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Furosemide

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Furosemide is a laboratory reagent used in biochemical research. It is a diuretic compound that inhibits the Na-K-2Cl cotransporter, a key ion transport protein. Furosemide is commonly used in various in vitro and ex vivo studies to investigate cellular and molecular mechanisms related to fluid and electrolyte balance.

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Lab products found in correlation

Bumetanide, by Bio-Techne (4 mentions) Cariporide, by Merck Group (2 mentions) Amiloride, by Bio-Techne (2 mentions) Hydrochlorothiazide, by Merck Group (2 mentions) Calphostin c, by Merck Group (2 mentions) Nickel chloride nicl2, by Merck Group (2 mentions) Kb r7943 mesylate, by Bio-Techne (2 mentions) 1 2 bis o aminophenoxy ethane n n n n tetraacetic acid bapta am, by Bio-Techne (2 mentions) Benzamil hydrochloride hydrate, by Merck Group (2 mentions) Indomethacin, by Merck Group (1 mentions) Bicuculline methochloride, by Bio-Techne (1 mentions) Gabazine, by Bio-Techne (1 mentions) Brain derived neurotrophic factor (bdnf), by Santa Cruz Biotechnology (1 mentions) Trkb fc chimera, by R&D Systems (1 mentions) Gapdh, by Merck Group (1 mentions) Dimethyl sulfoxide (dmso), by Merck Group (1 mentions) Kynurenic acid, by Merck Group (1 mentions) Cgp55845, by Bio-Techne (1 mentions) Sr95531, by Bio-Techne (1 mentions) Vu0240551, by Bio-Techne (1 mentions)

8 protocols using furosemide

1

Furosemide and Indomethacin Protocol

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Furosemide was from Tocris Bioscience (Abingdon, UK) and indomethacin from Sigma (Saint Quentin Fallavier, France).
Yao A.N., Kamagaté M., Amonkan A.K., Chabert P., Kpahé F., Koffi C., Kouamé M.N., Auger C., Kati-Coulibaly S., Schini-Kerth V, & Die-Kakou H. (2018). The acute diuretic effect of an ethanolic fraction of Phyllanthus amarus (Euphorbiaceae) in rats involves prostaglandins. BMC Complementary and Alternative Medicine, 18, 94.
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2

Pharmacological Regulation of Ion Transport

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Furosemide (20 µM Tocris Bioscience), hydrochlorothiazide (20 µM, Sigma), amiloride (20 µM, Tocris Bioscience), benzamil hydrochloride hydrate (10 µM, Sigma), KB-R7943 mesylate (2 nM, Tocris Bioscience), 1,2-bis(o-aminophenoxy) ethane-N,N,N′,N′-tetraacetic acid (BAPTA, AM) (Tocris Bioscience), calphostin C (20 nM, Sigma), cariporide (10 µM, Sigma), and nickel chloride (NiCl2) (10 mM, Sigma).
Barbaro N.R., Foss J.D., Kryshtal D.O., Tsyba N., Kumaresan S., Xiao L., Mernaugh R.L., Itani H.A., Loperena R., Chen W., Dikalov S., Titze J.M., Knollmann B.C., Harrison D.G, & Kirabo A. (2017). Dendritic Cell Amiloride-Sensitive Channels Mediate Sodium-Induced Inflammation and Hypertension. Cell reports, 21(4), 1009-1020.
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3

Neurochemical Modulation of TrkB Signaling

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Kynurenic acid was purchased from Sigma. DNQX (Tocris) was kept at a stock concentration of 20 μM in dimethyl sulfoxide (DMSO) (Sigma). Bicuculline methochloride, furosemide, bumetanide, and gabazine were obtained from Tocris. V1R antagonist dGly[Phaa1,d-tyr(et), Lys, Arg]VP was purchased from Bachem. TrkB-Fc chimera was purchased from R&D Systems. Antibodies from commercial sources: KCC2 (1:500), pan-TrkB (1:1,000), and GAPDH (1:5,000) from Millipore; BDNF (Santa Cruz Biotechnology; 1:100 for WB, 1:300 for IHC); Y515 phosphorylated TrkB from Abcam (1:100); and Iba1 from Wako chemicals (1:1,000). NKCC1 antibody (1:500) was generously provided by Dr. R. James Turner (NIH). VP-neurophysin antibody (mouse monoclonal, 1:100) was kindly provided by Dr. Hal Gainer (NIH).
Choe K.Y., Han S.Y., Gaub P., Shell B., Voisin D.L., Knapp B.A., Barker P.A., Brown C.H., Cunningham J.T, & Bourque C.W. (2015). High Salt Intake Increases Blood Pressure via BDNF-Mediated Downregulation of KCC2 and Impaired Baroreflex Inhibition of Vasopressin Neurons. Neuron, 85(3), 549-560.
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4

Electrophysiology Protocols with Tocris Compounds

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SR95531, CGP55845, furosemide, bumetanide, and VU0240551 were from Tocris Bioscience. All other chemicals used for electrophysiology were from Sigma. DMSO (0.001%) was used as vehicle for all drugs and controls. All tubing was replaced after furosemide and bumetanide use.
Rinetti-Vargas G., Phamluong K., Ron D, & Bender K.J. (2017). Periadolescent Maturation of GABAergic Hyperpolarization at the Axon Initial Segment. Cell reports, 20(1), 21-29.
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5

