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Angii

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AngII is a laboratory reagent used for research purposes. It is a synthetic peptide that corresponds to the sequence of angiotensin II, a hormone involved in the regulation of blood pressure and fluid balance. AngII is commonly used in scientific experiments to study the physiological effects of this peptide on various biological systems.

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Lab products found in correlation

Ang 1 7, by Bachem (4 mentions) Losartan, by Merck Group (3 mentions) Mitotracker red, by Thermo Fisher Scientific (3 mentions) Bp 2000 blood pressure analysis system, by Visitech (3 mentions) Pd123319, by Merck Group (2 mentions) Alzet osmotic minipump, by Durect (2 mentions) Alzet model 2004, by Durect (2 mentions) Td 88137, by Inotiv (2 mentions) Ang 2, by Merck Group (2 mentions) Ldlr mice, by Jackson ImmunoResearch (1 mentions) Ms550d, by Fujifilm (1 mentions) Parthenolide, by Merck Group (1 mentions) Irbesartan, by Merck Group (1 mentions) Smgm 2 singlequot kit, by Lonza (1 mentions) Cholesterol mβcd, by Merck Group (1 mentions) Tgf β, by R&D Systems (1 mentions) Dulbecco modified eagle medium (dmem), by GenDEPOT (1 mentions) Matlab, by MathWorks (1 mentions) Hamilton syringe, by Hamilton Company (1 mentions) Vps34 in1, by Selleck Chemicals (1 mentions)

56 protocols using angii

1

High-Fat Diet and Angiotensin II Infusion in Mice

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Mice were fed a high-fat diet (HFD; 60% kcal fat, 20% kcal protein, 20% kcal carbohydrates; Research Diets D17041409), or a low-fat equivalent chow (CTRL; 20% kcal fat, 20%kcal protein, 60% kcal carbohydrates; Research diets D17041407) for 12 consecutive weeks, as described.21 (link) After 8 weeks of diet, mice were anaesthetised with oxygen and isoflurane (2–3%), and a mouth mask was put over the nose and mouth of the mice to deliver this mixture throughout the pump placement, which lasted 10 min. The mice were then allowed to wake up and put back in their cage. All mice underwent surgery and an ALZET® osmotic mini-pump (Model 2004) was implanted in a subcutaneous pocket on the back. For Sham-treated mice, the subcutaneous pocket was closed without placement of a pump. Mice were infused with angiotensin II (ANGII) (1.25 mg/kg/day) (Bachem) for 4 weeks, as previously described.22 (link) Mice were randomized to treatment groups based upon body weight, and a total of four experimental groups were studied: (i) CTRL—control diet for 12 weeks, Sham surgery; (ii) CTRL + ANGII—control diet for 12 weeks with 4 weeks of ANGII—infusion via osmotic mini-pump; (iii) HFD for 12 weeks, Sham surgery; (iv) HFD + ANGII—HFD for 12 weeks with 4 weeks of ANGII—infusion via the osmotic mini-pump. A schematic overview of the experiment is shown in Figure 1A.
Withaar C., Meems L.M., Markousis-Mavrogenis G., Boogerd C.J., Silljé H.H., Schouten E.M., Dokter M.M., Voors A.A., Westenbrink B.D., Lam C.S, & de Boer R.A. (2020). The effects of liraglutide and dapagliflozin on cardiac function and structure in a multi-hit mouse model of heart failure with preserved ejection fraction. Cardiovascular Research, 117(9), 2108-2124.
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2

