Losartan

Manufactured by Santa Cruz Biotechnology

Sourced in United States

Losartan is a pharmaceutical compound that functions as an angiotensin II receptor antagonist. It is used in the treatment of hypertension and other cardiovascular conditions.

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Losartan potassium (2 citations) Losartan carboxylic acid (2 citations)

9 protocols using losartan

Angiotensin II-Induced Podocyte Injury

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Differentiated podocytes were treated with 1 μM Ang II (Tocris Bioscience) for 24 h. To examine the beneficial effects of losartan on Ang II-induced podocyte injury, differentiated cells were incubated with culture media containing 1 μM losartan (DuPont 753, Merck Pharmaceuticals) for 30 min, followed by incubation with Ang II plus losartan for 24 h. To inhibit NHE1 and p38 MAPK activity, cariporide (10 μM, Santa Cruz Biotechnology, Dallas, TX, USA) and SB203580 (0.1 μM, Merck Millipore, Temecula, CA, USA) were added for 30 min, followed by incubation with Ang II plus specific inhibitors for 24 h.

Cardoso V.G., Gonçalves G.L., Costa-Pessoa J.M., Thieme K., Lins B.B., Casare F.A., de Ponte M.C., Camara N.O, & Oliveira-Souza M. (2018). Angiotensin II-induced podocyte apoptosis is mediated by endoplasmic reticulum stress/PKC-δ/p38 MAPK pathway activation and trough increased Na+/H+ exchanger isoform 1 activity. BMC Nephrology, 19, 179.

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Genetic Mouse Models of Aortic Disease

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All mouse experiments were performed in accordance with institutional guidelines set forth by The University of Texas Health Science Center at Houston Animal Welfare Committee. Standard methods were used to rederive Acta2^−/− mice (C57/Bl6 background) from frozen embryos obtained from Dr. Warren Zimmer at Texas A&M University. Agtr1a^−/− mice were purchased from The Jackson Laboratory (strain B6.129P2-Agtr1a^tm1Unc/J.).
For all animal treatment trials, sample sizes were determined using a statistical power calculator based on the initial observed effect size. Doses and timepoints for drug treatments in animal models were based on published protocols. All mice underwent echocardiography at 4 weeks of age, then were randomly assigned to control or treatment groups. Losartan (Santa Cruz Biotechnology, Cat#: sc-204796A) was administered at 0.6g/L in the drinking water for six months, with echocardiography performed every 8 weeks, and aortas harvested for histology at the end of the study. Shorter treatments were used for RNA and protein analysis to eliminate possible secondary effects. NAC (Sigma, Cat#: A9165) was administered at 500 mg/kg/day in drinking water. For all protein and mRNA analyses, only ascending aortic tissue was used.

Chen J., Peters A., Papke C.L., Villamizar C., Ringuette L.J., Cao J., Wang S., Ma S., Gong L., Byanova K.L., Xiong J., Zhu M.X., Madonna R., Kee P., Geng Y.J., Brasier A.R., Davis E.C., Prakash S., Kwartler C.S, & Milewicz D.M. (2017). Loss of Smooth Muscle α-actin Leads to NF-κB-Dependent Increased Sensitivity to Angiontensin II in Smooth Muscle Cells and Aortic Enlargement. Circulation research, 120(12), 1903-1915.

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Puromycin Aminonucleoside Injection Protocol

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The puromycin aminonucleoside for injection was purchased from Enzo Life Sciences, Inc. (Farmingdale, NY, USA). Losartan, used as the positive control drug, was purchased from Santa Cruz Biotechnology (Santa Cruz, CA, USA).

Kho M.C., Park J.H., Han B.H., Tan R., Yoon J.J., Kim H.Y., Ahn Y.M., Lee Y.J., Kang D.G, & Lee H.S. (2017). Plantago asiatica L. Ameliorates Puromycin Aminonucleoside-Induced Nephrotic Syndrome by Suppressing Inflammation and Apoptosis. Nutrients, 9(4), 386.

