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Bumetanide

Bumetanide is a potent loop diuretic medication used to treat fluid retention and edema associated with various medical conditions, such as congestive heart failure, liver disease, and kidney disease.
It works by inhibiting the sodium-potassium-chloride cotransporter in the thick ascending limb of the loop of Henle, leading to increased urine output and reduced fluid buildup.
Bumetanide is known for its rapid onset of action and high potency, making it a valuable tool for managing acute and chronic fluid imbalances.
Researchers studying the pharmacology, clinical applications, and therapeutic potential of bumetanide can leverage PubCompare.ai's AI-driven optimization platform to streamline their research, locate the best protocols, and ensure reproducable and accurate results.

Most cited protocols related to «Bumetanide»

Acute Decompensated Heart Failure Protocol

Cited 20 times

Patients were eligible for enrollment if they had presented within the previous 24 hours with acute decompensated heart failure, diagnosed on the basis of the presence of at least one symptom (dyspnea, orthopnea, or edema) and one sign (rales, peripheral edema, ascites, or pulmonary vascular congestion on chest radiography) of heart failure. Additional eligibility criteria were a history of chronic heart failure and receipt of an oral loop diuretic for at least 1 month before hospitalization, at a dose between 80 mg and 240 mg daily in the case of furosemide and an equivalent dose in the case of a different loop diuretic (20 mg of torsemide or 1 mg of bumetanide was considered to be equivalent to 40 mg of furosemide). Thiazide diuretics were permitted if the patient had been taking them on a long-term basis. There was no prespecified inclusion criterion with respect to ejection fraction. Patients with systolic blood pressure of less than 90 mm Hg or a serum creatinine level that was greater than 3.0 mg per deciliter (265.2 μmol per liter) and patients requiring intravenous vasodilators or inotropic agents (other than digoxin) for heart failure were excluded.

Felker G.M., Lee K.L., Bull D.A., Redfield M.M., Stevenson L.W., Goldsmith S.R., LeWinter M.M., Deswal A., Rouleau J.L., Ofili E.O., Anstrom K.J., Hernandez A.F., McNulty S.E., Velazquez E.J., Kfoury A.G., Chen H.H., Givertz M.M., Semigran M.J., Bart B.A., Mascette A.M., Braunwald E, & O'Connor C.M. (2011). Diuretic Strategies in Patients with Acute Decompensated Heart Failure. The New England journal of medicine, 364(9), 797-805.

Publication 2011

Ascites Blood Vessel Bumetanide Creatinine Digoxin Dyspnea Edema Eligibility Determination Furosemide Heart Failure Hospitalization Loop Diuretics Lung Patients Radiography, Thoracic Serum Systolic Pressure Thiazide Diuretics Torsemide Vasodilator Agents

