Angiotensin II human


CAS No. : 4474-91-3

(Synonyms: Angiotensin II; Ang II; DRVYIHPF)

4474-91-3
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Cat. No. : HY-13948
M.Wt: 1046.18
Formula: C50H71N13O12
Purity: >98 %
Solubility: DMSO : 10 mg/mL (ultrasonic;warming;heat to 60°C);H2O : ≥ 10 mg/mL
Introduction of 4474-91-3 :

Angiotensin II (Angiotensin II) is a vasoconstrictor and a major bioactive peptide of the renin/angiotensin system. Angiotensin II human 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 stimulates sympathetic nervous stimulation, increases aldosterone biosynthesis and renal actions. Angiotensin II human 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 also induces apoptosis. Angiotensin II induces capillary formation from endothelial cells via the LOX-1 dependent redox-sensitive pathway[1][2][3][4]. IC50 & Target:Angiotensin receptor (AT receptor)[1] In Vitro:Most of the known actions of Angiotensin II (Ang II) are mediated by AT1 receptors, the AT2 receptor contributes to the regulation of blood pressure and renal function[1]
. Angiotensin II 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 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) 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]. In Vivo:Note:
Please do not refer to only one article to determine the experimental conditions. It is recommended to determine the optimal experimental conditions (animal strain, age, dosage, frequency and cycle, detection time and indicators, etc.) through preliminary experiments before the formal experiment.

Angiotensin II is internalized by various cell types through receptor-mediated endocytosis and is highly enriched in tissues such as the heart, kidney, and adrenal glands. The concentration in skeletal muscle tissue is 8%-41% of the plasma concentration, 64%-150% in the heart, 340%-550% in the kidney, and as high as 680%-2100% in the adrenal gland. It takes only about 5 minutes for Angiotensin II in plasma to reach a steady-state concentration, while it takes 30-60 minutes to reach a steady-state concentration in tissues. The half-life of Angiotensin II in the circulation system is extremely short (about 0.5 minutes), while in the heart, kidney, and adrenal tissues, the in vivo half-life of Angiotensin II formed after endocytosis is significantly extended to about 15 minutes[6]. Angiotensin II human can be used to induce models of hypertension, cardiac hypertrophy and abdominal aortic aneurysm[6][7][8][9].

1. Induction of hypertension[7]
Background
Angiotensin II human induces hypertension by activating AT1 receptors, leading to vasoconstriction, sodium and water retention, sympathetic nervous system activation, and oxidative stress.
Specific Modeling Methods
Mice: C57/BL6J • male and female • 12-16 wk old • 21-27 g
Administration: 800 ng/kg/min, 0.003 mL/min • 7 days • sc, osmotic pump implanted subcutaneously
Note
Effect of gender: Chronic ANG II-induced hypertension differs by gender in awake mice. Female mice may be protected from the ANG II-induced increase in blood pressure.
Modeling Indicators
Key Factor: Blood pressure ↑ on day 7, blood pressure in male was greater than in female.
2. Induction of Cardiac Hypertrophy[8]
Background
Angiotensin II human induces cardiac hypertrophy by activating the AT1 receptor, leading to inflammation, oxidative stress, and extracellular matrix remodeling, which cause myocardial cell proliferation and hypertrophy.
Specific Modeling Methods
Mice: C57/BL6J • male • 8 wk old •
Administration: 2 μg/kg/min • 4 weeks • sc, osmotic pump implanted subcutaneously
Note
Modeling Indicators
Indicator changes: Blood pressure in WT mice increased significantly.
Appearance monitoring: cardiac hypertrophy and fibrosis.
Opposite Product(s): Eplerenone (HY-B0251)
3. Abdominal aortic aneurysm model[9]
Pathogenic mechanism
Angiotensin II induces atherosclerosis by stimulating monocyte recruitment, macrophage activation, and enhancing oxidative stress, ultimately leading to local dilation and thinning of the abdominal aorta in mice and the formation of abdominal aortic aneurysm.
Specific modeling method
Mice: ApoE–/– mice • female • 6-month-old
Administration: 500 or 1000 ng/min/kg • s.c. • 28 days
Modeling success index
Cellular changes: Increased in lipid-laden macrophages and lymphocytes in the aortic intima.
Phenotype observation: There are a large number of atherosclerotic lesions in the mice. The size of the abdominal area of the aorta is significantly increased, there is a large amount of adventitial tissue, and blood clots exist in the adventitial tissue, and new blood vessels appear on the outer surface.
Antagonist products: (±)-Clopidogrel bisulfate (HY-107867)

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