It regulates blood pressure by binding to AT1R and AT2R receptors, stimulates the sympathetic nervous system, promotes aldosterone synthesis and renal function, induces vascular smooth muscle cell proliferation and collagen synthesis, leading to vascular and myocardial hypertrophy and fibrosis, while also promoting apoptosis and endothelial capillary formation. It is commonly used to induce hypertension and cardiac hypertrophy models.

Alamandine TFA , a member of the renin-angiotensin system (RAS), a vasoactive peptide, is an endogenous ligand of the G protein-coupled receptor MrgD. Alamandine TFA targets to protect the kidney and heart through anti-hypertensive actions[1][2].

Angiotensinogen (1-14), human acetate is a fragment of angiotensinogen which is a passive substrate of the renin-angiotensin system.

Aldosterone, the primary mineralocorticoid, is synthesized and secreted by the zona glomerulosa of the adrenal cortex in response to activation of the renin-angiotensin system or high dietary potassium.

Angiotensin 1/2 (5-7) is a peptide with the sequence H2N-Ile-His-Pro-OH. Angiotensin is an oligopeptide and is a hormone and a powerful dipsogen. It is derived from the precursor molecule angiotensinogen, a serum globulin produced in the liver. It plays a

Angiotensin 1 2 (5-7) acetate is a peptide with the sequence H2N-Ile-His-Pro-OH. Angiotensin is an oligopeptide and is a hormone and a powerful dipsogen. It is derived from the precursor molecule angiotensinogen, a serum globulin produced in the liver. It

Angiotensin Fragment 1-7 is a type 1 angiotensin II receptor agonist. In the renin-angiotensin system, angiotensin I is cleaved by the angiotensin-converting enzyme to form angiotensin II, which has effects on fluid and electrolyte, as well as homeostasis

A 65317 is a selective renin inhibitor that causes a blockade of the renin-angiotensin system.

Angiotensin I II (1-6) TFA is a chemical compound comprising amino acids 1-6, derived from the Angiotensin I II peptide. This peptide is formed by the cleavage of angiotensinogen by renin, with Angiotensin I subsequently hydrolyzed by angiotensin-converting enzyme (ACE) to produce biologically active Angiotensin II. Angiotensin II has been extensively studied for its potential applications in the treatment of Hypertension, Renin Angiotensin System, and Idiopathic Membranous Nephropathy[1][2][3].

Angiotensin II human TFA is a potent vasoconstrictor in the renin-angiotensin system that regulates blood pressure through interactions with AT1R and AT2R receptors. It activates sympathetic nerve activity, promotes aldosterone synthesis and renal function, induces proliferation of vascular smooth muscle cells, and enhances type I and III collagen production in fibroblasts, leading to vascular and myocardial thickening and fibrosis. It also triggers apoptosis and promotes capillary formation, making it suitable for establishing models of cardiac hypertrophy, hypertension, and abdominal aortic aneurysm.

Angiotensin I (human, mouse, rat) is the precursor to the vasoconstrictor peptide angiotensin II, cleaved by the angiotensin-converting enzyme (ACE). This peptide hormone causes vasoconstriction and increases blood pressure as part of the renin–angiotensin system, also stimulating aldosterone release from the adrenal cortex to promote sodium retention by the kidneys.