Diuretic Efficiency and Renal Outcomes in ADHF

Cited 11 times

The ESCAPE Trial was a National Heart, Lung and Blood Institute sponsored, randomized, multicenter trial of therapy guided by pulmonary artery catheter vs. clinical assessment in hospitalized patients with ADHF. Methods and results have been published previously.^{11 (link), 12} Briefly, 433 patients were enrolled at 26 sites from January 2000 to November 2003. Inclusion criteria included an ejection fraction of 30% or less, systolic blood pressure of 125 mmHg or less, hospitalization for HF within the preceding year, treatment during the preceding month with more than 160 mg of furosemide equivalents daily, and at least 1 sign and 1 symptom of congestion. Exclusion criteria included an admission creatinine level >3.5 mg/dL. Patients were randomized to therapy guided by clinical assessment alone vs. pulmonary artery catheter and clinical assessment. Treatment goals were resolution of the signs and symptoms of congestion and investigators were encouraged to “avoid progressive renal dysfunction or symptomatic systemic hypotension.” Patients in the ESCAPE population that did not have data available to calculate net urine output (n=19) and patients that did not have data available on peak loop diuretic dose (n=24) were not included in the current analysis. All-cause mortality was determined 180 days after randomization.
The relative diuretic efficiency in each patient was determined as the fluid output per mg of loop diuretic received (expressed as mL of net fluid output per 40 mg of furosemide equivalents). Forty milligrams of furosemide equivalents was chosen as a reference since this is a dose reported to produce near maximal rate of instantaneous natriuresis in a healthy volunteer naive to diuretics.¹³ For the Penn cohort, where detailed information on diuretic administration was available, diuretic efficiency was calculated using the cumulative in-hospital net fluid output divided by the cumulative in-hospital amount of intravenous (IV) loop diuretic received (Cumulative diuretic efficiency). For the ESCAPE cohort, only maximum loop diuretic dose received in a 24 hour period was available, thus diuretic efficiency was calculated using the average daily fluid output divided by the peak IV loop diuretic (Peak diuretic efficiency). Given the desire to compare effect sizes across variables and between cohorts, the median values for diuretic efficiency [Penn cohort median 480 (interquartile range 195–1024) mL net fluid output/40 mg furosemide equivalents; ESCAPE cohort median 148 (interquartile range 61–283) mL net fluid output/40 mg furosemide equivalents] was primarily employed. To allow direct comparison between the cohorts, the primary analyses were repeated using Peak diuretic efficiency in the Penn cohort calculated using the median from the ESCAPE cohort. Estimated glomerular filtration rate (eGFR) was calculated using the four variable Modified Diet and Renal Disease equation.^{14 (link)} Worsening renal function (WRF) was defined as a ≥ 20% decrease in eGFR at any time during the hospitalization, unless otherwise specified.^{15 (link)–20 (link)} Loop diuretic doses were converted to furosemide equivalents with 1 mg bumetanide = 20 mg torsemide = 80 mg furosemide for oral diuretics, and 1 mg bumetanide = 20 mg torsemide = 40 mg furosemide for intravenous diuretics.^{21 (link), 22 (link)} The study was approved or determined to qualify as exempt from Institutional Review Board review by the Hospital of the University of Pennsylvania and Yale University Institutional Review Boards.

Testani J.M., Brisco M.A., Turner J.M., Spatz E.S., Bellumkonda L., Parikh C.R, & Wilson Tang W.H. (2013). Loop Diuretic Efficiency: A Metric of Diuretic Responsiveness with Prognostic Importance in Acute Decompensated Heart Failure. Circulation. Heart failure, 7(2), 261-270.

Publication 2013

BLOOD Bumetanide Catheters Creatinine Diet Diuretics Ethics Committees, Research Furosemide Glomerular Filtration Rate Healthy Volunteers Heart Hospitalization Kidney Kidney Diseases Kidney Failure Loop Diuretics Lung Natriuresis Patients Pulmonary Artery Systolic Pressure Torsemide Urine

Propofol Anesthesia in Neonatal Rats

Cited 6 times

P4, P5, or P6 rat pups of both genders were kept in a temperature-controlled chamber (+37 °C) with a continuous supply of oxygen (1.5 L/min) during anesthesia. The anesthesia protocol with propofol (40 mg/kg intraperitoneally for induction for the first 60 min and then 20 mg/kg/h intraperitoneally for maintenance for 5 h in total) is a shorter version of the anesthesia protocol originally described by Briner et al.^{13 (link)} in neonatal rats consisting of six injections of propofol at the same doses and lasting for 6 h. Neither Briner et al. nor other authors using a single injection of propofol at 75 mg/kg intraperitoneally detected significant changes in blood gasses or glucose in neonatal rats.^{13 (link),14 (link)} In order to study the role of GABA_AR-mediated excitation in the effects of propofol, a subgroup of P4, P5 or P6 rats received the NKCC1inhibitor, bumetanide (1.82 mg/kg, intraperitoneally), 15 min prior to initiation of anesthesia with propofol for 5 h. Another subgroup of P4–P6 rats received a single injection of corticosterone (0.2 mg/kg, intraperitoneally) followed by intraperitoneal injections of saline at hours 2, 3 and 4. The animals in the corticosterone group were not exposed to anesthesia with propofol. This dose of corticosterone (0.2 mg/kg) is in the range of glucocorticoid doses administered to children in the early postnatal period to alleviate respiratory distress syndrome and to modulate the inflammatory response associated with cardiopulmonary bypass.^{15 (link),16 (link)} There were two control groups in which animals received equal numbers and volumes of intraperitoneal injections of saline or intralipid (the vehicle for propofol). All rat pups were separated from the dams for 5 h, the time equal to the duration of anesthesia with propofol, except rats in the negative control groups, which were neither separated from their dams nor injected. Mortality in the range of 10% occurred in P4–P6 rats during anesthesia with propofol for 5 h. Investigators analyzing data were blind to the experimental conditions. The sample sizes in this study were based on previous experience with the same experimental techniques.