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Angiotensin II and TRV023 Synthesis

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AngII and TRV023 (Sar-Arg-Val-Tyr-Lys-His-Pro-Ala-OH) were synthesized by GenScript USA with quality control assessed by high-performance chromatography and mass spectrometry. Losartan was purchased from Santa Cruz Biotechnology (sc-204796). AngII was also obtained from Sigma (A9525-1MG).

Ma Z., Viswanathan G., Sellig M., Jassal C., Choi I., Garikipati A., Xiong X., Nazo N, & Rajagopal S. (2021). β-Arrestin–Mediated Angiotensin II Type 1 Receptor Activation Promotes Pulmonary Vascular Remodeling in Pulmonary Hypertension. JACC: Basic to Translational Science, 6(11), 854-869.

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Quantification of Cardiovascular Drugs

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Amlodipine besylate, barnidipine, bumetanide, doxazosin, hydrochlorothiazide, irbesartan, metoprolol, nifedipine, spironolactone, telmisartan, lercanidipine, and valsartan were purchased from Sigma-Aldrich Chemie (Zwijndrecht, Netherlands). Canrenone, doxazosin-d8, enalapril, enalapril-d5, hydrochlorothiazide-13Cd2, losartan, losartan-carboxylic acid, perindopril, and perindoprilat were purchased from Santa Cruz Biotechnology (Heidelberg, Germany). Enalaprilat and candesartan were purchased from Alfa Aesar (Kandel, Germany), and chlorthalidone was purchased from EDQM (Strasbourg, France) and Cayman (Ann Arbor, MI).
Acetonitrile [99.9%, high performance liquid chromatography (HPLC)-R grade], absolute methanol [liquid chromatography/mass spectrometry (LC/MS) grade], and formic acid (FA) (99.9%, UHPLC/MS grade) were purchased from Biosolve (Valkenswaard, Netherlands). Ammonium hydroxide (AH) was purchased from Merck Millipore (Darmstadt, Germany). Deionized water was produced with a Milli-Q Advantage A10 purification system from Merck-Millipore (Darmstadt, Germany). Fresh human blood without AHDs was obtained from patients who provided consent to use the remnant material for other purposes.

Peeters L.E., Bahmany S., Dekker T., Aliawi A., van Domburg B., Versmissen J, & Koch B.C. (2022). Development and Validation of a Dried Blood Spot Assay Using UHPLC-MS/MS to Identify and Quantify 12 Antihypertensive Drugs and 4 Active Metabolites: Clinical Needs and Analytical Limitations. Therapeutic Drug Monitoring, 44(4), 568-577.

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Signaling Pathways in Androgen Metabolism

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The following reagents and antibodies were used: Angiotensin II (4474-91-3), [1β- 3 H]androst-4-ene3,17-dione (#46033), 17β-estradiol (50-28-2), and anti-AGTR1 (SAB2100073) from Sigma Aldrich (St. Louis, MI, USA); Losartan (#S5067), anti-β-Actin (sc. 69879), and anti-GAPDH (sc. 25778) antibodies from Santa Cruz Biotechnology (Santa Cruz, CA, USA); human anti-STAT3, anti-pSTAT3^Tyr705, and MAPK/STAT3/pMAPK^{Thr202/Tyr204}/pSTAT3 ^Thr705 from Cell Signaling Technology (Beverly, MA, USA); human anti-Aromatase (MCA2077S) from Bio-Rad Laboratories (Berkeley, CA, USA); Ki-67 (#M724029-2) from Dako Italia Spa (MI, Italy); PD-L1 (#PA5-20343) from Thermo Fisher Scientific, Waltham, MA, USA.

Panza S., Malivindi R., Caruso A., Russo U., Giordano F., Győrffy B., Gelsomino L., De Amicis F., Barone I., Conforti F.L., Giordano C., Bonofiglio D., Catalano S, & Andò S. (2021). Novel Insights into the Antagonistic Effects of Losartan against Angiotensin II/AGTR1 Signaling in Glioblastoma Cells. Cancers, 13(18), 4555.

