A sulfamyl diuretic.
Agents that inhibit SODIUM-POTASSIUM-CHLORIDE SYMPORTERS which are concentrated in the thick ascending limb at the junction of the LOOP OF HENLE and KIDNEY TUBULES, DISTAL. They act as DIURETICS. Excess use is associated with HYPOKALEMIA and HYPERGLYCEMIA.
A subclass of symporters that specifically transport SODIUM CHLORIDE and/or POTASSIUM CHLORIDE across cellular membranes in a tightly coupled process.
Na-K-Cl transporter ubiquitously expressed. It plays a key role in salt secretion in epithelial cells and cell volume regulation in nonepithelial cells.
Agents that promote the excretion of urine through their effects on kidney function.
A benzoic-sulfonamide-furan. It is a diuretic with fast onset and short duration that is used for EDEMA and chronic RENAL INSUFFICIENCY.
Inorganic compounds derived from hydrochloric acid that contain the Cl- ion.
An element in the alkali group of metals with an atomic symbol K, atomic number 19, and atomic weight 39.10. It is the chief cation in the intracellular fluid of muscle and other cells. Potassium ion is a strong electrolyte that plays a significant role in the regulation of fluid volume and maintenance of the WATER-ELECTROLYTE BALANCE.
A member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23.
Unstable isotopes of rubidium that decay or disintegrate emitting radiation. Rb atoms with atomic weights 79-84, and 86-95 are radioactive rubidium isotopes.
An inhibitor of anion conductance including band 3-mediated anion transport.
The movement of ions across energy-transducing cell membranes. Transport can be active, passive or facilitated. Ions may travel by themselves (uniport), or as a group of two or more ions in the same (symport) or opposite (antiport) directions.
A pyrazine compound inhibiting SODIUM reabsorption through SODIUM CHANNELS in renal EPITHELIAL CELLS. This inhibition creates a negative potential in the luminal membranes of principal cells, located in the distal convoluted tubule and collecting duct. Negative potential reduces secretion of potassium and hydrogen ions. Amiloride is used in conjunction with DIURETICS to spare POTASSIUM loss. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p705)
A cardioactive glycoside consisting of rhamnose and ouabagenin, obtained from the seeds of Strophanthus gratus and other plants of the Apocynaceae; used like DIGITALIS. It is commonly used in cell biological studies as an inhibitor of the NA(+)-K(+)-EXCHANGING ATPASE.
A non-penetrating amino reagent (commonly called SITS) which acts as an inhibitor of anion transport in erythrocytes and other cells.
An element that is an alkali metal. It has an atomic symbol Rb, atomic number 37, and atomic weight 85.47. It is used as a chemical reagent and in the manufacture of photoelectric cells.
Butylamines are a class of organic compounds containing a butyl group and an amine functional group, which may have various medical applications such as as vasodilators, local anesthetics, and anti-inflammatory agents.
Inorganic salts that contain the -HCO3 radical. They are an important factor in determining the pH of the blood and the concentration of bicarbonate ions is regulated by the kidney. Levels in the blood are an index of the alkali reserve or buffering capacity.
Benzoic acid or benzoic acid esters substituted with one or more nitro groups.
Membrane transporters that co-transport two or more dissimilar molecules in the same direction across a membrane. Usually the transport of one ion or molecule is against its electrochemical gradient and is "powered" by the movement of another ion or molecule with its electrochemical gradient.
Transport proteins that carry specific substances in the blood or across cell membranes.
Negatively charged atoms, radicals or groups of atoms which travel to the anode or positive pole during electrolysis.
A subclass of symporters found in KIDNEY TUBULES, DISTAL that are the major pathway for salt resorption. Inhibition of these symporters by BENZOTHIADIAZINES is the basis of action of some DIURETICS.
Cell membrane glycoproteins that form channels to selectively pass chloride ions. Nonselective blockers include FENAMATES; ETHACRYNIC ACID; and TAMOXIFEN.
The movement of materials (including biochemical substances and drugs) through a biological system at the cellular level. The transport can be across cell membranes and epithelial layers. It also can occur within intracellular compartments and extracellular compartments.
An enzyme that catalyzes the active transport system of sodium and potassium ions across the cell wall. Sodium and potassium ions are closely coupled with membrane ATPase which undergoes phosphorylation and dephosphorylation, thereby providing energy for transport of these ions against concentration gradients.
Sweat-producing structures that are embedded in the DERMIS. Each gland consists of a single tube, a coiled body, and a superficial duct.
The movement of materials across cell membranes and epithelial layers against an electrochemical gradient, requiring the expenditure of metabolic energy.
Compounds based on 4-aminobenzenesulfonamide. The '-anil-' part of the name refers to aniline.
The concentration of osmotically active particles in solution expressed in terms of osmoles of solute per liter of solution. Osmolality is expressed in terms of osmoles of solute per kilogram of solvent.
The selectively permeable barrier, in the EYE, formed by the nonpigmented layer of the EPITHELIUM of the CILIARY BODY, and the ENDOTHELIUM of the BLOOD VESSELS of the IRIS. TIGHT JUNCTIONS joining adjacent cells keep the barrier between cells continuous.

Acetylcholine-induced membrane potential changes in endothelial cells of rabbit aortic valve. (1/485)

1. Using a microelectrode technique, acetylcholine (ACh)-induced membrane potential changes were characterized using various types of inhibitors of K+ and Cl- channels in rabbit aortic valve endothelial cells (RAVEC). 2. ACh produced transient then sustained membrane hyperpolarizations. Withdrawal of ACh evoked a transient depolarization. 3. High K+ blocked and low K+ potentiated the two ACh-induced hyperpolarizations. Charybdotoxin (ChTX) attenuated the ACh-induced transient and sustained hyperpolarizations; apamin inhibited only the sustained hyperpolarization. In the combined presence of ChTX and apamin, ACh produced a depolarization. 4. In Ca2+-free solution or in the presence of Co2+ or Ni2+, ACh produced a transient hyperpolarization followed by a depolarization. In BAPTA-AM-treated cells, ACh produced only a depolarization. 5. A low concentration of A23187 attenuated the ACh-induced transient, but not the sustained, hyperpolarization. In the presence of cyclopiazonic acid, the hyperpolarization induced by ACh was maintained after ACh removal; this maintained hyperpolarization was blocked by Co2+. 6. Both NPPB and hypertonic solution inhibited the membrane depolarization seen after ACh washout. Bumetanide also attenuated this depolarization. 7. It is concluded that in RAVEC, ACh produces a two-component hyperpolarization followed by a depolarization. It is suggested that ACh-induced Ca2+ release from the storage sites causes a transient hyperpolarization due to activation of ChTX-sensitive K+ channels and that ACh-activated Ca2+ influx causes a sustained hyperpolarization by activating both ChTX- and apamin-sensitive K+ channels. Both volume-sensitive Cl- channels and the Na+-K+-Cl- cotransporter probably contribute to the ACh-induced depolarization.  (+info)

Isosmotic modulation of Ca2+-regulated exocytosis in guinea-pig antral mucous cells: role of cell volume. (2/485)