Tan S., Xu C., Zhu W., Willis J., Seubert C.N., Gravenstein N., Sumners C, & Martynyuk A.E. (2014). Endocrine and neurobehavioral abnormalities induced by propofol administered to neonatal rats. Anesthesiology, 121(5), 1010-1017.

Publication 2014

Anesthesia Animals BLOOD Bumetanide Cardiopulmonary Bypass Child Corticosterone Glucocorticoids Glucose Infant, Newborn Inflammation Injections, Intraperitoneal Intralipid Oxygen Propofol Rattus norvegicus Respiratory Distress Syndrome, Adult Saline Solution Training Programs

Choroid Plexus Rb+ Efflux Assay

Cited 5 times

Choroid plexus was isolated as above, initially in cold aCSF (in mM: 120 NaCl, 2.5 KCl, 2.5 CaCl₂, 1.3 MgSO₄, 1 NaH₂PO₄, 25 NaHCO₃, 10 glucose, pH 7.4, equilibrated with 95% O₂/5% CO₂) but allowed to recover at 37 °C for 5–10 min before beginning of the experiment. Choroidal isotope accumulation was performed by a 10 min incubation in equilibrated (95% O₂/5% CO₂) aCSF-based isotope medium (2 μCi ml^{−1 86}Rb⁺, NEZ07200 (congener for K⁺ transport) and 8 μCi ml^{−1 3}H-mannitol, NET101 (extracellular marker), both from PerkinElmer), followed by 15 s wash prior to incubation in 0.5 ml equilibrated (95% O₂/5% CO₂) efflux medium (aCSF containing 20 μM bumetanide, 1 mM furosemide or vehicle (DMSO), each choroid plexus randomly assigned to each group). 0.2 ml of the efflux medium was collected into scintillation vials every 20 s (time points: 0, 20, and 40 s) and replaced with fresh aCSF. At the end of the experiment, choroid plexus was solubilized at room temperature with 1 ml Solvable (6NE9100, PerkinElmer) in the leftover efflux medium. The isotope content was determined by liquid scintillation counting with Ultima Gold^TM XR scintillation liquid (6013119, PerkinElmer) in a Tri-Carb 2900TR Liquid Scintillation Analyzer (Packard). The choroid plexus ⁸⁶Rb⁺ content corrected for ³H-mannitol (extracellular background) was calculated for each time point, and the natural logarithm of the choroid plexus content A_t/A₀ was plotted against time⁴⁷. Slopes indicating the ⁸⁶Rb⁺ efflux rate constants (s⁻¹) were determined from linear regression analysis.

Steffensen A.B., Oernbo E.K., Stoica A., Gerkau N.J., Barbuskaite D., Tritsaris K., Rose C.R, & MacAulay N. (2018). Cotransporter-mediated water transport underlying cerebrospinal fluid formation. Nature Communications, 9, 2167.

