ライフサイエンスコーパス: bumetanide

1 esence of bound loop diuretic (furosemide or bumetanide).

2 Na(+)/K(+)/2Cl(-) cotransporter inhibition (bumetanide).

3 xperiments using the specific NKCC inhibitor bumetanide.

4 in its sensitivity to the specific inhibitor bumetanide.

5 ive to the Na+-K+-2Cl- cotransport inhibitor bumetanide.

6 er NMDA receptor activation was inhibited by bumetanide.

7 d acidic by approximately 0.1 pH units after bumetanide.

8 the Na(+)/K(+)/2Cl(-) cotransport inhibitor, bumetanide.

9 osure to 10 microM benzmetanide or 10 microM bumetanide.

10 d a 3-fold higher affinity for the inhibitor bumetanide.

11 ilbene-2,2'-disulfonic acid), furosemide, or bumetanide.

12 ffect similar to that seen in the absence of bumetanide.

13 and the patients with GS in the presence of bumetanide.

14 ffinities for the cotransported ions and for bumetanide.

15 stored by application of the NKCC1 inhibitor bumetanide.

16 w-variable-pressure perfusion with 10 microM bumetanide.

17 the transported ions and with the inhibitor bumetanide.

18 ior chamber with 2 ml 10, 100, or 500 microM bumetanide.

19 duced reductions in [Na+]i were sensitive to bumetanide.

20 as not substantially reduced by amiloride or bumetanide.

21 f sodium reabsorption through the loop using bumetanide.

22 ere characterized: ouabain (1 mM) sensitive, bumetanide (0.1 mM) sensitive, and ouabain-bumetanide in

23 n of K+ (Rb+) influx with the NKCC inhibitor bumetanide (1, 10 and 100 microM) revealed a highly bume

24 ansducer system after exposure to 100 microM bumetanide +/-1 microM carbachol.

25 Bumetanide (10 microM) produced a fall in intracellular

26 )-K(+)-2Cl(-) cotransporter (NKCC) inhibitor bumetanide (10 microM), or the Na(+)-K(+)-ATPase inhibit

27 Bumetanide (10 mM), an inhibitor of K(+)-Cl- cotransport

28 Cl-free perfusate and/or bumetanide (10(-5) M) was used to inhibit Na-K-Cl cotran

29 Bumetanide (100 microM) applied to the blood (pigmented

30 + or exposure to the Cl- transport inhibitor bumetanide (100 microM) shifted RB cell EREV to move neg

31 ransport were completely inhibited by apical bumetanide (100 microM).

32 2,2'-stilbenedisulfonic acid), furosemide or bumetanide; (2) exposure of swollen astrocytes to MeHg i

33 rgely reduced in the presence of basolateral bumetanide (20 microM) or in the absence of extracellula

34 median dose of 3 mg (2-4 mg) of intravenous bumetanide, 40% of the population had a poor natriuretic

35 Moreover, blocking of NKCC1 activity with bumetanide (5-10 microm) abolished glutamate- or OGD-ind

36 During furosemide (frusemide, 1 mM) or bumetanide (50 microM) application, a slow decrease in [

37 ted cAMP in the presence of amiloride nor to bumetanide, a blocker of Na(+),K(+),2Cl(-) cotransporter

38 There is considerable interest in using bumetanide, a chloride importer Na-K-Cl cotransporter an

39 based on the sensitivity of ion transport to bumetanide, a NKCC inhibitor.

40 contrast, phenobarbital in combination with bumetanide abolished seizures in 70% of hippocampi and s

41 We tested bumetanide added to phenobarbital to treat neonatal seiz

42 Under some conditions, bumetanide addition resulted in a small reduction in sec

43 g (1-4 mg), 1 mg (0-2 mg), and 1 mg (0-1 mg) bumetanide administered in bolus during consecutive 24-h

44 We observed that blocking NKCC1 activity by bumetanide administration induces a selective effect on

45 -fold lower Rb affinity, and a 4-fold higher bumetanide affinity.