1. Exocytotic events and changes of cell volume in mucous cells from guinea-pig antrum were examined by video-enhanced optical microscopy. 2. Acetylcholine (ACh) evoked exocytotic events following cell shrinkage, the frequency and extent of which depended on the ACh concentration. ACh actions were mimicked by ionomycin and thapsigargin, and inhibited by Ca2+-free solution and Ca2+ channel blockers (Ni2+, Cd2+ and nifedipine). Application of 100 microM W-7, a calmodulin inhibitor, also inhibited the ACh-induced exocytotic events. These results indicate that ACh actions are mediated by intracellular Ca2+ concentration ([Ca2+]i) in antral mucous cells. 3. The effects of ion channel blockers on exocytotic events and cell shrinkage evoked by ACh were examined. Inhibition of KCl release (quinine, Ba2+, NPPB or KCl solution) suppressed both the exocytotic events and cell shrinkage evoked by ACh. 4. Bumetanide (inhibition of NaCl entry) or Cl--free solution (increasing Cl- release and inhibition of NaCl entry) evoked exocytotic events following cell shrinkage in unstimulated antral mucous cells and caused further cell shrinkage and increases in the frequency of exocytotic events in ACh-stimulated cells. However, Cl--free solution did not evoke exocytotic events in unstimulated cells in the absence of extracellular Ca2+, although cell shrinkage occurred. 5. To examine the effects of cell volume on ACh-evoked exocytosis, the cell volume was altered by increasing the extracellular K+ concentration. The results showed that cell shrinkage increases the frequency of ACh-evoked exocytotic events and cell swelling decreases them. 6. Osmotic shrinkage or swelling caused the frequency of ACh-evoked exocytotic events to increase. This suggests that the effects of cell volume on ACh-evoked exocytosis under anisosmotic conditions may not be the same as those under isosmotic conditions. 7. In antral mucous cells, Ca2+-regulated exocytosis is modulated by cell shrinkage under isosmotic conditions.  (+info)

Isoforms of the Na-K-2Cl cotransporter in murine TAL II. Functional characterization and activation by cAMP. (3/485)

The functional properties of alternatively spliced isoforms of the mouse apical Na+-K+-2Cl- cotransporter (mBSC1) were examined, using expression in Xenopus oocytes and measurement of 22Na+ or 86Rb+ uptake. A total of six isoforms, generated by the combinatorial association of three 5' exon cassettes (A, B, and F) with two alternative 3' ends, are expressed in mouse thick ascending limb (TAL) [see companion article, D. B. Mount, A. Baekgaard, A. E. Hall, C. Plata, J. Xu, D. R. Beier, G. Gamba, and S. C. Hebert. Am. J. Physiol. 276 (Renal Physiol. 45): F347-F358, 1999]. The two 3' ends predict COOH-terminal cytoplasmic domains of 129 amino acids (the C4 COOH terminus) and 457 amino acids (the C9 terminus). The three C9 isoforms (mBSC1-A9/F9/B9) all express Na+-K+-2Cl- cotransport activity, whereas C4 isoforms are nonfunctional in Xenopus oocytes. Activation or inhibition of protein kinase A (PKA) does not affect the activity of the C9 isoforms. The coinjection of mBSC1-A4 with mBSC1-F9 reduces tracer uptake, compared with mBSC1-F9 alone, an effect of C4 isoforms that is partially reversed by the addition of cAMP-IBMX to the uptake medium. The inhibitory effect of C4 isoforms is a dose-dependent function of the alternatively spliced COOH terminus. Isoforms with a C4 COOH terminus thus exert a dominant negative effect on Na+-K+-2Cl- cotransport, a property that is reversed by the activation of PKA. This interaction between coexpressed COOH-terminal isoforms of mBSC1 may account for the regulation of Na+-K+-2Cl- cotransport in the mouse TAL by hormones that generate cAMP.  (+info)

UTP inhibits Na+ absorption in wild-type and DeltaF508 CFTR-expressing human bronchial epithelia. (4/485)

Ca2+-mediated agonists, including UTP, are being developed for therapeutic use in cystic fibrosis (CF) based on their ability to modulate alternative Cl- conductances. As CF is also characterized by hyperabsorption of Na+, we determined the effect of mucosal UTP on transepithelial Na+ transport in primary cultures of human bronchial epithelia (HBE). In symmetrical NaCl, UTP induced an initial increase in short-circuit current (Isc) followed by a sustained inhibition. To differentiate between effects on Na+ absorption and Cl- secretion, Isc was measured in the absence of mucosal and serosal Cl- (INa). Again, mucosal UTP induced an initial increase and then a sustained decrease that reduced amiloride-sensitive INa by 73%. The Ca2+-dependent agonists histamine, bradykinin, serosal UTP, and thapsigargin similarly induced sustained inhibition (62-84%) of INa. Mucosal UTP induced similar sustained inhibition (half-maximal inhibitory concentration 296 nM) of INa in primary cultures of human CF airway homozygous for the DeltaF508 mutation. BAPTA-AM blunted UTP-dependent inhibition of INa, but inhibitors of protein kinase C (PKC) and phospholipase A2 had no effect. Indeed, direct activation of PKC by phorbol 12-myristate 13-acetate failed to inhibit Na+ absorption. Apyrase, a tri- and diphosphatase, did not reverse inhibitory effects of UTP on INa, suggesting a long-term inhibitory effect of UTP that is independent of receptor occupancy. After establishment of a mucosa-to-serosa K+ concentration gradient and permeabilization of the mucosal membrane with nystatin, mucosal UTP induced an initial increase in K+ current followed by a sustained inhibition. We conclude that increasing cellular Ca2+ induces a long-term inhibition of transepithelial Na+ transport across normal and CF HBE at least partly due to downregulation of a basolateral membrane K+ conductance. Thus UTP may have a dual therapeutic effect in CF airway: 1) stimulation of a Cl- secretory response and 2) inhibition of Na+ transport.  (+info)

Amino acids are compatible osmolytes for volume recovery after hypertonic shrinkage in vascular endothelial cells. (5/485)

The response to chronic hypertonic stress has been studied in human endothelial cells derived from saphenous veins. In complete growth medium the full recovery of cell volume requires several hours and is neither associated with an increase in cell K+ nor hindered by bumetanide but depends on an increased intracellular pool of amino acids. The highest increase is exhibited by neutral amino acid substrates of transport system A, such as glutamine and proline, and by the anionic amino acid glutamate. Transport system A is markedly stimulated on hypertonic stress, with an increase in activity roughly proportional to the extent and the duration of the osmotic shrinkage. Cycloheximide prevents the increase in transport activity of system A and the recovery of cell volume. It is concluded that human endothelial cells counteract hypertonic stress through the stimulation of transport system A and the consequent expansion of the intracellular amino acid pool.  (+info)

Bicarbonate and chloride secretion in Calu-3 human airway epithelial cells. (6/485)

Serous cells are the predominant site of cystic fibrosis transmembrane conductance regulator expression in the airways, and they make a significant contribution to the volume, composition, and consistency of the submucosal gland secretions. We have employed the human airway serous cell line Calu-3 as a model system to investigate the mechanisms of serous cell anion secretion. Forskolin-stimulated Calu-3 cells secrete HCO-3 by a Cl-offdependent, serosal Na+-dependent, serosal bumetanide-insensitive, and serosal 4,4'-dinitrostilben-2,2'-disulfonic acid (DNDS)-sensitive, electrogenic mechanism as judged by transepithelial currents, isotopic fluxes, and the results of ion substitution, pharmacology, and pH studies. Similar studies revealed that stimulation of Calu-3 cells with 1-ethyl-2-benzimidazolinone (1-EBIO), an activator of basolateral membrane Ca2+-activated K+ channels, reduced HCO-3 secretion and caused the secretion of Cl- by a bumetanide-sensitive, electrogenic mechanism. Nystatin permeabilization of Calu-3 monolayers demonstrated 1-EBIO activated a charybdotoxin- and clotrimazole- inhibited basolateral membrane K+ current. Patch-clamp studies confirmed the presence of an intermediate conductance inwardly rectified K+ channel with this pharmacological profile. We propose that hyperpolarization of the basolateral membrane voltage elicits a switch from HCO-3 secretion to Cl- secretion because the uptake of HCO-3 across the basolateral membrane is mediated by a 4,4 '-dinitrostilben-2,2'-disulfonic acid (DNDS)-sensitive Na+:HCO-3 cotransporter. Since the stoichiometry reported for Na+:HCO-3 cotransport is 1:2 or 1:3, hyperpolarization of the basolateral membrane potential by 1-EBIO would inhibit HCO-3 entry and favor the secretion of Cl-. Therefore, differential regulation of the basolateral membrane K+ conductance by secretory agonists could provide a means of stimulating HCO-3 and Cl- secretion. In this context, cystic fibrosis transmembrane conductance regulator could serve as both a HCO-3 and a Cl- channel, mediating the apical membrane exit of either anion depending on basolateral membrane anion entry mechanisms and the driving forces that prevail. If these results with Calu-3 cells accurately reflect the transport properties of native submucosal gland serous cells, then HCO-3 secretion in the human airways warrants greater attention.  (+info)

