Angiotensin I (human, mouse, rat)
(Synonyms: 血管紧张素 1 (人)) 目录号 : GP10087
Angiotensin I (human, mouse, rat)是一种十肽激素，为血管紧张素II的前体。
Cas No.:484-42-4
Sample solution is provided at 25 µL, 10mM.
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Angiotensin I (human, mouse, rat), a decapeptide hormone, is the precursor of Angiotensin II[1]. Angiotensin I is specifically cleaved to Angiotensin II by the angiotensin-converting enzyme (ACE) in vivo[2]. Angiotensin II activates AT1 and AT2 receptors, raises blood pressure, and stimulates aldosterone release[3]. As a standard tool peptide in renin-angiotensin system (RAS) research, Angiotensin I is widely used in cardiovascular studies of hypertension, heart failure, and kidney disease[4].
In vitro, Treatment of murine peritoneal cells with Angiotensin I (10ng/μl；10 min–6h) results in cooperative conversion to Angiotensin II by mast-cell chymase mMCP-4 and carboxypeptidase A, peaking at 10–30min and degrading by 3h, concomitantly yielding Ang-(1–9), Ang-(5–10) and Ang-(1–7)[5]. Angiotensin I (500µM; 2h pre-incubation followed by 48h co-infection) significantly increases the invasion efficiency of SARS-CoV-2 spike-pseudotyped virus (PVP) into human ACE2-overexpressing HEK-ACE2 cells independently of the Angiotensin II AT1 receptor[6].
In vivo, Angiotensin I (1000ng/kg/min; 4 weeks; s.c. osmotic minipump) induced both thoracic and abdominal aortic aneurysms in Ldlr⁻/⁻ mice, and increased ascending aortic intima area by 2.4-fold and suprarenal abdominal aortic diameter by 1.9-fold[7]. Angiotensin I (0.2µg/g BW; single i.p.; 5min ) increased systolic blood pressure by 28 ± 4mmHg in male C57BL/6J mice[8].
References:
[1] Manabe K, Shirahase H, Usui H, Kurahashi K, Fujiwara M. Endothelium-dependent contractions induced by angiotensin I and angiotensin II in canine cerebral artery. J Pharmacol Exp Ther. 1989;251(1):317-320.
[2] Fuchs S, Xiao HD, Hubert C, et al. Angiotensin-converting enzyme C-terminal catalytic domain is the main site of angiotensin I cleavage in vivo. Hypertension. 2008;51(2):267-274.
[3] Mulrow PJ. Angiotensin II and aldosterone regulation. Regul Pept. 1999;80(1-2):27-32.
[4] Lazartigues E, Llorens-Cortes C, Danser AHJ. New Approaches Targeting the Renin-Angiotensin System: Inhibition of Brain Aminopeptidase A, ACE2 Ubiquitination, and Angiotensinogen. Can J Cardiol. 2023;39(12):1900-1912.
[5] Lundequist A, Tchougounova E, Abrink M, Pejler G. Cooperation between mast cell carboxypeptidase A and the chymase mouse mast cell protease 4 in the formation and degradation of angiotensin II. J Biol Chem.
2004;279(31):32339-32344.
[6] Zorad S, Skrabanova M, Zilkova M, et al. Angiotensin I and II Stimulate Cell Invasion of SARS-CoV-2: Potential Mechanism via Inhibition of ACE2 Arm of RAS. Physiol Res. 2024;73(1):27-35.
[7] Sawada H, Kukida M, Chen X, et al. Angiotensin I Infusion Reveals Differential Effects of Angiotensin-Converting Enzyme in Aortic Resident Cells on Aneurysm Formation. Circ J. 2020;84(5):825-829.
[8] Forster P, Wysocki J, Abedini Y, et al. Aminopeptidase A Effect on Angiotensin Peptides and Their Blood Pressure Action. Int J Mol Sci. 2025;26(14):6990.
