Disease relevance of Fordiuran

• Exposure of preconditioned hearts to ethylisopropylamiloride or bumetanide in the last reperfusion period limited in the increase in Nai during ischemia and reduced the beneficial effects of preconditioning [1].
• HCl-induced cell edema in rabbit esophageal epithelium: a bumetanide-sensitive process [2].
• Letter: Bumetanide in renal failure [3].
• Bumetanide-induced hyperamylaseaemia in patients with renal insufficiency [4].
• Bumetanide reduces cerebral edema formation in rats with diabetic ketoacidosis [5].

Psychiatry related information on Fordiuran

• Effects of water deprivation on the pharmacokinetics and pharmacodynamics of bumetanide in rats [6].

High impact information on Fordiuran

• The transport mechanisms involved include the cystic fibrosis transmembrane conductance regulator (CFTR) present in the apical membrane of the cystic cells and a bumetanide-sensitive transporter located in the basolateral membrane [7].
• The NKCC1 blocker bumetanide shifted E(Cl) negative in immature neurons, suppressed epileptiform activity in hippocampal slices in vitro and attenuated electrographic seizures in neonatal rats in vivo [8].
• We show here that a (Na+)-(K+)-(2Cl-) cotransporter, NKCC1, is required for this Cl- current, in that ORNs deficient in Nkcc1 or incubated with an NKCC blocker (bumetanide) lack the Cl- current [9].
• COX-2 expression also increased after administration of the Na(+)/K(+)/2Cl(-) cotransport inhibitor, bumetanide [10].
• Western blot analysis and immunoelectron microscopic studies showed that the loss of functional V2Rs had no significant effect on the basal expression levels of aquaporin-2 and the bumetanide-sensitive Na-K-2Cl cotransporter (BSC-1) [11].

Chemical compound and disease context of Fordiuran

• In addition to being time- and pH-dependent, cell edema was dependent on bathing solution osmolytes, specifically Na+, K+, and Cl-, and could be inhibited by tissue pretreatment with bumetanide (or ethacrynic acid) [2].
• These data suggest that one means by which sodium ions are accumulated during liver ischemia might be the Na+-K+-2Cl- cotransporter, which is blocked by furosemide and bumetanide [12].
• We showed previously that a luminal BBB Na-K-Cl cotransporter is stimulated by hypoxia and arginine vasopressin (AVP), factors present during cerebral ischemia, and that inhibition of the cotransporter by intravenous bumetanide greatly reduces edema in rats subjected to permanent middle cerebral artery occlusion (MCAO) [13].
• We explored if the K(+) efflux stimulator amphotericin B, with or without the Na(+), K(+), 2Cl(-)-cotransport (K(+) influx) blocker bumetanide, could affect cisplatin- and carboplatin-induced apoptosis and cytotoxicity in the pulmonary mesothelioma cell line (P31) [14].
• The efficacy of xipamide 20 to 40 mg once daily in patients with mild to moderate hypertension is comparable to that of bendrofluazide 5 mg, bumetanide 1 mg or hydrochlorothiazide 50 mg when used alone in newly treated or previously treated patients [15].

Biological context of Fordiuran

• In order to explore the role of the Na+/K+/Cl- cotransport in the mitogenic signal, the effect of two specific inhibitors of the cotransport, furosemide and bumetanide, was tested on cell proliferation induced by the above recombinant growth factors [16].
• The human and shark Na-K-Cl cotransporters (NKCC), although 74% identical in amino acid sequence, exhibit marked differences in ion transport and bumetanide binding [17].
• By mediating the coupled movement of Na, K, and Cl ions across the plasma membrane of most animal cells, the bumetanide-sensitive Na-K-Cl cotransporter (NKCC) plays a vital role in the regulation of ionic balance and cell volume [18].
• Bumetanide delays cell cycle progression and hampers volume increase [19].
• As sodium-free perfusions of the isolated rat liver proved impossible because of extensive vasoconstriction, we assessed the effects of two inhibitors of the Na+-K+-2Cl- cotransporter, the loop diuretics furosemide and bumetanide, on ischemic liver injury [12].