Contributions of K+:Cl- cotransport and Na+/K+-ATPase to basolateral ion transport in malpighian tubules of Drosophila melanogaster. (7/485)

Mechanisms of Na+ and K+ transport across the basolateral membrane of isolated Malpighian tubules of Drosophila melanogaster were studied by examining the effects of ion substitution and putative inhibitors of specific ion transporters on fluid secretion rates, basolateral membrane potential and secreted fluid cation composition. Inhibition of fluid secretion by [(dihydroindenyl)oxy]alkanoic acid (DIOA) and bumetanide (10(-)4 mol l-1) suggested that a K+:Cl- cotransporter is the main route for K+ entry into the principal cells of the tubules. Differences in the effects of bumetanide on fluxes of K+ and Na+ are inconsistent with effects upon a basolateral Na+:K+:2Cl- cotransporter. Large differences in electrical potential across apical (>100 mV, lumen positive) and basolateral (<60 mV, cell negative) cell membranes suggest that a favourable electrochemical gradient for Cl- entry into the cell may be used to drive K+ into the cell against its electrochemical gradient, via a DIOA-sensitive K+:Cl- cotransporter. A Na+/K+-ATPase was also present in the basolateral membrane of the Malpighian tubules. Addition of 10(-)5 to 10(-)3 mol l-1 ouabain to unstimulated tubules depolarized the basolateral potential, increased the Na+ concentration of the secreted fluid by 50-73 % and increased the fluid secretion rate by 10-19 %, consistent with an increased availability of intracellular Na+. We suggest that an apical vacuolar-type H+-ATPase and a basolateral Na+/K+-ATPase are both stimulated by cyclic AMP. In cyclic-AMP-stimulated tubules, K+ entry is stimulated by the increase in the apical membrane potential, which drives K+:Cl- cotransport at a faster rate, and by the stimulation of the Na+/K+-ATPase. Fluid secretion by cyclic-AMP-stimulated tubules was reduced by 26 % in the presence of ouabain, suggesting that the Na+/K+-ATPase plays a minor role in K+ entry into the tubule cells. Malpighian tubules secreted a Na+-rich (150 mmol l-1) fluid at high rates when bathed in K+-free amino-acid-replete saline (AARS). Secretion in K+-free AARS was inhibited by amiloride and bafilomycin A1, but not by bumetanide or hydrochlorothiazide, which inhibit Na+:Cl- cotransport. There was no evidence for a Na+ conductance in the basolateral membrane of unstimulated or cyclic-AMP-stimulated tubules. Possible mechanisms of Na+ entry into the tubule cells include cotransport with organic solutes such as amino acids and glucose.  (+info)

Endothelial cell shrinkage increases permeability through a Ca2+-dependent pathway in single frog mesenteric microvessels. (8/485)

1. We tested whether calcium (Ca2+)-dependent mechanisms were essential for our previous observation that a change in the endothelial cell (EC)-extracellular matrix (ECM) attachment caused an increase in microvessel hydraulic permeability (Lp) after exposure to hypertonic solutions in single perfused mesenteric microvessels in pithed frogs (Rana pipiens). 2. In microvessels where integrin-dependent EC-ECM attachments were disrupted by pretreatment with the peptide Gly-Arg-Gly-Asp-Thr-Pro (GRGDTP; 0.3 mmol l-1), we measured microvessel Lp after exposure to hypertonic solutions under experimental conditions that reduced Ca2+ influx into endothelial cells. 3. High K+ solutions (59.7 and 100 mmol l-1 K+) were used to depolarize the endothelial membrane and therefore to reduce the electrochemical driving force for Ca2+ influx through conductive Ca2+ channels. These solutions abolished the increase in Lp caused by hypertonic solutions in the microvessels pretreated with GRGDTP. 4. We previously suggested that the removal of albumin from the perfusate may reduce EC-ECM attachment because hypertonic solutions increased the Lp of microvessels above that due to removal of albumin alone. This additional increase in Lp was attenuated by the 59.7 mmol l-1 K+ solution and was completely abolished by the 100 mmol l-1 K+ solution. 5. Bumetanide, an inhibitor of the Na+-K+-2Cl- co-transporter and one of the mechanisms of regulatory volume increase after exposure to hypertonic solutions in endothelial cells, did not change the response of microvessels to high K+ solutions. 6. Our findings indicate that Ca2+ entry into endothelial cells via passive conductance channels is necessary to increase microvessel Lp after exposure to hypertonic solutions in microvessels where EC-ECM attachments are disrupted.  (+info)

Bumetanide is a loop diuretic medication that is used to treat fluid retention (edema) and high blood pressure. It works by blocking the reabsorption of sodium and chloride ions in the kidneys, which helps to increase the amount of urine produced and reduce the amount of fluid in the body. Bumetanide is often used in combination with other diuretics or with other medications to treat heart failure, liver disease, and kidney disease. It is available in oral tablet and intravenous forms. Common side effects of bumetanide include dizziness, headache, nausea, and vomiting.

Sodium-Potassium-Chloride Symporters (NKCCs) are a group of membrane transport proteins that play a crucial role in regulating the movement of sodium, potassium, and chloride ions across cell membranes. These transporters are found in various tissues and cells throughout the body, including the kidney, brain, and muscle cells. NKCCs are responsible for actively transporting sodium and chloride ions into cells, while potassium ions are transported out of cells. This process is important for maintaining the proper balance of ions within cells and for regulating various physiological processes, such as cell volume regulation, nerve impulse transmission, and muscle contraction. In the medical field, NKCCs are often studied in relation to various diseases and conditions, such as hypertension, heart failure, and neurological disorders. For example, drugs that block NKCCs have been shown to be effective in treating certain types of epilepsy and may also have potential as treatments for other neurological disorders. Additionally, changes in the expression or function of NKCCs have been implicated in the development of certain types of cancer.

Solute Carrier Family 12, Member 2 (SLC12A2) is a protein that plays a crucial role in the transport of chloride ions across cell membranes in various tissues in the human body. It is also known as the thiazide-sensitive sodium-chloride cotransporter (NCC) and is primarily expressed in the distal convoluted tubule (DCT) of the kidneys. The function of SLC12A2 is to regulate the reabsorption of sodium and chloride ions from the filtrate in the DCT, which is an essential process for maintaining the body's fluid and electrolyte balance. When the body is dehydrated or under stress, SLC12A2 activity is increased, leading to the reabsorption of more sodium and chloride ions, which helps to conserve water and maintain blood pressure. SLC12A2 is also involved in the regulation of blood pressure and the renin-angiotensin-aldosterone system (RAAS). Mutations in the SLC12A2 gene can lead to various kidney disorders, such as Gitelman syndrome and pseudohypoaldosteronism type 1 (PHA-1), which are characterized by low blood pressure, low levels of potassium in the blood, and high levels of calcium in the urine.