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Publication 2018

Bicarbonate, Sodium Bumetanide Choroid Cold Temperature Furosemide Glucose Isotopes Mannitol Plexus, Chorioid Sodium Chloride Sulfate, Magnesium Sulfoxide, Dimethyl

Electrophysiological Characterization of Cultured Hippocampal Neurons

Cited 5 times

All the data points are presented as replicates of experiments performed on the same rat cultured hippocampal DIV14–21 day neuron both before and after the glutamate treatment. We did not obtain any data from a neuron exclusively before or after glutamate exposure. We excluded from our analysis all neurons with E_M values above −50 mV at any point other than during the glutamate pulse. As mentioned in the text, we discarded nearly 25% of DIV14–21 neurons patched because they exhibited depolarizing GABA responses at the beginning of the experiment. Although neurons which exhibit depolarizing responses to GABA can still express KCC2, which could be verified by a combination of immunocytochemical and electrophysiological assays^{23 (link)}, a sustained hyperpolarizing GABA response is a simple measure by which one can verify the presence of functional KCC2 using only electrophysiological techniques.
We used the perforated patch-clamp technique in every recording. We used gramicidin D (50 μg/mL, Sigma) to establish access resistances between 30–40 MΩ throughout the recording period. We performed the recordings at 34°C and applied all compounds locally to neurons by a gravity-fed three-barreled pipette driven by a fast-step motor (Warner Instruments). The recording pipette saline contained (in mM) 140 KCl and 10 HEPES, pH 7.4 KOH. Bath saline contained (in mM) 140 NaCl, 4.7 KCl, 2.5 CaCl₂, 1.2 MgCl₂, 10 HEPES, 11 glucose, pH 7.4 NaOH., We performed all the experiments for the determination of E_GABA values in the presence of TTX (500 nM), DNQX (20 μM), and AP5 (50 μM) to block voltage-gated sodium channels, AMPA receptors, and NMDA receptors, respectively. However, we applied glutamate (20 μM) for 2 min without these antagonists and it was always applied in I=0 mode, never in voltage-clamp mode. After glutamate treatment, we immediately re-exposed neurons to the ion channel blocker/antagonists for 8 min prior to recording GABA-evoked currents. For the I–V experiments, we voltage-clamped neurons at specified holding potentials (20 mV increments in either direction beginning at −60 mV) for 30 s prior to the application of GABA. We performed the experiments testing furosemide inhibition, the role of excitatory GABA, and the time-course of E_GABA shifts on separate groups of neurons. We employed voltage-ramp protocols prior to glutamate application to determine the reversal potential of leak currents for a secondary assessment of resting membrane potential. These data revealed our I=0 measurements of resting membrane potential were accurate to within 5 mV (data not shown). Furosemide, bumetanide, and okadaic acid were dissolved in DMSO (0.1% final concentration), all other compounds were dissolved in deionized H₂O. We used a three-barreled (0.7 mm diameter per barrel) glass perfusion pipette (Warner Instruments) placed just above the target neuron to apply all agonists, antagonists, compounds, and control saline. We applied these solutions through the perfusion pipette at a rate of 0.5 mL/min and we used a computer controlled perfusion fast-step device (Warner Instruments) to ensure rapid and complete exchange of solutions. We obtained all data using an Axopatch 200B amplifier and pClamp 8 software (Axon Instruments). Data were recorded onto a personal computer for offline analysis using Clampfit. All records were filtered at 2 kHz and digitized at 10 kHz.

Lee H.H., Deeb T.Z., Walker J.A., Davies P.A, & Moss S.J. (2011). NMDA receptor activity downregulates KCC2 resulting in depolarizing GABAA receptor mediated currents. Nature neuroscience, 14(6), 736-743.