46 The administration of bumetanide after SCI in mouse improved locomotor recover

47 However, although [Cl-]i fell more than with bumetanide alone, it remained significantly above equili

48 Here we found that, after SCI, a prolonged bumetanide (an FDA-approved antagonist of the sodium-pot

49 Luminal application of bumetanide (an NKCC inhibitor) did not affect intestinal

50 xia after SCI, we investigated the effect of bumetanide, an FDA-approved sodium-potassium-chloride in

51 y 79.6% with an IC50 of 42.1 microM, whereas bumetanide, an inhibitor of (Na-K-Cl) cotransport, had n

52 obutyric acid (GABA) action by administering bumetanide, an inhibitor of early GABA depolarization, r

53 e removal of bath Cl(-) and addition of bath bumetanide, an inhibitor of Na-K-2Cl cotransport and Cl(

54 y removal of bath Cl(-), by addition of bath bumetanide, an inhibitor of Na-K-2Cl cotransport and Cl(

55 sulin and intravenous saline with or without bumetanide, an inhibitor of Na-K-2Cl cotransport, using

56 t model of DKA and determined the effects of bumetanide, an inhibitor of Na-K-Cl cotransport.

57 Thus, it was determined if bumetanide, an inhibitor of NKCC1, alters transepithelia

58 Finally, we show that application of bumetanide, an inhibitor of NKCC1, significantly decreas

59 induced electrical activity was prevented by bumetanide, an inhibitor of the Na+-K+-2Cl- co-transport

60 Bumetanide, an inhibitor of the Na+-K+-2Cl- co-transport

61 carboxylate, a chloride channel blocker, and bumetanide, an inhibitor of the Na/K/2Cl cotransporter,

62 inhibiting basolateral chloride uptake with bumetanide and 4,4'-diisothiocyanatostilbene-2,2'-disulf

63 ectory was corrected by the NKCC1 antagonist bumetanide and accompanied by alterations in ultrasonic

64 arger on warming, whereas in the presence of bumetanide and amiloride (blockers of electroneutral Na(

65 lapse is speeded by warming, and exposure to bumetanide and amiloride slows the temperature-dependent

66 inephrine responses were inhibited by apical bumetanide and basal 4,4'-diisothiocyanostilbene-2,2' di

67 dary decline of I(SC) was also attenuated by bumetanide and by Ba2+, indicating that it is partly due

68 A combination of bumetanide and DIDS decreased the response more than eit

69 Maximal inhibitory concentrations of bumetanide and dimethylamiloride, which respectively blo

70 rmine whether the loop diuretics furosemide, bumetanide and ethacrynic acid, which block the KCC1 pot

71 Cl- channel blockers NPPB, glibenclamide, or bumetanide and experiments using Cl- free alveolar insti

72 PGE2 was blocked by basolateral addition of bumetanide and furosemide at concentrations that are sel

73 ore residues had large effects on binding of bumetanide and furosemide, consistent with the hypothesi

74 Among them, bumetanide and furosemide, two blockers of Na(+)/K(+)/Cl

75 s the molecular target of the loop diuretics bumetanide and furosemide, we asked about their effects

76 Bumetanide and furosemide, which inhibit Cl- influx thro

77 The effects of bumetanide and other drugs on Isc and transepithelial 36

78 Future trials of bumetanide and other drugs should include a control grou

79 ed excitation of AVP neurons was reversed by bumetanide, and furosemide blocked AVP release, both in

80 hree were withdrawn for reasons unrelated to bumetanide, and one because of dehydration.

81 he anticonvulsant efficacy of phenobarbital, bumetanide, and the combination of these drugs was studi

82 ed by the so-called loop diuretics including bumetanide, and these drugs are a mainstay for treating

83 Loop diuretics, including furosemide, bumetanide, and torsemide, antagonize both NKCC1 and NKC

84 sm partially involves p75(NTR) signaling, as bumetanide application reduced SE-induced p75(NTR) expre

85 Bumetanide applied to the aqueous (nonpigmented epitheli

86 iuretics, such as furosemide, torsemide, and bumetanide, are the primary treatment for fluid overload

87 eptibility to ictal weakness and establishes bumetanide as a potential therapy for hypokalaemic perio

88 Our findings suggest that bumetanide as an add-on to phenobarbital does not improv

89 o assess dose and feasibility of intravenous bumetanide as an add-on to phenobarbital for treatment o

90 miloride and strongly reduced by basolateral bumetanide as well as by depletion of basolateral Cl(-),

91 electrolyte transport inhibitors ouabain and bumetanide, as well as bath Cl(-) and HCO(3)(-) levels.