Angiotensin I (human, mouse, rat)是一种十肽激素，为血管紧张素II的前体[1]。Angiotensin I在体内可被血管紧张素转换酶（ACE）特异性裂解生成Angiotensin II[2]。Angiotensin II激活AT1和AT2受体，升高血压并刺激醛固酮释放[3]。作为肾素-血管紧张素系统（RAS）研究的标准工具肽，Angiotensin I被广泛用于高血压、心力衰竭及肾脏疾病等心血管研究[4]。
体外实验中，用Angiotensin I（10ng/μl；10min–6h）处理小鼠腹腔细胞，可经肥大细胞糜酶mMCP-4与羧肽酶A协同转化为Angiotensin II，10–30min达峰，3h内降解，并伴随生成Ang-(1–9)、Ang-(5–10) 和Ang-(1–7)[5]。Angiotensin I（500µM；2h预孵育+48h共感染）显著且不依赖Angiotensin II AT1受体地提高SARS-CoV-2刺突假型病毒（PVP）对人ACE2过表达HEK-ACE2细胞的入侵效率[6]。
体内实验中，Angiotensin I（1000ng/kg/min；4周；皮下渗透泵）在Ldlr⁻/⁻小鼠中诱发胸、腹主动脉瘤，使升主动脉内膜面积增加2.4倍，肾下腹主动脉外径增加1.9倍[7]。Angiotensin I（0.2µg/g体重；单次腹腔注射；5min）使雄性C57BL/6J小鼠收缩压升高28 ± 4 mmHg[8]。
| Cell experiment [1]: | |
Cell lines | HEK-ACE2 cells |
Preparation Method | The recipient cells (HEK-ACE2) were seeded in density 4×104 cells per well of 96-well plate and cultured overnight in normal growth medium (DMEM, pH=7.6) supplemented with 10% FBS. Next day, the cells were pre-incubated with 500µM Angiotensin I for 2h then SARS-CoV-2 Spike pseudovirus (in 50µl of cultivation medium) was added to the cells. The cells were lysed with 70µl of cell lysis buffer 48h post-infection and 30µl of lysate was used to determine the luciferase activity. |
Reaction Conditions | 500µM; 2h pre-incubation followed by 48h co-infection |
Applications | Angiotensin I significantly reduced the viability of human ACE2-overexpressing HEK-ACE2 cells infected with SARS-CoV-2 spike-pseudotyped virus. |
| Animal experiment [2]: | |
Animal models | Male low density lipoprotein receptor (Ldlr)-/- mice |
Preparation Method | Male low density lipoprotein receptor (Ldlr)-/- mice were fed a standard rodent diet and provided with water purified by reverse osmosis (pH 6.0-6.2). Hypercholesterolemia was induced by feeding a diet supplemented with saturated fat. When mice were 8–16 weeks old, saline, Angiotensin I (1,000ng/kg/min) was infused subcutaneously using osmotic pump (Alzet model 1004 for 4 weeks). Aortas were dissected from the ascending region to iliac bifurcation and placed in 10% (wt/vol) neutrally buffered formalin overnight. After removal of adventitia, aortas were pinned and photographed. To quantify abdominal aortic dilation, maximal ex vivo diameters of suprarenal aortas were measured using ImagePro Plus software. Subsequently, aortas were cut open longitudinally, secured with pins, and imaged. To determine formation of thoracic aortic aneurysms, the intimal area of the ascending aorta was measured. |
Dosage form | 1000ng/kg/min; 4 weeks; s.c. osmotic minipump |
Applications | Angiotensin I induced both thoracic and abdominal aortic aneurysms in Ldlr⁻/⁻ mice, and increased ascending aortic intima area by 2.4-fold and suprarenal abdominal aortic diameter by 1.9-fold. |
References: | |
| Cas No. | 484-42-4 | SDF | |
| 别名 | 血管紧张素 1 (人) | ||
| 化学名 | Angiotensin I (human, mouse, rat) | ||
| Canonical SMILES | CCC(C)C(C(=O)NC(CC1=CN=CN1)C(=O)N2CCCC2C(=O)NC(CC3=CC=CC=C3)C(=O)NC(CC4=CN=CN4)C(=O)NC(CC(C)C)C(=O)O)NC(=O)C(CC5=CC=C(C=C5)O)NC(=O)C(C(C)C)NC(=O)C(CCCN=C(N)N)NC(=O)C(CC(=O)O)N | ||
| 分子式 | C62H89N17O14 | 分子量 | 1296.5 |
| 溶解度 | ≥ 129.6mg/mL in DMSO, ≥ 124.2 mg/mL in Water | 储存条件 | Desiccate at -20°C |
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1 mg | 5 mg | 10 mg |
| 1 mM | 771.3 μL | 3.8565 mL | 7.7131 mL |
| 5 mM | 154.3 μL | 771.3 μL | 1.5426 mL |
| 10 mM | 77.1 μL | 385.7 μL | 771.3 μL |
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| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
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| % DMSO % % Tween 80 % saline | ||||||||||
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2.
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