Angiotensin II human TFA  (Synonyms: Angiotensin II TFA; Ang II TFA; DRVYIHPF TFA)

Angiotensin II human (Angiotensin II) TFA is a vasoconstrictor and a major bioactive peptide of the renin/angiotensin system. Angiotensin II human TFA plays a central role in regulating human blood pressure, which is mainly mediated by interactions between Angiotensin II and the G-protein-coupled receptors (GPCRs) Angiotensin II type 1 receptor (AT1R) and Angiotensin II type 2 receptor (AT2R). Angiotensin II human TFA stimulates sympathetic nervous stimulation, increases aldosterone biosynthesis and renal actions. Angiotensin II human TFA induces growth of vascular smooth muscle cells, increases collagen type I and III synthesis in fibroblasts, leading to thickening of the vascular wall and myocardium, and fibrosis. Angiotensin II human TFA also induces apoptosis. Angiotensin II human TFA induces capillary formation from endothelial cells via the LOX-1 dependent redox-sensitive pathway^[1][2][3][4].

Most of the known actions of Angiotensin II (Ang II) human are mediated by AT1 receptors, the AT2 receptor contributes to the regulation of blood pressure and renal function^[1].
Angiotensin II human raises blood pressure (BP) by a number of actions, the most important ones being vasoconstriction, sympathetic nervous stimulation, increased aldosterone biosynthesis and renal actions. Other Angiotensin II human actions include induction of growth, cell migration, and mitosis of vascular smooth muscle cells, increased synthesis of collagen type I and III in fibroblasts, leading to thickening of the vascular wall and myocardium, and fibrosis. These actions are mediated by type 1 Ang II receptors (AT₁)^[2].
Angiotensin II (1 nM) TFA induces the expression of LOX-1 and VEGF and enhances capillary formation from human coronary endothelial cells in Matrigel assay. Angiotensin II-mediated expression of LOX-1 and VEGF, capillary formation, intracellular reactive oxygen species generation, and phosphorylation of p38 as well as p44/42 mitogen-activated protein kinases, are suppressed by anti-LOX-1 antibody, nicotinamide-adenine dinucleotide phosphate oxidase inhibitor apocynin and the Ang II type 1 receptor blocker Losartan, but not by the Ang II type 2 receptor blocker PD123319^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Angiotensin II human TFA can be used to create models of hypertension and cardiac hypertrophy. In 200-250 g Sprague-Dawley rats, intraperitoneal injection of 5 mL 1 nM Angiotensin II human TFA significantly induces neutrophil recruitment, which peaks at 4 hours and resolves within 24 hours. To specifically investigate the role of AT₁ receptors in the pathogenesis of hypertension, osmotic mini-pumps are used to continuously infuse Angiotensin II human TFA (1000 ng/kg/min) into each rat for 4 weeks. This process promotes sodium reabsorption by activating renal AT₁ receptors, leading to the development of hypertension^[4][5].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

1046.18 (free acid)

C₅₀H₇₁N₁₃O₁₂.xC₂HF₃O₂

2761969-44-0

Solid

White to off-white

Asp-Arg-Val-Tyr-Ile-His-Pro-Phe

DRVYIHPF

Room temperature in continental US; may vary elsewhere.

Sealed storage, away from moisture and light, under nitrogen

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light, under nitrogen)

• [1]. de Gasparo M, et al. International union of pharmacology. XXIII. The angiotensin II receptors. Pharmacol Rev. 2000 Sep;52(3):415-72.  [Content Brief]

  [2]. Fyhrquist F, et al. Role of angiotensin II in blood pressure regulation and in the pathophysiology of cardiovascular disorders. J Hum Hypertens. 1995 Nov;9 Suppl 5:S19-24.  [Content Brief]

  [3]. Hu C, et al. Angiotensin II induces capillary formation from endothelial cells via the LOX-1 dependent redox-sensitive pathway. Hypertension. 2007;50(5):952-957.  [Content Brief]

  [4]. Nabah YN, et al. Angiotensin II induces neutrophil accumulation in vivo through generation and release of CXC chemokines. Circulation. 2004;110(23):3581-3586.  [Content Brief]

  [5]. Crowley SD, et al. Angiotensin II causes hypertension and cardiac hypertrophy through its receptors in the kidney. Proc Natl Acad Sci U S A. 2006 Nov 21;103(47):17985-90.  [Content Brief]