Preparation and Use of Ionic Solutions

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CaCCinh-A01 (Tocris), benzbromarone (Tocris), nicardipine (Sigma), TTA-A2 (Alamone), and isradipine (Tocris) were dissolved in DMSO (concentration of DMSO in solution did not exceed 0.01%). ZD7288 (Tocris) was dissolved in water. Furosemide (Tocris) and bumetanide (Tocris) were dissolved in 100% ethanol (ethanol concentration did not exceed 0.01%). Nominal Ca2+ solutions (0 mM Ca2+ + 1 mM EGTA) contained (in mM): 120.35 NaCl 5.9 KCl, 15.5 NaHCO3, 1.2 Na2HPO4, 1.2 MgCl2, 11.5 glucose, 2.5 MgCl2, and 1.0 EGTA.
Grainger N., Shonnard C.C., Quiggle S.K., Fox E.B., Presley H., Daugherty R., Shonnard M.C., Drumm B.T, & Sanders K.M. (2022). Propagation of Pacemaker Activity and Peristaltic Contractions in the Mouse Renal Pelvis Rely on Ca2+-activated Cl− Channels and T-Type Ca2+ Channels. Function, 3(6), zqac041.
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6

Pharmacological Regulation of Ion Transport

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Furosemide (20 µM Tocris Bioscience), hydrochlorothiazide (20 µM, Sigma), amiloride (20 µM, Tocris Bioscience), benzamil hydrochloride hydrate (10 µM, Sigma), KB-R7943 mesylate (2 nM, Tocris Bioscience), 1,2-bis(o-aminophenoxy) ethane-N,N,N′,N′-tetraacetic acid (BAPTA, AM) (Tocris Bioscience), calphostin C (20 nM, Sigma), cariporide (10 µM, Sigma), and nickel chloride (NiCl2) (10 mM, Sigma).
Barbaro N.R., Foss J.D., Kryshtal D.O., Tsyba N., Kumaresan S., Xiao L., Mernaugh R.L., Itani H.A., Loperena R., Chen W., Dikalov S., Titze J.M., Knollmann B.C., Harrison D.G, & Kirabo A. (2017). Dendritic Cell Amiloride-Sensitive Channels Mediate Sodium-Induced Inflammation and Hypertension. Cell reports, 21(4), 1009-1020.
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7

Pharmacological Modulation of Neuronal Signaling

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GABA, Bicuculline methochloride, Tetrodotoxin citrate, NBQX and D-APV were purchased from Abcam Biochemicals (Cambridge, UK); Furosemide (100 mM in dimethyl sulfoxide (DMSO)), Bumetanide (50 mM in EtOH) and PP2 (10 mM in DMSO) were purchased from Tocris Biosciences (Bristol, UK); FluoZin-3AM (Invitrogen, 5 mM DMSO); K252a (Calbiochem, Merck S.p.a., Milano, Italy); DIOA (Santa Cruz Biotechnology, Inc., Heidelberg, Germany; 200 mM in EtOH); BDNF (PeproTech EC Ltd., London, UK); TPEN (10 mM in EtOH), Gramicidin (50 mg/ml in DMSO), Sulfasalazine (500 mM in DMSO), platelet-derived growth factor and all chemicals used were purchased from Sigma-Aldrich, Milan, Italy. Where not indicated, all drugs were dissolved in water. Antibodies were purchased and used as follows: rabbit anti-Phospho TrkB (phospho Y515, 1 : 500, Abcam, Cambridge, UK), rabbit anti-Phospho Src (phospho Y416, 1 : 2000, Abcam), mouse anti- Neuronal Class III β-tubulin (TuJ1, 1 : 2000, n.cat MMS-435P, Covance, San Diego, CA, USA), rabbit anti-actin (1 : 5000, Sigma-Aldrich); rabbit anti-KCC2 (1 : 1000; Millipore, Temecula, CA, USA).
Di Angelantonio S., Murana E., Cocco S., Scala F., Bertollini C., Molinari M.G., Lauro C., Bregestovski P., Limatola C, & Ragozzino D. (2014). A role for intracellular zinc in glioma alteration of neuronal chloride equilibrium. Cell Death & Disease, 5(10), e1501-.
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8

Synthesis and Characterization of Novel Compounds

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Compound 6, LAU 463, DK-I-56-1 and DK-I-58-1 were synthesized as previously described (Knutson et al., 2018) . Harmaline and propranolol were purchased from Sigma-Aldrich (St. Louis, MO, USA) and furosemide from Tocris Bioscience (Bristrol, UK). Compound 6, LAU463, DK-I-56-1, DK-I-58-1 (Fig. 1, A-D, respectively) and propranolol were dissolved in a vehicle containing 20% DMSO, 20% Cremophor® EL (polyoxyethylene castor; Sigma-Aldrich) and 60% normal saline.
Harmaline was dissolved in normal saline. furosemide administered by i.cb. microinjection was dissolved in DMSO as reported previously (Chiou et al., 2018; Liao et al., 2016) .
(which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission.
Huang Y., Lee M.T., Sieghart W., Knutson D.E., Wimmer L., Sharmin D., Cook J.M., Mihovilovič M.D., & Chiou L. (2021). Positive modulation of cerebellar α6GABAA receptors for treating essential tremor: a proof-of-concept study in harmaline-treated mice.
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