Furosemide is a medication that is used to treat fluid retention (edema) and high blood pressure (hypertension). It is a type of diuretic, which means that it increases the amount of urine that the body produces. This helps to reduce the amount of fluid in the body and lower blood pressure. Furosemide is also used to treat heart failure, liver disease, and some types of kidney disease. It is usually taken by mouth, but it can also be given intravenously (by injection into a vein). Furosemide is a relatively potent diuretic and can cause side effects such as dehydration, low blood pressure, and electrolyte imbalances. It is important to follow the dosage instructions provided by your healthcare provider and to let them know if you experience any side effects while taking furosemide.

Chlorides are a type of anion that are commonly found in the human body. They are produced when chlorine combines with other elements, such as sodium or potassium, to form compounds. In the body, chlorides are primarily found in the fluid that surrounds cells, known as extracellular fluid, and in the fluid that fills the lungs and other cavities, known as intracellular fluid. Chlorides play an important role in maintaining the balance of fluids in the body and in regulating the pH of the blood. They also help to transport nutrients and waste products throughout the body. Chlorides are an essential component of many bodily functions, including the production of hydrochloric acid in the stomach, which aids in the digestion of food. In the medical field, chlorides are often measured as part of a routine blood test to assess the overall health of the body. Abnormal levels of chlorides in the blood can be a sign of a variety of medical conditions, including kidney disease, liver disease, and respiratory disorders.

Potassium is a mineral that is essential for the proper functioning of many bodily processes. It is the most abundant positively charged ion in the body and plays a crucial role in maintaining fluid balance, regulating muscle contractions, transmitting nerve impulses, and supporting the proper functioning of the heart. In the medical field, potassium is often measured in blood tests to assess its levels and determine if they are within the normal range. Abnormal potassium levels can be caused by a variety of factors, including certain medications, kidney disease, hormonal imbalances, and certain medical conditions such as Addison's disease or hyperaldosteronism. Low levels of potassium (hypokalemia) can cause muscle weakness, cramps, and arrhythmias, while high levels (hyperkalemia) can lead to cardiac arrhythmias, muscle weakness, and even cardiac arrest. Treatment for potassium imbalances typically involves adjusting the patient's diet or administering medications to correct the imbalance.

Sodium is an essential mineral that plays a crucial role in various bodily functions. In the medical field, sodium is often measured in the blood and urine to assess its levels and monitor its balance in the body. Sodium is primarily responsible for regulating the body's fluid balance, which is essential for maintaining blood pressure and proper functioning of the heart, kidneys, and other organs. Sodium is also involved in nerve impulse transmission, muscle contraction, and the production of stomach acid. Abnormal levels of sodium in the body can lead to various medical conditions, including hyponatremia (low sodium levels), hypernatremia (high sodium levels), and dehydration. Sodium levels can be affected by various factors, including diet, medications, and underlying medical conditions. In the medical field, sodium levels are typically measured using a blood test called a serum sodium test or a urine test called a urine sodium test. These tests can help diagnose and monitor various medical conditions related to sodium levels, such as kidney disease, heart failure, and electrolyte imbalances.

In the medical field, Rubidium Radioisotopes refer to radioactive isotopes of the chemical element Rubidium. These isotopes are used in various medical applications, including diagnostic imaging and radiation therapy. One commonly used Rubidium Radioisotope in medical imaging is Rubidium-82 (82Rb), which is produced by bombarding a target with neutrons. 82Rb is taken up by the heart muscle and can be imaged using a gamma camera to assess blood flow and detect areas of ischemia or infarction. This technique is known as Rubidium-82 myocardial perfusion imaging (MPI) and is used to diagnose coronary artery disease. Another Rubidium Radioisotope used in medical imaging is Rubidium-86 (86Rb), which is used in positron emission tomography (PET) scans to study blood flow in the brain. 86Rb is taken up by the brain and can be imaged using PET to detect areas of reduced blood flow, which may indicate the presence of neurological disorders such as Alzheimer's disease or stroke. In radiation therapy, Rubidium Radioisotopes such as Rubidium-86 and Rubidium-87 (87Rb) are used as sources of beta radiation to treat certain types of cancer. These isotopes emit beta particles that can damage cancer cells and shrink tumors. However, they are also toxic to normal cells and can cause side effects, so their use in radiation therapy is carefully controlled and monitored.

'4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid' is a chemical compound that is used in the medical field as a contrast agent for magnetic resonance imaging (MRI) scans. It is also known by its chemical name, Gadodiamide, and is marketed under the brand name Omniscan. Gadodiamide is a paramagnetic contrast agent that enhances the visibility of certain structures in the body on MRI scans. It works by increasing the relaxation time of water molecules in the tissues, which allows for better visualization of the affected area on the MRI image. Gadodiamide is commonly used to diagnose and monitor a variety of medical conditions, including brain and spinal cord disorders, kidney disease, and cardiovascular disease. It is administered intravenously and is generally well-tolerated by most patients. However, like all contrast agents, it can cause some side effects, including headache, nausea, and allergic reactions.

Amiloride is a medication that is used to treat high blood pressure and fluid retention caused by various medical conditions, such as heart failure, kidney disease, and diabetes. It works by blocking the sodium channels in the kidneys, which helps to reduce the amount of sodium and water that is reabsorbed by the kidneys and excreted in the urine. This, in turn, helps to lower blood pressure and reduce swelling in the body. Amiloride is available in both oral and intravenous forms and is usually taken once or twice a day, depending on the condition being treated. It is generally well-tolerated, but can cause side effects such as dizziness, headache, and an increased risk of potassium levels becoming too high.

Ouabain is a cardiac glycoside that is extracted from the plant Digitalis purpurea, also known as the foxglove plant. It is a potent inhibitor of the sodium-potassium ATPase pump, which is responsible for maintaining the electrochemical gradient across the cell membrane. In the medical field, ouabain is used as a medication to treat heart failure, particularly in cases where other treatments have been ineffective. It works by increasing the strength of the heart's contractions and decreasing the workload on the heart, which can help to improve symptoms and reduce the risk of complications such as heart failure and arrhythmias. However, ouabain can also have side effects, including nausea, vomiting, dizziness, and an irregular heartbeat. It is therefore typically used under close medical supervision and with careful monitoring of the patient's response to the medication.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic acid, also known as SITS, is a synthetic compound that is commonly used as a fluorescent dye in biological research. It is a fluorescent probe that is used to study the transport of ions across cell membranes, particularly chloride ions. SITS is also used as a pH indicator and as a fluorescent probe for studying the activity of various enzymes and proteins. In the medical field, SITS has been used to study the function of ion channels and transporters in various diseases, including cystic fibrosis, epilepsy, and hypertension.

In the medical field, Rubidium is not commonly used as a treatment or diagnostic tool. However, it is sometimes used in medical imaging studies, particularly in nuclear medicine. Rubidium-82 is a radioactive isotope of rubidium that is used in positron emission tomography (PET) scans to evaluate blood flow to the heart muscle. This can help diagnose conditions such as coronary artery disease, heart failure, and myocarditis. Rubidium-82 is produced by bombarding a target material with high-energy protons, and the resulting radioactive isotope is then purified and administered to the patient as a liquid or gas. The rubidium-82 is taken up by the heart muscle and emits positrons, which are detected by the PET scanner. The resulting images can help doctors identify areas of reduced blood flow and plan treatment accordingly.

Butylamines are a class of organic compounds that contain a butyl group (-C4H9) attached to an amine functional group (-NH2). They are derivatives of ammonia and are commonly used in the pharmaceutical industry as intermediates in the synthesis of various drugs and as solvents for drug delivery systems. In the medical field, butylamines have been used in the treatment of a variety of conditions, including depression, anxiety, and insomnia. They work by increasing the levels of certain neurotransmitters in the brain, such as serotonin and dopamine, which can help to improve mood and reduce symptoms of mental health disorders. However, butylamines can also have side effects, including dizziness, nausea, and dry mouth. They may also interact with other medications, so it is important to consult with a healthcare provider before taking them.