92 Mucosal 8-Br cAMP at 3 mM, serosal bumetanide at 0.5 mM, and both mucosal and serosal bathi

93 ablation of NKCC1 or inhibition of NKCC1 by bumetanide-attenuated OGD-mediated swelling.

94 h Na+ with NMDG+; it was stimulated by 10 nM bumetanide (bath).

95 e, suggesting a specific modification of the bumetanide binding site.

96 Finally, unlike Cl, bumetanide binding was strongly affected by shark-human

97 ibit marked differences in ion transport and bumetanide binding.

98 transmembrane domain 2, indicating that the bumetanide-binding site is not the same as the Cl-bindin

99 did not significantly increase the number of bumetanide-binding sites and only marginally increased s

100 ene-targeted deletion of NKCC1 (NKCC1-/-) or bumetanide blockade of NKCC1.

101 locking the activity of the transporter with bumetanide (BMN).

102 150 mmHg O2) in the presence of ouabain and bumetanide (both 100 microM).

103 ne-triggered GLP-1 secretion was impaired by bumetanide but not bendrofluazide, suggesting that a hig

104 fall in [Cl-]i similar to that observed with bumetanide, but the hyperpolarization of Em was larger.

105 nor the inhibitor of Na+-K+-2Cl- cotransport bumetanide by itself was effective.

106 cent evidence in mouse models indicated that bumetanide can prevent attacks of hypokalaemic periodic

107 That bumetanide can produce a previously unobserved lowering

108 However, it remains unknown whether bumetanide can rescue earlier circuit phenotypes or sens

109 Bumetanide caused a rapid rise in ADCs of DKA rats witho

110 free Ringer solutions and in the presence of bumetanide, chlorothiazide and ouabain.

111 In the presence of bumetanide, chlorothiazide produced a further dose-depen

112 affected by 100 microM levels of amiloride, bumetanide, chlorothiazide, or stilbene.

113 The bumetanide concentrations used had little effect on outf

114 Cl- and was inhibited by the NKCC inhibitor, bumetanide, consistent with the involvement of a Na+/K+/

115 removing extracellular Cl(-) or exposure to bumetanide, consistent with the involvement of the trans

116 chloride transporter NKCC1 with the diuretic bumetanide could rescue synaptic circuit phenotypes in t

117 the pilocarpine model in mice, BUM5, but not bumetanide, counteracted the alteration in seizure thres

118 n step-trained SCI rats an acute delivery of bumetanide decreased presynaptic inhibition of the H-ref

119 r, in step-trained SCI, an acute delivery of bumetanide decreases presynaptic inhibition of the H-ref

120 The aquaporin ligand bumetanide derivative AqB011 was the most potent blocker

121 Serosal bumetanide did not further reduce the I(sc) beyond the i

122 Inhibition of this activity by bumetanide diminished ammonia-induced astrocyte swelling

123 tional dose of phenobarbital and one of four bumetanide dose levels by use of a bivariate Bayesian se

124 Light-cell generation was inhibited by 1 mM bumetanide during both oxy incubation and oxy/deoxy cycl

125 Blocking NKCC1 with the diuretic bumetanide during development leads to similar persisten

126 ibition were altered and the NKCC1 inhibitor bumetanide eliminated seizures in a subgroup of mice.

127 TATION: Thus, alteration of Cl- transport by bumetanide enables the anticonvulsant action of phenobar

128 We therefore tested whether bumetanide enhances the anticonvulsant action of phenoba

129 In the presence of bumetanide, ethacrynic acid and N-ethyl maleimide caused

130 justify add-on trials of the NKCC1 inhibitor bumetanide for the treatment of TSC and FCD type IIb-rel

131 y resolve the problems associated with using bumetanide for treatment of neurological disorders.

