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Angiotensin II human acetate

CAS No. : 68521-88-0

MCE 国际站：Angiotensin II human acetate

产品活性：Angiotensin II human (Angiotensin II) acetate 是一种血管收缩剂，是肾素/血管紧张素系统的主要生物活性肽。Angiotensin II human acetate 在调节人类血压中起着核心作用，主要通过血管紧张素 II 与 G 蛋白偶联受体 (GPCRs)、血管紧张素II 1型受体 (AT1R) 和血管紧张素II 2型受体 (AT2R) 之间的相互作用来介导。Angiotensin II human acetate 刺激交感神经刺激，增加醛固酮生物合成和肾脏活动。Angiotensin II human acetate 诱导血管平滑肌细胞生长，增加成纤维细胞中 I 型和 III 型胶原的合成，导致血管壁和心肌增厚，并导致纤维化。Angiotensin II human acetate 也诱导细胞凋亡。Angiotensin II human acetate 通过 LOX-1 依赖的氧化还原敏感途径诱导内皮细胞毛细血管形成。

研究领域：GPCR/G Protein  |  Apoptosis

作用靶点：Angiotensin Receptor  |  Apoptosis

In Vitro: Most of the known actions of Angiotensin II (Ang II) human acetate are mediated by AT1 receptors, the AT2 receptor contributes to the regulation of blood pressure and renal function.
Angiotensin II human acetate 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 acetate 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).
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, were 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.

In Vivo: Angiotensin II human (5 mL of 1 nM; intraperitoneal injection; 200-250 g Sprague-Dawley rats) acetate induces a significant neutrophil recruitment that was maximal at 4 hours and had resolved by 24 hours.
To distinguish the AT₁ receptor population that is critical for the pathogenesis of hypertension, osmotic minipumps are implanted s.c. into each animal to infuse Angiotensin II human (1000 ng/kg/min) acetate continuously for 4 weeks. Angiotensin II human acetate causes hypertension by activating AT₁ receptors in the kidney promoting sodium reabsorption.

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