Angiotensin II human(Synonyms: 血管紧张素Ⅱ Angiotensin II Ang II DRVYIHPF)

Angiotensin II human;(Synonyms: 血管紧张素Ⅱ; Angiotensin II; Ang II; DRVYIHPF) 纯度: 99.48%

Angiotensin II (Angiotensin II) 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 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 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 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 也诱导细胞凋亡 (apoptosis)。Angiotensin II human 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。

Angiotensin II humanamp;;(Synonyms: 血管紧张素Ⅱ; Angiotensin II;  Ang II;  DRVYIHPF)

Angiotensin II human Chemical Structure

CAS No. : 4474-91-3

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生物活性

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]

体外研究
(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].

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

体内研究
(In Vivo)

Angiotensin II human (5 mL of 1 nM; intraperitoneal injection; 200-250 g Sprague-Dawley rats) induces a significant neutrophil recruitment that was maximal at 4 hours and had resolved by 24 hours[4].
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 (1000 ng/kg/min) continuously for 4 weeks. Angiotensin II causes hypertension by activating AT1 receptors in the kidney promoting sodium reabsorption[5].

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

Clinical Trial

分子量

1046.18

Formula

C50H71N13O12

CAS 号

4474-91-3

Sequence

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

Sequence Shortening

DRVYIHPF

中文名称

血管紧张素Ⅱ

运输条件

Room temperature in continental US; may vary elsewhere.

储存方式

Protect from light, stored under nitrogen

Powder -80deg;C 2 years
-20deg;C 1 year

*In solvent : -80deg;C, 6 months; -20deg;C, 1 month (protect from light, stored under nitrogen)

溶解性数据
In Vitro:;

DMSO : 100 mg/mL (95.59 mM; Need ultrasonic)

H2O : 50 mg/mL (47.79 mM; Need ultrasonic)

配制储备液
浓度 溶剂体积 质量 1 mg 5 mg 10 mg
1 mM 0.9559 mL 4.7793 mL 9.5586 mL
5 mM 0.1912 mL 0.9559 mL 1.9117 mL
10 mM 0.0956 mL 0.4779 mL 0.9559 mL

*

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液;一旦配成溶液,请分装保存,避免反复冻融造成的产品失效
储备液的保存方式和期限:-80°C, 6 months; -20°C, 1 month (protect from light, stored under nitrogen)。-80°C 储存时,请在 6 个月内使用,-20°C 储存时,请在 1 个月内使用。

In Vivo:

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液,再依次添加助溶剂:

——为保证实验结果的可靠性,澄清的储备液可以根据储存条件,适当保存;体内实验的工作液,建议您现用现配,当天使用; 以下溶剂前显示的百
分比是指该溶剂在您配制终溶液中的体积占比;如在配制过程中出现沉淀、析出现象,可以通过加热和/或超声的方式助溶

  • 1.

    请依序添加每种溶剂:;PBS

    Solubility: 30 mg/mL (28.68 mM); Clear solution; Need ultrasonic

  • 2.

    请依序添加每种溶剂:;10% DMSO ;; 40% PEG300 ;; 5% Tween-80 ;; 45% saline

    Solubility: ≥ 2.5 mg/mL (2.39 mM); Clear solution

    此方案可获得 ≥ 2.5 mg/mL (2.39 mM,饱和度未知) 的澄清溶液。

    以 1 mL 工作液为例,取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中,混合均匀;向上述体系中加入50 μL Tween-80,混合均匀;然后继续加入 450 μL生理盐水定容至 1 mL。

    将 0.9 g 氯化钠,完全溶解于 100 mL ddH₂O 中,得到澄清透明的生理盐水溶液

  • 3.

    请依序添加每种溶剂:;10% DMSO ;; 90% corn oil

    Solubility: ≥ 2.5 mg/mL (2.39 mM); Clear solution

    此方案可获得 ≥ 2.5 mg/mL (2.39 mM,饱和度未知) 的澄清溶液,此方案不适用于实验周期在半个月以上的实验。

    以 1 mL 工作液为例,取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中,混合均匀。

  • 4.

    请依序添加每种溶剂:;10% DMSO ;; 90% (20% SBE-β-CD in saline)

    Solubility: ≥ 0.83 mg/mL (0.79 mM); Clear solution

    此方案可获得 ≥ 0.83 mg/mL (0.79 mM,饱和度未知) 的澄清溶液。

    以 1 mL 工作液为例,取 100 μL 8.3 mg/mL 的澄清 DMSO 储备液加到 900 μL 20% 的 SBE-β-CD 生理盐水水溶液中,混合均匀。

    将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中,再用生理盐水定容至 10 mL,完全溶解,澄清透明
*以上所有助溶剂都可在 MCE 网站选购。
参考文献
  • [1]. de Gasparo M, et al. International union of pharmacology. XXIII. The angiotensin II receptors. Pharmacol Rev. 2000 Sep;52(3):415-72.

    [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.

    [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.

    [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.

    [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.

Animal Administration
[3]

Mice[3]
(129×C57BL/6) F1 mice lacking AT1A receptors for Angiotensin II are used. The mice are fed 10 gm/day gelled 0.25% NaCl diet that contains all nutrients and water. After 1 week of baseline collections, the animals are implanted with osmotic minipumps infusing Angiotensin II and are returned to the metabolic cage for 5 more days. Urinary sodium content is determined by using an IL943 Automatic Flame photometer. After 28 days of Angiotensin II infusion, hearts are harvested, weighed, fixed in formalin, sectioned, and stained with Masson trichrome. All of the tissues are examined by a pathologist (P.R.) without knowledge of genotypes.

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

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

    [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.

    [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.

    [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.

    [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.