Anatomical context of Fordiuran

• NTCP-mediated taurocholate uptake into oocytes was inhibited by all major bile acid derivatives (100 microM), bumetanide (500 microM), and bromosulphophthalein (100 microM) [20].
• Utilizing cellular ion uptake techniques, we describe an interdependence of bumetanide-sensitive 22Na+, 86Rb+, and 36Cl- uptake, which is indicative of a Na+,K+,Cl- cotransport system in this cell line [21].
• Butyrate but not acetate or proprionate decreased basal and cAMP-stimulated bumetanide-sensitive K+ (86Rb) uptake in both HT29 cells and the Cl--secreting T84 line [22].
• Bumetanide decreases canine cerebrospinal fluid production. In vivo evidence for NaCl cotransport in the central nervous system [23].
• Expression of the bumetanide-sensitive Na-K-Cl cotransporter BSC2 is differentially regulated by fluid mechanical and inflammatory cytokine stimuli in vascular endothelium [24].

Associations of Fordiuran with other chemical compounds

• The ouabain- and bumetanide-resistant K efflux from CC cells was not inhibited by some inhibitors of the Ca2+-activated K permeability [25].
• Bumetanide added to the basolateral side effectively inhibited the Isc responses of T84 cells to either guanylin or ST 5-17 [26].
• The NKCC1 blocker bumetanide or a temperature decrease of 10 degrees C shifted the GABA-current E(GABA) more negative in oocytes injected with membranes from TLE hippocampal subiculum, matching the E(GABA) of TL neocortex-injected oocytes [27].
• When expressed in Xenopus laevis oocytes and cosM6 cells, both clones mediate methotrexate and bumetanide transport [28].
• During intestinal chloride secretion, epithelial uptake of salts is accomplished largely by a bumetanide-sensitive Na:K:2Cl cotransporter designated here as NKCC [29].

Gene context of Fordiuran

• To analyze whether the Na(+)/K(+)/Cl(-) cotransporter has a role in the mitogenic signal of normal cells, we measured the effect of bumetanide on ERK phosphorylation in human peripheral blood lymphocytes [30].
• Use of Cl-free solutions and bumetanide reduced the ET-1-induced increases in Isc, indicating that ET-1 stimulates Cl secretion [31].
• Ouabain (inhibitor of Na+,K(+)-ATPase) and bumetanide (inhibitor of Na(+)-K(+)-Cl- cotransport) reduced (up to 40% and up to 70%, respectively) the ET-1-stimulated K+ uptake [32].
• This response was sensitive to bumetanide and largely abrogated in Cftr-null mice, indicating that it predominantly reflects CFTR-mediated Cl- secretion [33].
• The basolateral NKCC1 of the secretory coils of sweat glands would most likely account for the observed bumetanide-sensitive NaCl secretion in the secretory coils, and the basolateral NHE1 is likely to be involved in Na(+)-coupled acid-base transport [34].

Analytical, diagnostic and therapeutic context of Fordiuran

• We used ventriculo-cisternal perfusion (VCP) labeled with blue dextran with or without bumetanide and measured choroidal CSF production in anesthetized, and paralyzed, mechanically ventilated dogs [23].
• CONCLUSIONS: In patients with severe CRI, a continuous intravenous infusion of bumetanide is more effective and less toxic than conventional intermittent bolus therapy [35].
• Molecular cloning and functional expression of the bumetanide-sensitive Na-K-Cl cotransporter [18].
• Light-cell generation was inhibited by 1 mM bumetanide during both oxy incubation and oxy/deoxy cycling, providing evidence that a bumetanide-sensitive, deoxy-independent pathway, previously described in circulating light SSRBCs, also contributes to the rehydration of high-density SSRBCs [36].
• Thus, both furosemide and bumetanide showed a clear benificial effect on rat livers subjected to warm ischemia [12].

References