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Megalin Expression in TMAO-Induced HK-2 Cells

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HK-2 cells were stimulated with TMAO (300 µM), low glucose (5 mM, unstimulated) or high glucose (30 mM) for 24 h at 37 °C in 5% CO₂. The HK-2 cells were also treated with TMAO (300 µM) for 12 h followed by treatment with DMSO (vehicle), candesartan (10 µM, Santa Cruz Biotechnology), dapagliflozin (10 µM, Santa Cruz Biotechnology), losartan (10 µM, Santa Cruz Biotechnology) and enalaprilat (5 µM, Santa Cruz Biotechnology Inc) for an additional 12 h in the presence of TMAO. After 24 h, the cells were detached with Accutase (Sigma-Aldrich) and megalin was detected using the monoclonal mouse anti-human megalin/LRP2 Alexa Fluor 488-conjugated antibody (R&D Systems, Minneapolis, USA). Cells were stained with 0.25 µg antibody for 20 min at room temperature. The expression was evaluated using the Gallios (Beckman Coulter, Brea, CA, USA) flow cytometer with 488 nm laser and FL1 525/40 nm band-pass filter. The data were analyzed with Kaluza Flow Cytometry Analysis v1.3 (Beckman Coulter).

Kapetanaki S., Kumawat A.K., Persson K, & Demirel I. (2022). TMAO Suppresses Megalin Expression and Albumin Uptake in Human Proximal Tubular Cells Via PI3K and ERK Signaling. International Journal of Molecular Sciences, 23(16), 8856.

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Cardioprotective Effects of ACE Inhibition and Angiotensin II Receptor Blockade in Diabetic Rats

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A total of 96 rats were subdivided into 3 groups (n = 32 per group) and subjected to 4 different experimental protocols. The first group contained nondiabetic rats. All hearts isolated from these animals in this group were subdivided into 4 subgroups subjected to acute hyperglycemia which was created by adding 6 g/L to the perfusion buffer. One subgroup (Ctr) was subjected to only I/R and served as control. The second subgroup (Cap) was subjected to I/R and treated with Captopril (100 μM; cat. #:C4042 Sigma-Aldrich (St Louis, MI, USA)). The third subgroup (Los) was subjected to I/R and treated with Losartan (4.5 μM, Santa Cruz Biotechnology). The fourth subgroup (Cap + Los) was subjected to I/R and treated with Losartan (4.5 μM) and Captopril (100 μM). All drugs were injected 5 min before the end of ischemia and continued for 10 min thereafter (Figure 9). The second group was subjected to DM for four weeks, then divided into four subgroups, Ctr, Cap, Los, and Los + Cap (Figure 9). The third group was subjected to DM for six weeks, then like the previous groups, was subdivided into four similar subgroups (Ctr, Cap, Los, and Cap + Los (Figure 9).

Al-Kouh A., Babiker F, & Al-Bader M. (2023). Renin–Angiotensin System Antagonism Protects the Diabetic Heart from Ischemia/Reperfusion Injury in Variable Hyperglycemia Duration Settings by a Glucose Transporter Type 4-Mediated Pathway. Pharmaceuticals, 16(2), 238.

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Cardiac Hypertrophy Induction in Mice

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Hearts were rapidly dissected from mice following overdose anesthesia with 2.5% avertin (tribromoethanol; Sigma). Hearts were rinsed in 0.9% NaCl, blotted, and weighed. Heart weight was normalized to tibia length (HW/TL; mg/mm). Captopril (400 mg/L; Sigma) and losartan (90 mg/mL; Santa Cruz Biotechnology) were administered in drinking water for 4 weeks (water was changed every 3 days).

McClenaghan C., Huang Y., Matkovich S.J., Kovacs A., Weinheimer C.J., Perez R., Broekelmann T.J., Harter T.M., Lee J.M., Remedi M.S, & Nichols C.G. (2020). The Mechanism of High-Output Cardiac Hypertrophy Arising From Potassium Channel Gain-of-Function in Cantú Syndrome. Function, 1(1), zqaa004.

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