Publication 2011

6,7-dinitroquinoxaline-2,3-dione agonists AMPA Receptors antagonists Axon Bath Bumetanide Cardiac Arrest Electric Stimulation Therapy Furosemide gamma Aminobutyric Acid Glucose Glutamate Gramicidin Gravity HEPES Ion Channel Magnesium Chloride Medical Devices Membrane Potentials N-Methyl-D-Aspartate Receptors Neurons Okadaic Acid Perfusion Psychological Inhibition Pulse Rate Saline Solution Sodium Chloride Sulfoxide, Dimethyl Voltage-Gated Sodium Channels

Most recents protocols related to «Bumetanide»

iPSCod Tubuloids Sodium Uptake Assay

iPSCod tubuloids were dissociated, grown to a confluent 2D monolayer in EM, and differentiated for 5 to 7 d as described above. Prior to the sodium uptake experiment, iPSCod tubuloids were preincubated for 30 min with either isotonic buffer (140 mM NaCl, 5 mM KCl, 1 mM CaCl₂, 1 mM MgCl_2, and 5 mM HEPES, with pH adjusted to 7.4 using Tris) or, to stimulate sodium uptake, hypotonic low-chloride buffer (70 mM Na⁺ D-gluconate, 2.5 mM K⁺ D-gluconate, 0.5 mM CaCl₂, 0.5 mM MgCl₂ and 2.5 mM HEPES, with pH set to 7.4 using Tris). The inhibitors (0.1 mM) hydrochlorothiazide, bumetanide, amiloride, and/or ouabain were included in the preincubation to inhibit the transporters/channels NCC, NKCC2, ENaC, and Na/K-ATPase, respectively. Ouabain was added to prevent basolateral removal of absorbed ²²Na⁺. Same buffers including the radioactive tracer ²²Na⁺ replaced the preincubation buffers and incubated for 30 min at 37 °C. The cells were washed three times in ice-cold isotonic or hypotonic buffer to remove any extracellular ²²Na⁺ and lysed using 0.05% SDS for 30 min at 37 °C. Intracellular ²²Na⁺ radioactivity was measured using a liquid scintillation counter (Hidex 300SL).

Yousef Yengej F.A., Jansen J., Ammerlaan C.M., Dilmen E., Pou Casellas C., Masereeuw R., Hoenderop J.G., Smeets B., Rookmaaker M.B., Verhaar M.C, & Clevers H. (2023). Tubuloid culture enables long-term expansion of functional human kidney tubule epithelium from iPSC-derived organoids. Proceedings of the National Academy of Sciences of the United States of America, 120(6), e2216836120.

Publication 2023

Amiloride Buffers Bumetanide Cardiac Arrest Cells Chlorides Cold Temperature gluconate HEPES Hydrochlorothiazide inhibitors Magnesium Chloride Membrane Transport Proteins Na(+)-K(+)-Exchanging ATPase Ouabain Protoplasm Radioactive Tracers Radioactivity Scintillation Counters Sodium Sodium Chloride Tromethamine

Sprague-Dawley Rat Model for SCI Study

Thirty adult female Sprague-Dawley (SD) rats (8 week-old, weighing 250–280 g)
were used for all of the animal studies performed, which were purchased from the
Institute of Rehabilitation Medicine China Rehabilitation Science Institute
(Beijing, China). They were kept under standard conditions maintained at 22 ±
2°C, 55% ± 10% humidity, 12:12 h light/dark cycle with free access to food and
water. All animals were randomly divided into three groups for the current study
(sham, SCI, and bumetanide (BU) groups). Pharmacological studies involving BU
group were conducted with SCI animals. At the end of experiments and before
tissue harvesting, rats were deeply anesthetized by intraperitoneal injection of
10% chloral hydrate (mg kg⁻¹).

Wu Y, & Wang F. (2023). Inhibition of NKCC1 in spinal dorsal horn and dorsal root ganglion results in alleviation of neuropathic pain in rats with spinal cord contusion. Molecular Pain, 19, 17448069231159855.

