ライフサイエンスコーパス: glibenclamide

1 compared with ischemia/controls and ischemia/glibenclamide).

2 17+/-1 vs. 4+/-1 and 9+/-1% before and after glibenclamide).

3 1075 or the K(ATP) channel closer glyburide (glibenclamide).

4 the clinically used KATP channel inhibitor, glibenclamide.

5 t HCO3- secretion that was also inhibited by glibenclamide.

6 e effects of RIPC and RPostC were blocked by glibenclamide.

7 y pretreatment with the KATP channel blocker glibenclamide.

8 ly abolished by the K(ATP) channel inhibitor glibenclamide.

9 ter IRI (P=0.68) but not when coinfused with glibenclamide.

10 scle cells, both of which were attenuated by glibenclamide.

11 are caused by a defect in hepatic uptake of glibenclamide.

12 e in our model led to reduced sensitivity to glibenclamide.

13 saline (ischemia/control), and 3 intravenous glibenclamide.

14 endent K+ channels because it was blocked by glibenclamide.

15 s involved in the binding of tolbutamide and glibenclamide.

16 locked by the sulphonylureas tolbutamide and glibenclamide.

17 locked by the sulphonylureas tolbutamide and glibenclamide.

18 ated by elevated [K(+) ]o was insensitive to glibenclamide.

19 oidosis patients in Thailand were prescribed glibenclamide.

20 after systemic K(ATP) channel inhibition via glibenclamide.

21 ation, inhibited by the open-channel blocker glibenclamide.

22 gh after Nod-like receptor P3 inhibition via glibenclamide.

23 es by administering the KATP channel blocker glibenclamide.

24 is partially rescued by the K(ATP) inhibitor glibenclamide.

25 lornithine, or the K(ATP) channel inhibitor, glibenclamide.

26 administration of the K(ATP) channel blocker glibenclamide.

27 lly restored by the K(ATP) channel inhibitor glibenclamide.

28 sensitive potassium (K(ATP)) channel blocker glibenclamide.

29 -sensitive potassium channels inhibitor), or glibenclamide.

30 enuated by apocynin, 5-hydroxydecanoate, and glibenclamide.

31 t K(ATP) channels or adenosine A1 receptors, glibenclamide (0.1 mg/kg icv; n = 8), 5-hydroxydeconaoat

32 Local VMH microinjection of a small dose of glibenclamide (0.1% of the intracerebroventricular dose)

33 as significantly less in those animals given glibenclamide (0.16+/-0.10 mV) than in controls (0.35+/-

34 zocine pretreated with KATP channel blocker, glibenclamide (0.3 mg/kg), administered 45 mins before i

35 (IC(50) of 34.1 microM) and irreversibly by glibenclamide (0.3-3 nM) and had a low affinity for [ATP

36 K(ATP) channels were inhibited with glibenclamide (1 mg/kg intravenously).

37 s antagonized by the K(ATP) channel blockers glibenclamide (1 micromol/L) and 5-HD (300 micromol/L) i

38 Conversely, the K(ATP) channel blockers glibenclamide (1 micromol/L) and 5-hydroxydecanoate (5-H

39 The hyperpolarization was blocked by glibenclamide (1-10 microM).

40 Tetraethylammonium 10(-3) mol/L but not glibenclamide 10(-6) mol/L reduced FID.

41 Similarly, glibenclamide (10 microM) caused a 67% increase in adipo

42 microM minoxidil, diazoxide and NNC 55-0118; glibenclamide (10 microM) had no effect, but prevented s

43 -1.0 microm) and the K(ATP) channel blocker, glibenclamide (10 microm).

44 s control -44+/-2 mV; P<0.05) to BK, whereas glibenclamide (10(-6) mol/L), an ATP-sensitive K+ channe

45 ctance regulator (CFTR) Cl- channel blocker, glibenclamide (100 microM), were without effect in this

46 Both glucose (6.6 mm) and glibenclamide (100 micrometer) significantly increased a

47 Blockade of K(ATP) channels by glibenclamide (100 nM) or depletion of intracellular H2O

48 is required to mediate the renal effects of glibenclamide (15 mg/kg), clearance experiments were per

49 Shortening of AERP was not prevented by glibenclamide (180+/-20 to 153+/-33 ms) but was prevente

50 Administration of a K(ATP) channel blocker, glibenclamide (20 mg/kg, iv) 45 min prior to ZD6169 admi

51 resence of the CFTR chloride channel blocker glibenclamide (250 microM), but was DIDS insensitive (50