132 was a synergistic effect in combination with bumetanide (fractional excretion of sodium, 5.8+/-2.5% v

133 ons-a low concentration of the loop diuretic bumetanide had differential effects on AVP+ and VIP+ neu

134 Bumetanide had no effect in the presence of the GABA(A)-

135 Inhibition of Na(+)-K(+)-2Cl- cotransport by bumetanide had no effect on [Na+]i.

136 Bumetanide had no effect, but ouabain caused a decrease

137 In Na(+)-free media, bumetanide had no effect.

138 the Na-K-Cl cotransporter (NKCC1) inhibitor bumetanide has prominent positive effects on the pathoph

139 Our results suggest that bumetanide has the potential to decrease spastic symptom

140 l cerebral spinal fluid (aCSF) or 100 microM bumetanide in aCSF were continuously microdialyzed into

141 odel in rats, BUM5 was more efficacious than bumetanide in potentiating the anticonvulsant effect of

142 than the parent drug and are converted into bumetanide in the brain.

143 3 hours after administration of intravenous bumetanide in various diluents.

144 of intravenous loop diuretics (furosemide or bumetanide) in bolus (2-3 times per day) or continuous f

145 nificantly attenuated by the NKCC1 inhibitor bumetanide, in contrast to hyperpolarizing GABA(A)R-medi

146 otoneurons, we further show that a prolonged bumetanide increased postsynaptic inhibition by hyperpol

147 Intravenous bumetanide increased urine volume, regardless of the dil

148 eduction of external Cl(-) or application of bumetanide induced a decrease in [Cl(-)](i), whereas an

149 Application of bumetanide induced a positive shift of E(GABA), suggesti

150 Removal of Na+, K+, or Cl- or adding bumetanide inhibited acid-induced swelling.

151 +)-K(+)-2Cl(-) (NKCC1) cotransporter blocker bumetanide inhibited seizure-induced neuronal Cl(-) accu

152 Blocking NKCC1 with bumetanide inhibited the GABA-induced calcium transients

153 Bumetanide inhibited the PE-to-NPE chloride flux by 52%

154 macologic inhibition using the loop diuretic bumetanide inhibits in vitro Transwell migration by 25%

155 old stimulation of the residual (i.e. oubain-bumetanide insensitive) 86Rb+ influx across the human re

156 , bumetanide (0.1 mM) sensitive, and ouabain-bumetanide insensitive.

157 ) and did not affect bumetanide-sensitive or bumetanide-insensitive 86+Rb+ uptake.

158 NaK-ATPase (measured as ouabain-sensitive, bumetanide-insensitive 86Rb+ uptake) and bumetanide-inse

159 The bumetanide-insensitive K+ (Rb+) influx pathway was activ

160 Rb+) flux pathway at low PO2, and a relative bumetanide-insensitive pathway at high PO2.

161 ve, bumetanide-insensitive 86Rb+ uptake) and bumetanide-insensitive, ouabain-insensitive 86Rb+ uptake

162 ammonium)ethyl methanethiosulfonate, and the bumetanide insensitivity of M382W is consistent with try

163 consistent with tryptophan blocking entry of bumetanide into the cavity.

164 s into the brain, and chronic treatment with bumetanide is compromised by its potent diuretic effect.

165 Bumetanide is effective in preventing attacks in mouse m

166 However, bumetanide is heavily bound to plasma proteins (~98%) an

167 in Nkcc1 or incubated with an NKCC blocker (bumetanide) lack the Cl- current.

168 Analysis of bumetanide levels in plasma and brain showed that admini

169 Treatment with bumetanide may help diminish the adverse effects of init

170 genesis processes as well as contributing to bumetanide-mediated improvement of cognitive performance

171 clinical data suggest that the loop-diuretic bumetanide might be an effective treatment for neonatal

172 ted by loop diuretics such as furosemide and bumetanide, molecules used in clinical medicine because

173 plied ouabain (Na(+)/K(+)-ATPase inhibitor), bumetanide (Na(+)/K(+)/2Cl(-) tritransporter inhibitor),

174 colon, which was inhibited by either serosal bumetanide (NKCC1 inhibitor) or mucosal iberiotoxin (IbT

175 und that in scPCP mice, the NKCC1 antagonist bumetanide normalizes GABA(A) current polarity ex vivo a

176 The effect of bumetanide on Isc was Cl- dependent, suggesting a role f

177 3)(-)/CO(2)-buffered solutions, no effect of bumetanide on net K(+) flux was detected.