Angiotensin II-Induced Cell Injury Assay

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Ang II (Sigma Aldrich, MO) induced cell injury model was produced as previously reported [20 (link)–22 (link)]. In brief, confluent HbmECs were incubated with increasing concentrations of Ang II (10−9, 10−8, 10−7 and 10−6 M) for 24 h. After that, cells were collected for annexin V measurements. In order to determine the effective concentration of Ang-(1–7) (Bachem AG, CH) to suppress Ang II-induced pro-apoptotic activity, HbmECs were pre-treated with different concentrations of Ang-(1-7) (10−9, 10−8, 10−7 and 10−6 M) for 30 min before addition of Ang II (10−7 M) for 24 h. After that, HbmECs were collected for annexin V measurements. Upon completion of this study, we chose 10−7 M of Ang II and Ang-(1-7) for the subsequent experiments.
Xiao X., Zhang C., Ma X., Miao H., Wang J., Liu L., Chen S., Zeng R., Chen Y, & Bihl J.C. (2015). Angiotensin-(1-7) Counteracts Angiotensin II-induced Dysfunction in Cerebral Endothelial Cells via Modulating Nox2/ROS and PI3K/NO Pathways. Experimental cell research, 336(1), 58-65.
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3

Angiotensin II-Induced Hypertension Study

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Compound 21 (C-21; Vicore Pharma), a highly selective, non-peptide AT2R agonist (Ki=0.4 mol/L) was employed to activate systemic and renal AT2Rs (17 (link),18 (link)). C-21 demonstrates 25,000-fold selectivity at AT2Rs compared with AT1Rs (18 (link),19 (link)). Candesartan (CAND; 0.01 mg/kg/min; Astra Zeneca), a specific, potent, insurmountable inhibitor of AT1Rs (IC50>1×10-5 mol/L and 2.9×10-8 mol/L for AT2Rs and AT1Rs, respectively), was used for systemic AT1R blockade. PD-123319 (PD; 10 μg/kg/min; Parke Davis) a specific AT2R antagonist (IC50=2×10-8 mol/L and >1×10-4 mol/L for AT2R and AT1Rs, respectively) was employed interstitially to block intrarenal AT2Rs. L-NG-Nitroarginine methyl ester (L-NAME; 100 ng/kg/min; Sigma) was employed interstitially to block intrarenal NO synthase (NOS) activity. Icatibant (HOE-140; 100 ng/kg/min; Sigma), a specific, potent inhibitor of BK B2 receptors was employed interstitially to inhibit intrarenal BK B2 receptors. Ang II (200 ng/kg/min; Bachem) was employed to induce Ang II-dependent hypertension.
Kemp B.A., Howell N.L., Gildea J.J., Keller S.R., Padia S.H, & Carey R.M. (2014). At2 Receptor Activation Induces Natriuresis and Lowers Blood Pressure. Circulation research, 115(3), 388-399.
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4

Selective AT2R Agonist C-21 for Hypertension

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C-21 (60 ng/kg/min for chronic intrarenal studies, 300 ng/kg/min for chronic systemic studies, and 100, 200, and 300 ng/kg/min for acute systemic studies; Vicore Pharma), a highly selective, non-peptide AT2R agonist (Ki=0.4 mol/L) was employed to activate intrarenal and systemic AT2Rs. C-21 demonstrates 25,000-fold selectivity at AT2Rs compared with AT1Rs (14 (link)). C-21 was administered systemically at doses that are selective for AT2Rs in the rat (14 (link)). The intrarenal dose of C-21 was chosen as 20% of the systemic dose based on renal blood flow. Ang II (200 ng/kg/min; Bachem) was used to induce Ang II–dependent hypertension. PD-123319 (PD; 10 μg/kg/min; Parke-Davis) a specific AT2R antagonist (IC50=2×10−8 mol/L and >1×10−4 mol/L for AT2R and AT1Rs, respectively), was used to block intrarenal AT2Rs. Amiloride (0.8 μg/kg/min; Tocris) was used to inhibit intrarenal ENaC activity. Chlorothiazide (0.1 μg/kg/min; Sigma) was used to inhibit intrarenal NCC activity. Amiloride and Chlorothiazide doses were administered on the basis of dose-ranging studies with target incremental natriuretic responses of 1–2 μmol/min.
Kemp B.A., Howell N.L., Keller S.R., Gildea J.J., Padia S.H, & Carey R.M. (2016). AT2 Receptor Activation Prevents Sodium Retention and Reduces Blood Pressure in Angiotensin II-Dependent Hypertension. Circulation research, 119(4), 532-543.
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5