Publication 2023

Animals Bumetanide Food Humidity Hydrate, Chloral Injections, Intraperitoneal Rats, Sprague-Dawley Rattus norvegicus Rehabilitation Woman

Pharmacological Agents for Experimental Use

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Publication 2023

Bumetanide CLP257 Ethanol Furosemide Glucose Kynurenic Acid Mannitol Sulfoxide, Dimethyl

Resistant Hypertension Management Trial

Patients will be recruited from vascular, cardiology and nephrology outpatient clinics of 11 hospitals including two university hospitals. Patients are eligible for participation if they fulfill the criteria of resistant hypertension, use at least two AHDs for which DBS-analysis are available, are 18 years or older and are able to provide informed consent. Due to the large population of people orginating from Turkey in Rotterdam, the patient information leaflet is made available in both the Dutch and Turkish language.
Resistant hypertension is defined as having an office BP of > 140 mmHg (systolic) and/or 90 mmHg (diastolic) or, if available, a 24-h ambulatory blood pressure measurement (24-h ABPM) daytime BP of > 135 mmHg and/or 85 mmHg despite a medication regimen of AHDs in the maximal tolerable dose of at least three AHDs from different drug classes, including a diuretic, or at least four AHDs from different drug classes. In Table 1 the minimal drug dose needed at time of the inclusion and the lower limit of detection of each included drug are shown. DBS analysis includes the following AHDs and active metabolites: enalapril and enalaprilate, perindopril and perindoprilate, irbesartan, valsartan, losartan and losartan-carboxylic acid (losartan-CA), hydrochlorothiazide, bumetanide, spironolactone and canrenone, amlodipine, barnidipine, nifedipine, metoprolol and doxazosin [25 (link), 26 (link)].Table 1

Overview antihypertensive drugs included in the RHYME-RCT trial

Antihypertensive drug [metabolite]	Minimal drug dose for inclusion (mg)	LLOD (μg/L) [25 (link)]
Amlodipine	5	17.1
Barnidipine	10	2.1
Bumetanide	1	4.0
Doxazosin	4	18.1
Enalapril	20	0.4
[Enalaprilat]	–	1.1
Hydrochlorothiazide	12.5	40.2
Irbesartan	150	7.7
Losartan	50	1.7
[Losartan-CA]	–	2.6
Metoprolol	50 CR or 25 mg two times daily (normal release)	0
Nifedipine	30	3.5
Perindopril	4	0.7
[Perindoprilat]	–	1.3
Spironolactone	12.5	5.2
[Canrenone]	–	26.8
Valsartan	80	21.3

CA carboxylic acid; CR controlled release, LLOD lower limit of detection

Patients are excluded from participation if they are not able to give informed consent, have end-stage kidney disease (eGFR < 15 ml/min/m²), insufficient understanding of the Dutch or Turkish language or if secondary forms of hypertension are expected but have not been excluded. Patients with secondary forms of hypertension primarily treated with AHDs such as primary aldosteronism caused by bilateral hyperplasia can be eligible for participating in the trial.
This study is approved by the Institutional Review Board (IRB) of the Erasmus MC, University Medical Centre, Rotterdam, the Netherlands (MEC-2018–027).

Peeters L.E., Kappers M.H., Boersma E., Massey E.K., van Dijk L., van Gelder T., Koch B.C, & Versmissen J. (2023). The effect of combining therapeutic drug monitoring of antihypertensive drugs with personalised feedback on adherence and resistant hypertension: the (RHYME-RCT) trial protocol of a multi-centre randomised controlled trial. BMC Cardiovascular Disorders, 23, 87.