178 Inhibition of NKCC1 activity by bumetanide or ablation of the NKCC1 gene significantly a

179 n the absence and presence of loop diuretic (bumetanide or furosemide), using single-particle cryo-el

180 by a reduction in NaCl concentration and by bumetanide or furosemide.

181 was inhibited (approximately 50%) by either bumetanide or HCO(3)(-) removal and inhibited approximat

182 ol and LDL-C/HDL-C whereas administration of bumetanide or metolazone increased the concentration of

183 Pase and other transporters not sensitive to bumetanide or ouabain.

184 However, application of the NKCC1 inhibitor bumetanide or the potassium channel antagonist Tetraethy

185 egimen, (3) change from furosemide to either bumetanide or torsemide, and the change persists for at

186 ospho-activated NKCC1 bound with furosemide, bumetanide, or torsemide showing that furosemide and bum

187 reduction in seizure burden attributable to bumetanide over phenobarbital without increased serious

188 There was an additive increase in C with bumetanide plus Cl-free media.

189 DKA rats treated with bumetanide plus saline/insulin showed a trend toward mor

190 tion of it with the clinically used diuretic bumetanide potently suppresses ammonia-induced neurologi

191 Treatment with the CCC blocker bumetanide prevented neuronal swelling via a reversal in

192 Blocking the NKCC1 transporter with bumetanide prevents outward Cl- flux and causes a more n

193 Thus, application of bumetanide prevents p75(NTR) upregulation and neuronal d

194 data demonstrate that the goal of designing bumetanide prodrugs that specifically target the brain i

195 IPA, BIIB723, or dorzolamide, application of bumetanide produced an additional reduction in IOP of 3.

196 emic periodic paralysis and show herein that bumetanide protects against both muscle weakness from lo

197 early transient (3 days) post-SE infusion of bumetanide reduced rMF sprouting and recurrent seizures

198 Block of NKCC cotransport with bumetanide reduced the EOG in epithelia from wild-type m

199 owed that inhibition of chloride influx with bumetanide reduced the susceptibility to attacks of weak

200 Here, we found that bumetanide rescues parvalbumin-positive interneurons by

201 Arsenite had no effect on bumetanide-resistant 86Rb uptake.

202 f NKCC1 after SE with the specific inhibitor bumetanide restored NKCC1 and KCC2 expression, normalize

203 Tyzio et al. reported that bumetanide restored the impaired oxytocin-mediated gamma

204 were similar in calf eyes: Cl-free medium or bumetanide resulted in 41% and 52% increases in C, where

205 Treatment of Scn1b(-/-) mice with bumetanide resulted in a delay in SUDEP onset compared t

206 Na-K-Cl cotransport using Cl-free medium or bumetanide resulted in facility increases of 27% and 22%

207 exercise on FDD, whereas blocking NKCC1 with bumetanide returned FDD toward intact levels after SCI.

208 Inhibition of NKCC1 with bumetanide reversed the paclitaxel effect on GABA-mediat

209 he apparent affinities for Na+, K+, Cl-, and bumetanide segregated exactly according to whether the l

210 d to the plasma membrane, where it catalyzed bumetanide-sensitive (36)Cl(-), (22)Na(+), and (86)Rb(+)

211 oocytes and determined the ion dependence of bumetanide-sensitive (86)Rb influx.

212 Each carried out bumetanide-sensitive 86Rb influx with cation affinities

213 d in HEK-293 cells, each chimera carried out bumetanide-sensitive 86Rb influx, demonstrating transpor

214 NKCC1 activity was measured as bumetanide-sensitive 86Rb uptake or basolateral to apica

215 marker for K+ to study ouabain-insensitive, bumetanide-sensitive 86Rb+ uptake in cultured fetal huma

216 or K+ was used to study ouabain-insensitive, bumetanide-sensitive 86Rb+ uptake in cultured NPE monola

217 Bumetanide-sensitive and Cl(-)-dependent (86)Rb(+) uptak

218 KCC1 during hyperosmotic stress, measured as bumetanide-sensitive basolateral to apical (86)Rb flux.

219 1 yielded a similar inhibition and a loss of bumetanide-sensitive cell volume regulation.