52 Glibenclamide (3 to 300 microM) had virtually no effect

53 formation-sensitive channel antagonist [(3)H]glibenclamide ([(3)H]GBM), indicating that ATP can act a

54 s of ischemia), (3) IRI preceded by IPC with glibenclamide, (4) IPC followed by glibenclamide before

55 Glibenclamide (5 micromol/L), another K(ATP) channel clo

56 ucose (20 nmol) or the K-ATP channel blocker glibenclamide (5 nmol) attenuated the galanin-induced pe

57 itions, during K+(ATP) channel blockade with glibenclamide (50 microg x kg(-1) x min(-1) i.c.) in the

58 re and after K(+)(ATP) channel blockade with glibenclamide (50 microg/kg/min ic) or adenosine recepto

59 was inhibited by the Cl(-) channel blockers, glibenclamide (50 microM) and niflumic acid (100 microM)

60 Glibenclamide (50 microM) significantly blocked ICl,ATP

61 anoate (100 microm), HMR1098 (30 microm), or glibenclamide (50 microm), the respective blockers of mi

62 In contrast, intrathecal delivery of glibenclamide, a KATP channel blocker, or the specific K

63 Glibenclamide, a KATP channel blocker, when present only

64 Glibenclamide, a non-selective K(ATP) channel blocker, w

65 channel was investigated with 2 inhibitors: glibenclamide, a nonselective KATP channel inhibitor, an

66 iants to inhibition by the sulfonylurea drug glibenclamide, a potential pharmacotherapy for CS.

67 nt, 6 juvenile swine were given 0.5 mg/kg IV glibenclamide, a selective inhibitor of the K(+)(ATP) ch

68 Glibenclamide, a selective K(ATP) channel inhibitor, sig

69 Glibenclamide abolished IPC when given contemporaneously

70 5-Hydroxydecanoate and glibenclamide abolished PKGIalpha-mediated protection ag

71 r the delivery of the K(ATP) channel blocker glibenclamide abolished the glucose production-lowering

72 The KATP-channel antagonist glibenclamide abolished the H2O2-dependent increase in D

73 Glibenclamide abolishes and diazoxide mimics endothelial

74 In rats, glibenclamide acts as a K(+)-sparing diuretic by a mecha

75 of the core recognize a hydrophobic group in glibenclamide, adjacent to the sulfonylurea moiety, to p

76 Glibenclamide, administered 30 minutes before I/R in 48-

77 In the severe HI model, glibenclamide, administered immediately after HI and on

78 s of stroke, sulfonylurea (SU) drugs such as glibenclamide (adopted US name, glyburide) confer protec

79 However, the mechanisms by which glibenclamide affects cytokine production are unknown.

80 Glibenclamide also blocked the formation of cysts when i

81 orothioate (a protein kinase G-inhibitor) or glibenclamide (an ATP-sensitive potassium channel-inhibi

82 ster, an inhibitor of nitric oxide synthase; glibenclamide, an adenosine triphosphate-sensitive potas

83 -cyclic GMP could be reversed by exposure to glibenclamide, an antagonist of K(ATP) channels.

84 ; sodium hydrogen sulphide (NaHS); NaHS plus glibenclamide, an antagonist of K(ATP) opening (NaHS Gli

85 Glibenclamide, an inhibitor of ATP-sensitive K(+) channe

86 cretion and Ca(2+) uptake in the presence of glibenclamide, an inhibitor of the ATP-dependent potassi

87 Both 100 nM glibenclamide and 200 M tolbutamide, blockers of the -ce

88 l/L) in normoxic heart mitochondria, whereas glibenclamide and 5-HD alone had no effect.

89 affected by bimakalim but was attenuated by glibenclamide and 5-HD.

90 -) channel blockers, but sensitive to apical glibenclamide and arylaminobenzoates.

91 l bound to a high-affinity sulfonylurea drug glibenclamide and ATP at 3.63 A resolution, which reveal

92 ied as K(ATP) channels through blockade with glibenclamide and by comparison with recordings from Kir

93 harmacological chaperoning mechanism wherein glibenclamide and carbamazepine stabilize the heteromeri

94 igate how two chemically distinct compounds, glibenclamide and carbamazepine, correct biogenesis defe

95 ch are amenable to pharmacological rescue by glibenclamide and carbamazepine.

