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]。