Angiotensin II-Induced Aortic Aneurysm Model

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Fifteen male low density-lipoprotein receptor-deficient (LDLr -/-) mice (2 months of age, on a C57BL/6 background) were obtained from the Jackson Laboratory (Bar Harbor, ME). Eleven mice were used for aneurysm studies while four other mice were used as healthy age-matched controls. Aneurysms were induced by systemic infusion of angiotensin II (AngII, Bachem Americas, Torrance, CA) in combination with a diet with saturated fat (21% wt/wt) and cholesterol (0.2% wt/wt; catalog no. TD88137; Harlan Teklad) 13 (link). Briefly, mice were fed with high-fat diet for one week before, and six weeks during AngII infusion. Osmotic pumps (model 2004; Alzet, Cupertino, CA) filled with AngII were implanted subcutaneously through an incision at the right back shoulder of the mice. 2% to 3% isoflurane was inhaled by the mice as anesthesia throughout the surgical process. The pumping rate for AngII was set to 1000ng/kg/min. Pumps were explanted four weeks after the implantation and mice were allowed to recover for two weeks. Disease progression was monitored with a high-frequency ultrasound machine, Fujifilm VisualSonics Vevo 2100 (Fujifilm VisualSonics, Toronto, ON, Canada), by utilizing a linear array probe (MS-550D, broadband frequency 22 MHz -55 MHz). All animal use protocols for the study were approved by the Institutional Animal Care and Use Committee (IACUC) at Clemson University.
Wang X., Lane B.A., Eberth J.F., Lessner S.M, & Vyavahare N.R. (2019). Gold nanoparticles that target degraded elastin improve imaging and rupture prediction in an AngII mediated mouse model of abdominal aortic aneurysm. Theranostics, 9(14), 4156-4167.
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6

Cultured Coronary Artery Smooth Muscle Cells

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Human coronary artery smooth muscle cells (caHSMCs, Lonza Cat #CC-2583) were cultured in SmBM media (Lonza, Cat #CC-3181) with 5% fetal bovine serum and SmGM-2 SingleQuot Kit (Lonza, CC-4149) and maintained at 37 °C in a humidified atmosphere containing 5% CO2. Cells were used between passage 3–7 and at 80–90% confluency before treatment. caHSMCs were serum starved for 12 h and treated with Mβ-CD Cholesterol (10 µγ/ul, Sigma, Cat. #C4951) LPA (1 µM), AngII (1 µM, Bachem, Cat. # 4006473), transforming growth factor beta 1 (TGFβ) (1 µM, R&D Systems, Cat. #240-B002), parthenolide (1 µM, Sigma Cat. #P0667), Irbesartan (Sigma, Cat. #61188) or PD-123-319 (Sigma, Cat. #P186) for either: 24, 48 or 72 h.
Van Hoose P.M., Yang L., Kraemer M., Ubele M., Morris A.J, & Smyth S.S. (2022). Lipid phosphate phosphatase 3 in smooth muscle cells regulates angiotensin II-induced abdominal aortic aneurysm formation. Scientific Reports, 12, 5664.
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7