220 ved in both sexes, associated with decreased bumetanide-sensitive chloride cotransport, whereas KCC2

221 increase in KCC2 expression and decrease in bumetanide-sensitive chloride cotransport.

222 ransporter 2 (KCC2) expression and decreased bumetanide-sensitive chloride transport in females.

223 e cells swelled back to resting volume via a bumetanide-sensitive Cl(-) influx pathway, likely to be

224 stent with defective Cl(-) uptake, a loss of bumetanide-sensitive Cl(-) influx was observed in paroti

225 K(+) uptake with only a minimal increase in bumetanide-sensitive Cl(-) uptake.

226 The bumetanide-sensitive component was completely inhibited

227 Both the ouabain-sensitive and bumetanide-sensitive components increased in the presenc

228 re we demonstrate that the gene encoding the bumetanide-sensitive cotransporter BSC2, one of the two

229 ated with a approximately 3-fold increase in bumetanide-sensitive CSF secretion.

230 tor, did not alter NKCC1 activity or percent bumetanide-sensitive flux.

231 perkalemic rats, the sum of the ouabain- and bumetanide-sensitive fluxes could account for all of 86R

232 Two bumetanide-sensitive ion cotransporters that carry Na+,

233 asic, concentration- and chloride-dependent, bumetanide-sensitive Isc increase.

234 t activity, assessed as ouabain-insensitive, bumetanide-sensitive K influx using 86Rb as a tracer for

235 Cotransport activity was assessed as bumetanide-sensitive K influx.

236 ns, there is a significant activation of the bumetanide-sensitive K(+) uptake with only a minimal inc

237 prionate decreased basal and cAMP-stimulated bumetanide-sensitive K+ (86Rb) uptake in both HT29 cells

238 ide (1, 10 and 100 microM) revealed a highly bumetanide-sensitive K+ (Rb+) flux pathway at low PO2, a

239 The bumetanide-sensitive K+ (Rb+) influx pathway was activat

240 er known choroid plexus K+ uptake mechanism, bumetanide-sensitive K+ cotransport, was unaffected by d

241 ride cotransporters, which also includes two bumetanide-sensitive Na+-K+-2Cl- cotransporters and a th

242 paired Na+/H+ and Cl-/HCO3- antiports and a bumetanide-sensitive Na+-K+-2Cl- symport.

243 tors, increasing [Ca2+](in), and stimulating bumetanide-sensitive Na,K,2Cl uptake at the apical membr

244 sal expression levels of aquaporin-2 and the bumetanide-sensitive Na-K-2Cl cotransporter (BSC-1).

245 , mutations in the genes encoding either the bumetanide-sensitive Na-K-2Cl cotransporter (NKCC2) or t

246 he thick ascending limb of Henle's loop (the bumetanide-sensitive Na-K-2Cl cotransporter [NKCC2]), an

247 l sequence homology (24-25% identity) to the bumetanide-sensitive Na-K-Cl cotransporter (NKCC or BSC)

248 uptake of salts is accomplished largely by a bumetanide-sensitive Na:K:2Cl cotransporter designated h

249 molyte (and consequently water) uptake via a bumetanide-sensitive NaK2Cl cotransporter.

250 acellular pH (pHo) caused by activation of a bumetanide-sensitive NaK2Cl cotransporter.

251 P13 because of increase in the activity of a bumetanide-sensitive NKCC1 (sodium potassium chloride co

252 reported action on CFTR) and did not affect bumetanide-sensitive or bumetanide-insensitive 86+Rb+ up

253 accompanied by secretory volume decrease and bumetanide-sensitive regulatory volume increase, respect

254 asic, concentration- and chloride-dependent, bumetanide-sensitive short-circuit current (Isc) increas

255 was Cl- dependent, suggesting a role for the bumetanide-sensitive transport pathway in Cl- secretion.

256 t in ferret erythrocytes was measured as the bumetanide-sensitive uptake of 86Rb.