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Publication 2023

Allan-Herndon-Dudley syndrome Amlodipine Antihypertensive Agents Blood Vessel Bumetanide Canrenone Carboxylic Acids Cardiovascular System Conn Syndrome Determination, Blood Pressure Diastole Diuretics Doxazosin EGFR protein, human Enalapril Enalaprilat Ethics Committees, Research High Blood Pressures Hydrochlorothiazide Hyperplasia Irbesartan Kidney Failure, Chronic Losartan losartan carboxylic acid mepirodipine Metoprolol Nifedipine Patients Perindopril perindoprilat Pharmaceutical Preparations Spironolactone Systole Treatment Protocols Valsartan

Ion Transport Inhibitors in Epithelia

The following reagents and solutions were used in the experiment:

RH—iso-osmotic Ringer solution: K⁺ 4.0 mM; Na⁺ 147.2 mM; Ca²⁺ 2.2 mM; Mg²⁺ 2.6 mM; Cl⁻ 160.8 mM (Avantor Performance Materials, Gliwice, Poland); pH = 7.4, used as a basic solution;

B—bumetanide, 3-butylamino-4-phenoxy-5-sulfamoylbenzoic acid, 0.1 mM, 364.42 g/mol (Sigma-Aldrich, St. Louis, MO, USA), used as an inhibitor of transepithelial chloride transport pathways.

A—amiloride, 3,5-diamino-6-chloro-2-carboxylic acid, 0.1 mM, 266.09 g/mol (Sigma-Aldrich, St. Louis, MO, USA), used as an inhibitor of transepithelial sodium transport pathways.

AB—a solution of amiloride (A, 0.1 mM) and bumetanide (B, 0.1 mM).

Diclofenac—a gel containing diclofenacum natricum, 10 mg/g (Perrigo, Poland).

Dobrzeniecka W., Daca M., Nowakowska B., Sobiesiak M., Szewczyk-Golec K., Woźniak A, & Hołyńska-Iwan I. (2023). The Impact of Diclofenac Gel on Ion Transport in the Rabbit (Oryctolagus cuniculus) Skin: An In Vitro Study. Molecules, 28(3), 1332.

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Publication 2023

Amiloride Bumetanide Carboxylic Acids Chlorides Diclofenac Osmosis Ringer's Solution serum sodium transport inhibitor

Top products related to «Bumetanide»

Bumetanide by Merck Group

Sourced in United States, United Kingdom, Germany, Denmark

Bumetanide is a pharmaceutical compound used as a loop diuretic. It functions by inhibiting the Na-K-2Cl cotransporter in the thick ascending limb of the loop of Henle, leading to increased excretion of sodium, chloride, and water.

Bumetanide by Bio-Techne

Sourced in United Kingdom

Bumetanide is a biochemical compound used in research applications. It functions as a potent loop diuretic that inhibits the sodium-potassium-chloride cotransporter, which is responsible for the reabsorption of these ions in the thick ascending limb of the loop of Henle in the kidney.

Amiloride by Merck Group

Sourced in United States, Germany, Italy, Sao Tome and Principe, United Kingdom, Macao, China, Denmark

Amiloride is a laboratory product manufactured by Merck Group. It is a small molecule compound primarily used as a research tool in scientific investigations. Amiloride functions as a potassium-sparing diuretic, inhibiting the sodium-hydrogen exchanger and the epithelial sodium channel.

Dimethyl sulfoxide (dmso) by Merck Group

Sourced in United States, Germany, United Kingdom, China, Italy, Sao Tome and Principe, France, Macao, India, Canada, Switzerland, Japan, Australia, Spain, Poland, Belgium, Brazil, Czechia, Portugal, Austria, Denmark, Israel, Sweden, Ireland, Hungary, Mexico, Netherlands, Singapore, Indonesia, Slovakia, Cameroon, Norway, Thailand, Chile, Finland, Malaysia, Latvia, New Zealand, Hong Kong, Pakistan, Uruguay, Bangladesh

DMSO is a versatile organic solvent commonly used in laboratory settings. It has a high boiling point, low viscosity, and the ability to dissolve a wide range of polar and non-polar compounds. DMSO's core function is as a solvent, allowing for the effective dissolution and handling of various chemical substances during research and experimentation.

Forskolin by Merck Group

Sourced in United States, Germany, United Kingdom, France, Sao Tome and Principe, Canada, Italy, Japan, China, Switzerland, Macao, Australia

Forskolin is a lab equipment product manufactured by Merck Group. It is a compound derived from the roots of the Coleus forskohlii plant. Forskolin is used as a tool for research purposes in the laboratory setting.