Cardiac Hypertrophy in H9c2 Cells

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The H9c2 myoblast cell line, derived from embryonic rat heart, was obtained from ATCC (Manassas, VA, USA). Cells were grown in DMEM (GenDepot, Katy, TX, USA) with 10% fetal bovine serum (FBS), 1% penicillin (100 U/mL), and 1% streptomycin (100 μg/mL), at 37 °C in 5% CO2 and 95% air, at a relative humidity of 95%; they were split 1:4 at sub-confluence (80%). Before each experiment, the cells were seeded in six-well plates at a 5 × 104 cells/cm2 density and starved for 18 h in serum-free DMEM. H9c2 cells were treated with Ang II (Bachem, Torrance, CA, USA), with or without miR-25 TuD plasmid transfection, for 2 days. These were then used to verify the expression of miR-25, β-MHC, BNP, and KLF4. HEK-293T cells were grown in DMEM supplemented with 10% FBS, 1% penicillin (100 U/mL), and 1% streptomycin (100 μg/mL).
Lee C., Cho S, & Jeong D. (2023). Inhibition of miR-25 Ameliorates Cardiac Dysfunction and Fibrosis by Restoring Krüppel-like Factor 4 Expression. International Journal of Molecular Sciences, 24(15), 12434.
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8

Angiotensin II-Induced Renal Injury Model

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PAG (dissolved in saline 30 mg/mL, 37.5 mg/kg BW) was administered daily intraperitoneally (ip) for one or four weeks in healthy rats (n=6, CON + PAG), while healthy saline treated rats served as control group (n=6, CON) as previously described [15] . Hypertension-driven renal injury was induced by AngII infusion (435 ng/kg/min, Bachem, Weil am Rhein, Germany) for three weeks via a subcutaneous osmotic minipump (model 2004, Alzet, Cupertino, CA) which were implanted under isoflurane anesthesia with buprenorphine analgesia [12] . As a control for AngII infusion, saline-filled minipumps were implanted in a group of rats (n=5, VEH). AngII-infused rats were randomly divided over intraperitoneal injections with saline (saline twice daily, n=7; AngII) and PAG (18.75 mg/kg twice daily ip, n=7; AngII + PAG). At the end of the experiment rats were sacrificed, a blood sample was taken and kidneys were excised, weighed, fixed in formaldehyde and then embedded in paraffin or snap frozen and stored at -80°C for RNA isolation.
Oosterhuis N.R., Frenay A.R., Wesseling S., Snijder P.M., Slaats G.G., Yazdani S., Fernandez B.O., Feelisch M., Giles R.H., Verhaar M.C., Joles J.A, & van Goor H. (2015). DL-propargylglycine reduces blood pressure and renal injury but increases kidney weight in angiotensin-II infused rats. Nitric oxide : biology and chemistry, 49.
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9

Angiotensin II and Vasoconstrictor Effects

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After measuring responses to the physiological stressors (Pre), intravenous infusion of Ang II (2 ng/kg/min; Bachem AG, Switzerland; study day 1) or phenylephrine (0.6–1.2 μg/kg/min; Baxter Healthcare, Deerfield IL: study day 2) was begun and continued until the end of the study day. The dose of the control vasoconstrictor (phenylephrine) was titrated upward in 0.2 μg/kg/min increments at 3 min intervals until BP approximated levels achieved during the Ang II infusion on study day 1. Thus, infusion occurred in a single blind fashion. Thirty minutes after beginning the infusions the 3 physiological stressors were repeated (Post) in an identical manner to Pre (same order). Infusions were stopped after collection of the last blood sample (~90 min after they started), which occurred after completion of the last physiological stressor. At least 72 hours separated study days 1 and 2. The 2ng/kg/min dose of Ang II was chosen based on pilot studies in which we observed that this dose increases plasma Ang II levels to the lower end of the pathophysiological range in humans.
Solaiman A.Z., Feehan R.P., Chabitnoy A.M., Leuenberger U.A, & Monahan K.D. (2014). Ventilatory responses to chemoreflex stimulation are not enhanced by angiotensin II in healthy humans. Autonomic neuroscience : basic & clinical, 0, 72-79.
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10

Angiotensin II Pathway Modulation

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Ang II, Ang-(1–7) and A-779 were purchased from Bachem Bioscience (Torrance, CA). Human PRO was purchased from Innovative Research (Novi, MI).
Liu M., Shi P, & Sumners C. (2015). Direct anti-inflammatory effects of angiotensin-(1–7) on microglia. Journal of neurochemistry, 136(1), 163-171.
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