Bicarbonates, also known as bicarbonate ions or HCO3-, are a type of ion found in the blood and other body fluids. They play an important role in regulating the acid-base balance of the body and maintaining the proper pH of the blood. In the medical field, bicarbonate levels are often measured as part of a routine blood test. Abnormal levels of bicarbonate can indicate a variety of medical conditions, including metabolic acidosis (a condition in which the body produces too much acid), metabolic alkalosis (a condition in which the body produces too little acid), and respiratory acidosis (a condition in which the body is not able to remove enough carbon dioxide from the blood). Bicarbonate is also used in medicine to treat certain conditions, such as metabolic acidosis and respiratory acidosis. It is given intravenously (through a vein) or by mouth in the form of a salt, such as sodium bicarbonate.

In the medical field, nitrobenzoates are a class of organic compounds that contain a nitro group (-NO2) attached to a benzene ring. They are commonly used as vasodilators, which means they help to widen blood vessels and improve blood flow. One example of a nitrobenzoate is nitroglycerin, which is used to treat angina (chest pain caused by reduced blood flow to the heart) and heart attacks. Nitroglycerin works by relaxing the smooth muscles in the walls of blood vessels, allowing blood to flow more easily to the heart. Other nitrobenzoates that are used in medicine include molsidomine, which is used to treat Raynaud's disease (a condition that causes the fingers and toes to become cold and white), and isosorbide dinitrate, which is used to treat angina and heart failure. It's worth noting that nitrobenzoates can have side effects, including headache, dizziness, and low blood pressure. They should only be used under the guidance of a healthcare professional.

Symporters are a type of membrane transport protein that move molecules across a cell membrane in the same direction, using the energy of a chemical gradient. In other words, symporters use the downhill flow of one molecule to drive the uphill transport of another molecule. Symporters are important for the transport of a variety of molecules across cell membranes, including ions, sugars, amino acids, and neurotransmitters. They play a crucial role in maintaining the proper balance of these molecules inside and outside of cells, and are involved in many physiological processes, such as nutrient uptake, nerve impulse transmission, and hormone secretion. In the medical field, symporters are often targeted for therapeutic purposes. For example, some drugs are designed to bind to symporters and block their function, which can be useful for treating conditions such as epilepsy, depression, and cancer. Other drugs are designed to activate symporters, which can be useful for delivering drugs across cell membranes and increasing their bioavailability.

In the medical field, carrier proteins are proteins that transport molecules across cell membranes or within cells. These proteins bind to specific molecules, such as hormones, nutrients, or waste products, and facilitate their movement across the membrane or within the cell. Carrier proteins play a crucial role in maintaining the proper balance of molecules within cells and between cells. They are involved in a wide range of physiological processes, including nutrient absorption, hormone regulation, and waste elimination. There are several types of carrier proteins, including facilitated diffusion carriers, active transport carriers, and ion channels. Each type of carrier protein has a specific function and mechanism of action. Understanding the role of carrier proteins in the body is important for diagnosing and treating various medical conditions, such as genetic disorders, metabolic disorders, and neurological disorders.

In the medical field, anions are negatively charged ions that are found in the body fluids, such as blood and urine. They are important for maintaining the balance of electrolytes in the body and play a role in various physiological processes, including nerve function, muscle contraction, and acid-base balance. Anions can be classified into different types based on their chemical composition, such as chloride ions (Cl-), bicarbonate ions (HCO3-), and phosphate ions (PO43-). Each type of anion has a specific function in the body and can be affected by various medical conditions, such as kidney disease, acidosis, and electrolyte imbalances. In some cases, anions can be used as diagnostic markers for certain medical conditions, such as high levels of chloride ions in the blood may indicate dehydration or kidney disease, while low levels of bicarbonate ions may indicate acidosis. Therefore, monitoring the levels of anions in the body fluids is an important part of medical diagnosis and treatment.

Sodium chloride symporters are a group of proteins that transport both sodium and chloride ions across cell membranes. These transporters play a crucial role in maintaining the balance of electrolytes in the body and regulating various physiological processes, such as fluid balance, nerve impulse transmission, and muscle contraction. There are several types of sodium chloride symporters, including the thiazide-sensitive sodium chloride cotransporter (NCC), the epithelial sodium channel (ENaC), and the sodium-glucose cotransporter (SGLT). These transporters are found in various tissues throughout the body, including the kidneys, the brain, and the lungs. Disruptions in the function of sodium chloride symporters can lead to a variety of medical conditions, such as hypertension, edema, and cystic fibrosis. Therefore, understanding the mechanisms of sodium chloride symporters is important for developing new treatments for these conditions.

Chloride channels are ion channels that selectively allow chloride ions to pass through cell membranes. They play a crucial role in regulating the movement of chloride ions across cell membranes, which is important for many physiological processes, including the regulation of fluid balance, the transmission of nerve impulses, and the secretion and absorption of fluids in various organs and tissues. There are several types of chloride channels, including cystic fibrosis transmembrane conductance regulator (CFTR) channels, which are involved in the regulation of fluid balance in the lungs and other organs, and volume-regulated chloride channels, which are involved in the regulation of cell volume and the movement of fluids across cell membranes. Disruptions in the function of chloride channels can lead to a variety of medical conditions, including cystic fibrosis, which is caused by mutations in the CFTR gene that affect the function of CFTR channels in the lungs and other organs. Other conditions that may be associated with disruptions in chloride channel function include epilepsy, ataxia, and certain types of hearing loss.

The Sodium-Potassium-Exchanging ATPase (Na+/K+-ATPase) is an enzyme that plays a crucial role in maintaining the electrochemical gradient across the cell membrane in animal cells. It is responsible for actively pumping three sodium ions (Na+) out of the cell and two potassium ions (K+) into the cell, using energy from ATP hydrolysis. This process is essential for many cellular functions, including nerve impulse transmission, muscle contraction, and the maintenance of cell volume. The Na+/K+-ATPase is also involved in the regulation of intracellular pH and the transport of other ions across the cell membrane. It is a ubiquitous enzyme found in all animal cells, and its dysfunction can lead to various diseases, including cardiac arrhythmias, muscle weakness, and neurological disorders.

Sulfanilamides are a group of synthetic antimicrobial drugs that were first developed in the early 20th century. They are also known as sulfa drugs or sulphonamides. Sulfanilamides work by inhibiting the growth of bacteria by interfering with their ability to synthesize folic acid, which is essential for their growth and reproduction. Sulfanilamides are commonly used to treat a variety of bacterial infections, including urinary tract infections, bronchitis, and pneumonia. They are also used to treat some skin infections, such as acne and rosacea. However, sulfanilamides are not effective against viral infections or fungal infections. They can also cause side effects, such as nausea, vomiting, and allergic reactions. In some cases, sulfanilamides can cause more serious side effects, such as anemia, liver damage, and blood disorders. Sulfanilamides are no longer the first-line treatment for many bacterial infections, as newer antibiotics have been developed that are more effective and have fewer side effects. However, they are still used in some cases, particularly in developing countries where access to newer antibiotics may be limited.