Ouabain by Merck Group

Sourced in United States, Germany, United Kingdom, Sao Tome and Principe, Macao, India, France, Denmark, Poland

Ouabain is a cardiac glycoside that is used as a reference standard and research tool in the study of cardiac function and ion transport mechanisms. It acts by inhibiting the Na+/K+ ATPase pump, which is essential for maintaining the electrochemical gradient across the cell membrane. Ouabain is commonly used in various in vitro and in vivo experiments, particularly in the fields of physiology, pharmacology, and biochemistry.

Furosemide by Merck Group

Sourced in United States, Germany, Canada, United Kingdom

Furosemide is a diuretic medication commonly used in medical laboratories. It is a powerful loop diuretic that works by inhibiting the reabsorption of sodium, chloride, and water in the ascending limb of the loop of Henle in the kidney. This action leads to an increased excretion of water, sodium, and chloride.

Fetal bovine serum (fbs) by Thermo Fisher Scientific

Sourced in United States, China, United Kingdom, Germany, Australia, Japan, Canada, Italy, France, Switzerland, New Zealand, Brazil, Belgium, India, Spain, Israel, Austria, Poland, Ireland, Sweden, Macao, Netherlands, Denmark, Cameroon, Singapore, Portugal, Argentina, Holy See (Vatican City State), Morocco, Uruguay, Mexico, Thailand, Sao Tome and Principe, Hungary, Panama, Hong Kong, Norway, United Arab Emirates, Czechia, Russian Federation, Chile, Moldova, Republic of, Gabon, Palestine, State of, Saudi Arabia, Senegal

Fetal Bovine Serum (FBS) is a cell culture supplement derived from the blood of bovine fetuses. FBS provides a source of proteins, growth factors, and other components that support the growth and maintenance of various cell types in in vitro cell culture applications.

Ussing chamber by Physiologic Instruments

Sourced in United States

Ussing chambers are specialized laboratory equipment used to measure the transepithelial transport of ions, solutes, and water across epithelial cell layers. They provide a controlled environment for the study of physiological processes in biological membranes.

Gabazine by Bio-Techne

Sourced in United Kingdom

Gabazine is a laboratory reagent used in biochemical research. It functions as a GABAA receptor antagonist, blocking the inhibitory effects of gamma-aminobutyric acid (GABA) on neuronal activity. Gabazine is commonly utilized in experimental settings to investigate the role of GABA-mediated signaling in various biological processes.

More about "Bumetanide"

Bumetanide is a powerful loop diuretic medication used to treat fluid retention and edema associated with various medical conditions, such as congestive heart failure, liver disease, and kidney disease.
It functions by inhibiting the sodium-potassium-chloride cotransporter in the thick ascending limb of the loop of Henle, leading to increased urine output and reduced fluid buildup.
Bumetanide is known for its rapid onset of action and high potency, making it a valuable tool for managing acute and chronic fluid imbalances.
Researchers studying the pharmacology, clinical applications, and therapeutic potential of bumetanide can leverage PubCompare.ai's AI-driven optimization platform to streamline their research.
The platform helps locate the best protocols from literature, preprints, and patents, using intelligent comparisons to ensure reproducible and accurate results.
Researchers can also explore related compounds like amiloride, DMSO, forskolin, ouabain, and furosemide, as well as techniques such as Ussing chambers and FBS cell culture, to gain a more comprehensive understanding of bumetanide's mechanisms and potential applications.
By utilizing PubCompare.ai's powerful optimization tools, researchers can save time, improve the quality of their studies, and unlock new insights into the use of bumetanide for the treatment of fluid-related medical conditions.
Whether you're investigating the pharmacokinetics, pharmacodynamics, or clinical efficacy of bumetanide, PubCompare.ai can help you achieve more efficient and reliable research outcomes.