ライフサイエンスコーパス: bumetanide

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

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

3 er NMDA receptor activation was inhibited by bumetanide.

4 d acidic by approximately 0.1 pH units after bumetanide.

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

6 osure to 10 microM benzmetanide or 10 microM bumetanide.

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

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

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

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

11 ffinities for the cotransported ions and for bumetanide.

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

13 the transported ions and with the inhibitor bumetanide.

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

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

16 as not substantially reduced by amiloride or bumetanide.

17 stored by application of the NKCC1 inhibitor bumetanide.

18 in its sensitivity to the specific inhibitor bumetanide.

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

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

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

22 Bumetanide (10 microM) produced a fall in intracellular

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

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

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

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

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

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

29 2,2'-stilbenedisulfonic acid), furosemide or bumetanide; (2) exposure of swollen astrocytes to MeHg i

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

66 Bumetanide and furosemide, which inhibit Cl- influx thro

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

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

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

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

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

72 Bumetanide applied to the aqueous (nonpigmented epitheli

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

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

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

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

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

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

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

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

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

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

83 ibit marked differences in ion transport and bumetanide binding.

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

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

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

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

88 150 mmHg O2) in the presence of ouabain and bumetanide (both 100 microM).

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

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

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

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

93 That bumetanide can produce a previously unobserved lowering

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

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

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

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

98 The bumetanide concentrations used had little effect on outf

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

116 Bumetanide had no effect, but ouabain caused a decrease

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

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

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

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

121 3 hours after administration of intravenous bumetanide in various diluents.

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

123 Intravenous bumetanide increased urine volume, regardless of the dil

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

140 Bumetanide is effective in preventing attacks in mouse m

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

183 1 yielded a similar inhibition and a loss of bumetanide-sensitive cell volume regulation.

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

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

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

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

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

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

190 The bumetanide-sensitive component was completely inhibited

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

228 Also, intrathecal bumetanide significantly attenuated hyperalgesia and all

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

249 (+)-2Cl(-) cotransporter inhibitor, 10microM bumetanide, was without effect on either the RVI or the

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

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

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

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

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