... is a loop diuretic and works by decreasing the reabsorption of sodium by the kidneys. Bumetanide was patented in ... Bumetanide is 40 times more potent than furosemide for people with normal renal function. Bumetanide is synthesized from 4- ... Bumetanide, sold under the brand name Bumex among others, is a medication used to treat swelling and high blood pressure. This ... Bumetanide is a loop diuretic and works by decreasing the reabsorption of sodium by the kidneys. The main difference between ...
A dose of 40 mg of furosemide is equivalent to 20 mg of torsemide and 1 mg bumetanide. Loop diuretics are principally used in ... Furosemide Bumetanide Ethacrynic acid Torasemide Huxel, Chris; Raja, Avais; Ollivierre-Lawrence, Michelle D. (2022). "Loop ... Because furosemide, torsemide and bumetanide are technically sulfa drugs, there is a theoretical risk that patients sensitive ... However, for torsemide and bumetanide, their oral bioavailability is consistently higher than 90%. Torsemide has longer half ...
Bumetanide is a loop diuretic (water pill) that prevents your body from absorbing too much salt, allowing the salt to instead ... A brand name for bumetanide is Bumex. Several side effects with diuretics and masking agents are: dizziness, dehydration, heat ... Examples of diuretics and masking agents are: bumetanide, chlorothiazide, furosemide, hydrochlorothiazide, probenecid, ...
Bumetanide which can be delivered across the blood brain barrier is an inhibitor of NKCCl. Bumetanide significantly reduces ... Identifying the right dose of bumetanide that acts as an inhibitor of NKCCl could prevent cerebral edema to some extent. This ... Lu, K; Wu C; Yen H; Peng JF; Wang C; Yang Y (June 2007). "Bumetanide administration attenuated traumatic brain injury through ...
It is noticed that the risk of ototoxicity caused by furosemide is much higher than that of bumetanide. Several approaches can ... Common examples include furosemide, bumetanide and ethacrynic acid. Loop diuretics act on the thick ascending limb of the loop ...
Bumetanide confers a decreased risk of ototoxicity compared to furosemide. Platinum-containing chemotherapeutic agents, ...
Shankaran S, Liang KC, Ilagan N, Fleischmann L (April 1995). "Mineral excretion following furosemide compared with bumetanide ... results from a randomized controlled study with bumetanide". J. Bone Miner. Res. 21 (1): 163-70. doi:10.1359/JBMR.051003. PMID ...
If high doses of furosemide are inadequate, boluses or continuous infusions of bumetanide may be preferred. These loop ...
The NaCl/KCl symporters are specifically inhibited by bumetanide while the NaCl symporters are specifically inhibited by ...
The encoded protein is localized to the cell membrane and acts as a proton-linked transporter of bumetanide. Transport by the ...
... and chromosomal localization of the bumetanide-sensitive Na-K-Cl cotransporter in human colon". J. Biol. Chem. 270 (30): 17977- ...
Combined with amphotericin B, vancomycin, bacitracin, paromomycin, cyclosporine, kanamycin, cisplatin, bumetanide, etoricoxib, ...
In 2010, Nesbit sued the NFL, claiming that they knew that bumetanide was in StarCaps, but they did not notify any of the ... He had been using StarCaps, which contained the illegal loop diuretic bumetanide, which is used to mask steroids or performance ...
Loop diuretics (furosemide, bumetanide, torasemide) and thiazide diuretics (e.g., chlortalidone, hydrochlorothiazide, or ...
... is sometimes used together with loop diuretics such as furosemide or bumetanide, but these highly effective ...
On December 2, 2008, Smith was one of six players suspended for use of Bumetanide a diuretic, which can be used as a masking ...
... may refer to: Lixil Group, a Japanese manufacturer of building materials and housing equipment Bumetanide, a ...
A highly potent drug (e.g., fentanyl, clonazepam, risperidone, benperidol, bumetanide) evokes a given response at low ...
This includes loop diuretics such as furosemide and bumetanide, non-steroidal anti-inflammatory drugs (NSAIDs) both over-the- ...
Bumetanide and torasemide are alternatives For use in high‐risk patients. Atorvastatin, fluvastatin, lovastatin, and ... Bumetanide and torasemide are alternatives Chlorothiazide and chlorthalidone are alternatives Alternatives are 4th level ATC ...
... bumetanide MeSH D02.241.223.100.275 - dicamba MeSH D02.241.223.100.360 - hexobendine MeSH D02.241.223.100.380 - hydroxybenzoic ... bumetanide MeSH D02.065.884.344 - chloramines MeSH D02.065.884.365 - chlorthalidone MeSH D02.065.884.390 - clopamide MeSH ... bumetanide MeSH D02.886.590.700.344 - chloramines MeSH D02.886.590.700.365 - chlorthalidone MeSH D02.886.590.700.390 - ...
The molecular formula C17H20N2O5S (molar mass: 364.41 g/mol, exact mass: 364.1093 u) may refer to: Bumetanide Pheneticillin ...
... bumetanide (INN) bumetrizole (INN) Bumex (Roche) Buminate (Baxter International) bunaftine (INN) bunamidine (INN) bunamiodyl ( ...
Studies of piretanide in rats and dogs in comparison with other high-ceiling diuretics such as furosemide and bumetanide found ...
... hydrochloride with cyclopenthiazide Amiloride hydrochloride with bumetanide Amiloride is an inhibitor of NHE-1, which ...
Several classes are used, with combinations reserved for severe heart failure: Loop diuretics (e.g. furosemide, bumetanide) - ...
Edoxaban Enoxaparin Heparin Rivaroxaban Warfarin Fibrinolytics Alteplase Streptokinase Urokinase Diuretics Bumetanide, ...
Gliclazide Glyclopyramide Glimepiride Glipizide Gliquidone Glisoxepide Tolazamide Tolbutamide Acetazolamide Bumetanide ...
This includes loop diuretics such as furosemide and bumetanide, non-steroidal anti-inflammatory drugs (NSAIDs) both over-the- ...
... bumetanide, and torsemide), acetazolamide, sulfonylureas (including glipizide, glyburide, among others), and some COX-2 ...
Bumetanide: learn about side effects, dosage, special precautions, and more on MedlinePlus ... Bumetanide controls edema but does not cure it. Continue to take bumetanide even if you feel well. Do not stop taking ... Before taking bumetanide,. *tell your doctor and pharmacist if you are allergic to bumetanide, sulfonamide medications, any ... Bumetanide comes as a tablet to take by mouth. It usually is taken once a day. When used to treat edema, a second or third dose ...
Piña: The diuretic that you protocolized could have been bumetanide or furosemide; it didnt matter? ...
... bumetanide (B; 10?4 M) and ouabain (O; basolateral; 10?4M). Changes in lactate dehydrogenase (LDH) levels in apical medium also ...
bumetanide. Monitor Closely (1)aldesleukin increases effects of bumetanide by pharmacodynamic synergism. Use Caution/Monitor. ... bumetanide. aldesleukin increases effects of bumetanide by pharmacodynamic synergism. Use Caution/Monitor. Risk of hypotension. ...
Tubulointerstitial Nephritis - Learn about the causes, symptoms, diagnosis & treatment from the MSD Manuals - Medical Consumer Version.
Bumetanide increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits ... The use of loop diuretics (eg, furosemide, bumetanide) requires potassium supplementation and close monitoring of serum ...
BUMETANIDE 50710 BUPIVACAINE 50711 BUPRENORPHINE HCL 50713 BUSPRIONE HCL 50714 BUPROPION 50715 BUSULFAN 50720 BUTABARBITAL ...
Acute intermittent porphyria (AIP) is one of the porphyrias, a group of diseases involving defects in heme metabolism and that results in excessive secretion of porphyrins and porphyrin precursors. AIP manifests itself by abdomen pain, neuropathies, and constipation, but, unlike most types of porphyria, patients with AIP do not have a rash.
Clinical bumetanide doses for improved neurological deficits are reviewed. Regardless of mechanism, the efficacy of bumetanide ... Evaluation of bumetanide as a potential therapeutic agent for Alzheimers disease. Boyarko, Ben; Podvin, Sonia; Greenberg, ... Bumetanide is a loop diuretic which inhibits the kidney Na+-K+-2Cl- cotransporter isoform, NKCC2, for the treatment of ... In consideration of bumetanide as a repurposed drug for AD, this review evaluates its pharmaceutical properties with respect to ...