257 y was measured in ferret erythrocytes as the bumetanide-sensitive uptake of 86Rb.

258 NKCC1 activity (i.e. bumetanide-sensitive uptake), intracellular Ca(2+) and c

259 oxy/deoxy cycling, providing evidence that a bumetanide-sensitive, deoxy-independent pathway, previou

260 ulation in Na+,K+,Cl cotransport measured as bumetanide-sensitive, ouabain-insensitive 86Rb+ uptake.

261 in turkey red cells using Na+ dependence or bumetanide sensitivity of 86Rb+ influx to monitor activi

262 The NKCC1 blocker bumetanide shifted E(Cl) negative in immature neurons, s

263 es in the developing brain and indicate that bumetanide should be useful in the treatment of neonatal

264 Also, intrathecal bumetanide significantly attenuated hyperalgesia and all

265 BUM5, but not BUM1, was less diuretic than bumetanide, so that BUM5 was further evaluated in chroni

266 old increase in sensitivity to the inhibitor bumetanide, suggesting a specific modification of the bu

267 revented by treating slices with BAPTA-AM or bumetanide, suggesting that gp120 activates a mechanism

268 lted in significantly higher brain levels of bumetanide than administration of the parent drug.

269 e defines new pharmacological derivatives of bumetanide that selectively inhibit the ion channel, but

270 esigned lipophilic and uncharged prodrugs of bumetanide that should penetrate the blood-brain barrier

271 d that administration of 2 ester prodrugs of bumetanide, the pivaloyloxymethyl (BUM1) and N,N-dimethy

272 echanism, we propose the use of the diuretic bumetanide to prevent the requirement for BDNF and conse

273 However, with the application of bumetanide to the bath, J(Na) was +5.2 +/- 1.3 pmol/mm p

274 Addition of bumetanide to the blood-side bath inhibited FF by approx

275 Prior addition of bumetanide to the PE side blocked the increase due to is

276 on of the Na+-K+-2Cl- cotransport inhibitor, bumetanide, to the low-sodium perfusate reduced baseline

277 significantly decreased in the pre-ischemic bumetanide-treated group (P<0.05) but not in the post-is

278 Furthermore, chronic bumetanide treatment (postnatal days 5-14) restored S1 c

279 Bumetanide treatment also rectified the reduced feedforw

280 Bumetanide treatment increased ATP/Pi and PCr/Pi and ame

281 In SCI rats, a prolonged bumetanide treatment increased postynaptic inhibition bu

282 In a model of FASD, maternal bumetanide treatment prevented interneuronopathy in the

283 In addition, pre-ischemic bumetanide treatment reduced the ipsilateral water conte

284 Postnatal bumetanide treatment restored network activity by postna

285 Bumetanide treatment to inhibit Cl(-) secretion by block

286 Importantly, bumetanide treatment was associated with increased neuro

287 r placebo (control) or 0.1, 0.2, or 0.3mg/kg bumetanide (treatment).

288 r placebo (control) or 0.1, 0.2, or 0.3mg/kg bumetanide (treatment).

289 de, or torsemide showing that furosemide and bumetanide utilize a carboxyl group to coordinate and co

290 hamber for 45 to 60 minutes before and after bumetanide was administered by bolus intracameral inject

291 e, immediately after, and 2 to 6 weeks after bumetanide was administered intravitreally (final concen

292 Bumetanide was ineffective if added after 10-120 min of

293 atory volume increase (RVI) was prevented if bumetanide was present.

294 (+)-2Cl(-) cotransporter inhibitor, 10microM bumetanide, was without effect on either the RVI or the

295 utward-facing conformation of NKCC1, showing bumetanide wedged into a pocket in the extracellular ion

296 ](i)-stimulated mucus, and its inhibition by bumetanide were unexpected.

297 blockers, such as SITS, DIDS, furosemide, or bumetanide, when simultaneously added with EtOH to hypon

298 ateral Na(+),K(+),2Cl(-) co-transporter with bumetanide, which effectively blocked all cAMP-stimulate

299 with a Ki of approximately 40 microM and by bumetanide with a Ki of approximately 60 microM.

300 All babies received at least one dose of bumetanide with the second dose of phenobarbital; three