Loop Diuretics. Loop diuretics (e.g., furosemide, ethacrynic acid, bumetanide) affect the potassium gradient of the stria ...
D2.455.426.559.389.657.150 Bumetanide D2.241.223.100.215 D2.241.223.100.50.300.200 D2.455.426.559.389.127.20.452.500 Buruli ...
D2.455.426.559.389.657.150 Bumetanide D2.241.223.100.215 D2.241.223.100.50.300.200 D2.455.426.559.389.127.20.452.500 Buruli ...
D2.455.426.559.389.657.150 Bumetanide D2.241.223.100.215 D2.241.223.100.50.300.200 D2.455.426.559.389.127.20.452.500 Buruli ...
D2.455.426.559.389.657.150 Bumetanide D2.241.223.100.215 D2.241.223.100.50.300.200 D2.455.426.559.389.127.20.452.500 Buruli ...
D2.455.426.559.389.657.150 Bumetanide D2.241.223.100.215 D2.241.223.100.50.300.200 D2.455.426.559.389.127.20.452.500 Buruli ...
D2.455.426.559.389.657.150 Bumetanide D2.241.223.100.215 D2.241.223.100.50.300.200 D2.455.426.559.389.127.20.452.500 Buruli ...
D2.455.426.559.389.657.150 Bumetanide D2.241.223.100.215 D2.241.223.100.50.300.200 D2.455.426.559.389.127.20.452.500 Buruli ...
D2.455.426.559.389.657.150 Bumetanide D2.241.223.100.215 D2.241.223.100.50.300.200 D2.455.426.559.389.127.20.452.500 Buruli ...
Bumetanide is contraindicated in anuria. Although bumetanide can be used to induce diuresis in renal insufficiency, any marked ... Bumetanide decreases uric acid excretion and increases serum uric acid. Following oral administration of bumetanide the onset ... In cats, dogs and guinea pigs, bumetanide has been shown to produce ototoxicity. In these test animals bumetanide was 5 to 6 ... Reabsorption of chloride in the ascending limb is also blocked by bumetanide, and bumetanide is somewhat more chloruretic than ...
Bumetanide is contraindicated in anuria. Although bumetanide can be used to induce diuresis in renal insufficiency, any marked ... Bumetanide decreases uric acid excretion and increases serum uric acid. Following oral administration of bumetanide the onset ... In cats, dogs and guinea pigs, bumetanide has been shown to produce ototoxicity. In these test animals bumetanide was 5 to 6 ... Reabsorption of chloride in the ascending limb is also blocked by bumetanide, and bumetanide is somewhat more chloruretic than ...
Bumetanide Tablets, USP for oral administration are available as:. Bumetanide Tablets USP, 0.5 mg are supplied as white to off ... Bumetanide is contraindicated in anuria. Although bumetanide can be used to induce diuresis in renal insufficiency, any marked ... Bumetanide decreases uric acid excretion and increases serum uric acid. Following oral administration of bumetanide the onset ... In cats, dogs and guinea pigs, bumetanide has been shown to produce ototoxicity. In these test animals bumetanide was 5 to 6 ...
Bumetanide Bumetanide is used to treat edema (fluid retention; excess fluid held in body tissues) caused by various medical ... of loop diuretics (most commonly furosemide, torsemide, or bumetanide) A low level of urine calcium may be ... ... Esidrix, HydroDiuril), and metolazone (Mykrox, Zaroxolyn) Loop diuretics: Bumetanide (Bumex), furosemide (Lasix), and torsemide ... medicines and diuretics (water pills): Atenolol (Tenormin) Bethanidine Bumetanide (Bumex) Captopril (Capoten) Chlorothiazide ( ...
It is unknown if bumetanide is excreted into breastmilk. It should be avoided while breastfeeding a newborn because it may ... Bumetanide No authors listed In: Drugs and Lactation Database (LactMed®) [Internet]. Bethesda (MD): National Institute of Child ... It is unknown if bumetanide is excreted into breastmilk. It should be avoided while breastfeeding a newborn because it may ...
... bumetanide), frequency-based adverse effects, comprehensive interactions, contraindications, pregnancy & lactation schedules, ... bumetanide oral BUMETANIDE - ORAL (bue-MET-a-nide) COMMON BRAND NAME(S): Bumex WARNING: Bumetanide is a very potent medication ... encoded search term (bumetanide (Bumex%2C Burinex)) and bumetanide (Bumex, Burinex) What to Read Next on Medscape ... Metabolites: Bumetanide conjugates, desbutyl bumetanide, primary alcohols, aliphatic acid metabolite (inactive). Elimination. ...
It is unknown if bumetanide is excreted into breastmilk. It should be avoided while breastfeeding a newborn because it may ... Bumetanide - Drugs and Lactation Database (LactMed®). Bumetanide - Drugs and Lactation Database (LactMed®). ... It is unknown if bumetanide is excreted into breastmilk. It should be avoided while breastfeeding a newborn because it may ... Relevant published information on bumetanide was not found as of the revision date. Intense diuresis, fluid restriction and ...
Bumetanide increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits ... The use of loop diuretics (eg, furosemide, bumetanide) requires potassium supplementation and close monitoring of serum ...
Bumetanide is contraindicated in anuria. Although bumetanide can be used to induce diuresis in renal insufficiency, any marked ... Bumetanide decreases uric acid excretion and increases serum uric acid. Following oral administration of bumetanide the onset ... In cats, dogs and guinea pigs, bumetanide has been shown to produce ototoxicity. In these test animals bumetanide was 5 to 6 ... Reabsorption of chloride in the ascending limb is also blocked by bumetanide, and bumetanide is somewhat more chloruretic than ...
Bumetanide increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits ... The use of loop diuretics (eg, furosemide, bumetanide) requires potassium supplementation and close monitoring of serum ...
Bumetanide was identified as a top drug for apoE4 AD. Bumetanide treatment of apoE4 mice without or with Aβ accumulation ... In humans, bumetanide exposure was associated with a significantly lower AD prevalence in individuals over the age of 65 in two ... Experimental and real-world evidence supporting the computational repurposing of bumetanide for APOE4-related Alzheimers ... electronic health record databases, suggesting effectiveness of bumetanide in preventing AD. ...
Variable effects on Rt were observed in response to amiloride, and bumetanide. Generally, MMA-SS was more potent in altering ... MMA-SS or GMA-MS exposure potentiated Isc responses (decreases) to amiloride and bumetanide, while not affecting those to NPPB ... and bumetanide (basolateral), respectively. MMA-SS (0.0167-16.7mug/cm2) increased basal Vt. Only 16.7mug/cm2 GMA-MS increased ... responses to amiloride and bumetanide than GMA-MS. Hyperpolarization occurred in the absence of LDH release, but decreases in ...
The FDA-approved drug bumetanide stood out as the best candidate for further investigation. Bumetanide is used to treat high ... The researchers confirmed that bumetanide reversed AD-associated gene expression changes in the mice. Bumetanide had a similar ... Bumetanide treatment restored normal neuronal activity and reduced spatial learning problems.. Beta-amyloid plaques in the ... The researchers tested the effects of bumetanide on mouse models of AD with APOE4. These mice have abnormal electrical activity ...
Bumetanide is a common FDA-approved diuretic; further tests and clinical trials for its use in reducing Alzheimers risk are ... By combining precision medicine and big data methods, an NIH-funded study identified bumetanide as a candidate for lowering the ... Experimental and real-world evidence supporting the computational repurposing of bumetanide for APOE4-related Alzheimers ...
rxclassdata, ,drugMemberGroup, ,drugMember, ,minConcept, ,rxcui,1808,/rxcui, ,name,bumetanide,/name, ,tty,IN,/tty, ,/minConcept ... bumetanide,/attrValue, ,/nodeAttr, ,nodeAttr, ,attrName,Relation,/attrName, ,attrValue,DIRECT,/attrValue, ,/nodeAttr, ,/ ...
... bumetanide attenuated decreases in Isc. The effects of the transport blockers depended upon whether Isc was initially decreased ... basolateral bumetanide, basolateral ouabain, and Cl(-)-free solution, but not by basolateral iberiotoxin. Apical hyperosmolar ...
bumetanide. Serious - Use Alternative (1)bumetanide, paromomycin. Either increases toxicity of the other by Mechanism: ... bumetanide. bumetanide, paromomycin. Either increases toxicity of the other by Mechanism: pharmacodynamic synergism. Avoid or ...
Structural basis for inhibition of the Cation-chloride cotransporter NKCC1 by the diuretic drug bumetanide.. Zhao, Yongxiang; ...
The organic anion transport inhibitor probenecid increases brain concentrations of the NKCC1 inhibitor bumetanide.. Töllner K; ...
Bumetanide,N0000007386, bismuth subgallate,N0000007385, reteplase,N0000007384, Tyrothricin,N0000007931, Piperidones,N0000007930 ...
Tubulointerstitial Nephritis - Learn about the causes, symptoms, diagnosis & treatment from the MSD Manuals - Medical Consumer Version.
bumetanide-sensitive sodium-(potassium)-chloride cotransporter 1. *solute carrier family 12 (sodium/potassium/chloride ...
... and the bumetanide-sensitive sodium potassium 2chloride cotransporter (NKCC2), have been detected in human as well as rat urine ...
... and the bumetanide-sensitive sodium potassium 2chloride cotransporter (NKCC2), have been detected in human as well as rat urine ...
  • Bumetanide is 40 times more potent than furosemide (for patients with normal renal function). (the-medical-dictionary.com)
  • Loop diuretics (e.g., furosemide, ethacrynic acid, bumetanide) affect the potassium gradient of the stria vascularis, as well as the electrical potential of the endocochlear structure. (medscape.com)
  • acebutolol increases and bumetanide decreases serum potassium. (medscape.com)
  • albuterol and bumetanide both decrease serum potassium. (medscape.com)
  • Bumetanide is a strong diuretic ('water pill') and may cause dehydration and electrolyte imbalance. (medlineplus.gov)
  • Bumetanide is a loop diuretic of the sulfamyl category to treat heart failure. (the-medical-dictionary.com)
  • tell your doctor and pharmacist if you are allergic to bumetanide, sulfonamide medications, any other medications, or any ingredients in bumetanide tablets. (medlineplus.gov)
  • Bumetanide is also sometimes used to treat high blood pressure. (medlineplus.gov)
  • Using the substance bumetanide in newborn mice, the scientists succeeded in attenuating the disease progression, allowing the animals to develop almost normally. (epilepsyu.com)
  • At this stage, that is, for the first two weeks of life, the scientists treated mice carrying a mutation of the Kv7 channel using the substance 'bumetanide', which has previously been shown to help neurons mantaining their ionic balance. (epilepsyu.com)
  • Minnesota Vikings' Kevin Williams and Pat Williams and New Orleans Saints' Charles Grant, Deuce McAllister and Will Smith were each suspended for four games after testing positive for the banned substance bumetanide, an ingredient found in the dietary supplement StarCaps. (sportslitigationalert.com)
  • Bumetanide decreases uric acid excretion and increases serum uric acid. (nih.gov)
  • acebutolol increases and bumetanide decreases serum potassium. (medscape.com)
  • aceclofenac decreases effects of bumetanide by pharmacodynamic antagonism. (medscape.com)
  • bumetanide attenuated decreases in Isc. (cdc.gov)
  • Potassium excretion is also increased by bumetanide, in a dose-related fashion. (nih.gov)
  • albuterol and bumetanide both decrease serum potassium. (medscape.com)
  • Bumetanide was identified as a top drug for apoE4 AD. (nih.gov)
  • Bumetanide treatment of apoE4 mice without or with Aβ accumulation rescued electrophysiological, pathological, or cognitive deficits. (nih.gov)
  • The researchers tested the effects of bumetanide on mouse models of AD with APOE4 . (nih.gov)
  • Bumetanide had a similar effect on gene expression in cultured APOE4 human neurons. (nih.gov)
  • It is unknown if bumetanide is excreted into breastmilk. (nih.gov)
  • An FDA-approved drug used for high blood pressure and swelling, called bumetanide, alleviated symptoms of Alzheimer's disease in mice. (nih.gov)
  • In mice with plaques, bumetanide treatment significantly reduced the number of plaques. (nih.gov)
  • The researchers confirmed that bumetanide reversed AD-associated gene expression changes in the mice. (nih.gov)
  • Unlike mice treated with bumetanide within this time window, their littermates carrying the same genetic defect developed epilepsy. (epilepsyu.com)
  • Bumetanide inhibits sodium reabsorption in the ascending limb of the loop of Henle, as shown by marked reduction of free-water clearance (CH 2 O) during hydration and tubular free-water reabsorption (T C H 2 O) during hydropenia. (nih.gov)
  • The finding suggests that bumetanide warrants further investigation as a possible treatment for Alzheimer's disease. (nih.gov)
  • By combining precision medicine and big data methods, an NIH-funded study identified bumetanide as a candidate for lowering the risk of Alzheimer's disease in people who carry the APOE ε4 variant. (nih.gov)
  • Several pharmacokinetic studies have shown that bumetanide, administered orally or parenterally, is eliminated rapidly in humans, with a half-life of between 1 and 1½ hours. (nih.gov)
  • In humans, bumetanide exposure was associated with a significantly lower AD prevalence in individuals over the age of 65 in two electronic health record databases, suggesting effectiveness of bumetanide in preventing AD. (nih.gov)
  • Small pharmacokinetic studies of intravenous bumetanide in preterm and full-term neonates with respiratory disorders have reported an apparent half-life of approximately 6 hours, with a range up to 15 hours and a serum clearance ranging from 0.2 mL/min/kg to 1.1 mL/min/kg. (nih.gov)
  • In a population of neonates receiving bumetanide for volume overload, mean serum clearance rates were 2.2 mL/min/kg in patients less than 2 months of age and 3.8 mL/min/kg in patients aged 2 to 6 months. (nih.gov)
  • Oral administration of carbon-14 labeled bumetanide to human volunteers revealed that 81% of the administered radioactivity was excreted in the urine, 45% of it as unchanged drug. (nih.gov)
  • Elimination of bumetanide appears to be considerably slower in neonatal patients compared with adults, possibly because of immature renal and hepatobiliary function in this population. (nih.gov)
  • Dzhala VI, B rumback AC, Staley KJ: Bumetanide enhances phenobarbital efficacy in a neonatal seizure model. (utexas.edu)
  • Finally, the researchers used electronic health records to compare AD prevalence and orders for bumetanide among people over the age of 65. (nih.gov)
  • They found a 35-75% lower prevalence of AD in people who were exposed to bumetanide compared with those who weren't. (nih.gov)
  • bumetanide increases toxicity of squill by Other (see comment). (medscape.com)
  • Bumetanide is used to treat high blood pressure and swelling caused by heart, liver, or kidney disease. (nih.gov)
  • In adult patients, bumetanide is used for the treatment of kidney and heart diseases. (epilepsyu.com)
  • Bumetanide is also sometimes used to treat high blood pressure. (medlineplus.gov)
  • The results suggest that bumetanide warrants further investigation as an AD treatment. (nih.gov)
  • Bumetanide treatment restored normal neuronal activity and reduced spatial learning problems. (nih.gov)
  • There are also trials studying the treatment of epileptic seizures in newborns with bumetanide. (epilepsyu.com)
  • Relevant published information on bumetanide was not found as of the revision date. (nih.gov)
  • The major site of bumetanide action is the ascending limb of the loop of Henle. (nih.gov)