96 adenosine-5'-triphosphate release inhibitors glibenclamide and carbenoxolone.

97 nitrophenyl)glutathione (DNP-SG) and also by glibenclamide and frusemide but not by the monoclonal Ig

98 That lemakalim, as well as glibenclamide and glucose, increased hippocampal ACh out

99 mo cAMP (10(-8), 10(-6) M) was attenuated by glibenclamide and iberiotoxin (8+/-1 and 17+/-1 vs. 4+/-

100 Glibenclamide and iberiotoxin, K(ATP) and K(ca) channel

101 Glibenclamide and iberiotoxin, KATP and Kca channel anta

102 ound that the ratio of the concentrations of glibenclamide and its metabolites was moderately increas

103 cose and the direct K-ATP channel modulators glibenclamide and lemakalim on spontaneous alternation p

104 Glibenclamide and N(G)-nitro-l-arginine methyl ester par

105 Glibenclamide and PTX attenuated the acidosis-induced ar

106 nhibition of KATP channels and G proteins by glibenclamide and PTX, respectively.

107 ical closing and opening of the channel with glibenclamide and the specific mitoK(ATP) openers diazox

108 n in a Ca(2+)-free medium and was blocked by glibenclamide and tolbutamide, but not by charybdotoxin.

109 s the charge carrier: (1) the sulfonylureas, glibenclamide and tolbutamide, inhibited NCCa-ATP channe

110 However, glibenclamide and tolbutamide, two widely used antidiabe

111 1H nuclear magnetic resonance spectroscopy, glibenclamide and tolbutamide, were found to incorporate

112 ere inhibited by ATP but were insensitive to glibenclamide and tolbutamide.

113 on exhibited specific binding of FITC-tagged glibenclamide and were immunolabeled with anti-SUR1 anti

114 eriotoxin); (II) KATP channel-inhibited (via glibenclamide); and (III) controls.

115 Tetraethylammonium, glibenclamide, and a high concentration of extraluminal

116 ATP-sensitive potassium (K(ATP)) channels by glibenclamide, and inhibition of NO synthase by N(G)-nit

117 at, N omega-I-nitro-L-arginine methyl ester, glibenclamide, and meclofenamate had no significant effe

118 tabolic inhibition, decreased sensitivity to glibenclamide, and responds to both diazoxide and pinaci

119 was inhibited by the K(ATP) channel blocker, glibenclamide, and was mimicked by pinacidil, which is a

120 rrent with the addition of 4-AP, TEA-Cl, and glibenclamide; and 4) blocking I(Ca) with cadmium.

121 The selective KATP blocker glibenclamide antagonized the above vascular effects, co

122 orter proteins and ABC transporter inhibitor glibenclamide antagonizes secretion.

123 etraethylammonium chloride, 4-aminopyridine, glibenclamide, apamin or MK-499.

124 barium (Ba2+) and unaffected by iberiotoxin, glibenclamide, apamin, 3,4-DAP and ouabain.

125 Sulfonylurea inhibitors, such as glibenclamide, are potential therapies for CS.

126 glimepiride, and nateglinide and identified glibenclamide as a novel substrate of OATP1B3.

127 and provide evidence of in vivo efficacy of glibenclamide as a therapeutic agent in CS.

128 by minoxidil and pinacidil and attenuated by glibenclamide as well as tetraethylammonium, in agreemen

129 diately after HI and on postoperative Day 1, glibenclamide at 0.01 mg/kg improved several neurologica

130 in the presence of ATP and the sulfonylurea glibenclamide, at 6 A resolution reveals a closed Kir6.2

131 ereas K(ATP) channel blockers (quinidine and glibenclamide) attenuated DNA synthesis.

132 IPC with glibenclamide, (4) IPC followed by glibenclamide before IRI, (5) IRI preceded by diazoxide,

133 However, significant glibenclamide binding activity was observed when the hal

134 aculovirus expression system did not lead to glibenclamide binding activity, although studies with gr

135 us expression of Kir6.2 resulted in enhanced glibenclamide binding activity.

136 reveals unprecedented details of the ATP and glibenclamide binding sites.

137 Immunocytochemistry and glibenclamide binding studies showed increased K(ATP) ch

138 to 12-fold increase in the density of [(3)H]glibenclamide binding to the cortex, hippocampus, and st

139 linker has been reported to be required for glibenclamide binding, and DeltaNK(IR)6.2/SUR1 channels

140 ions of SUR1, that NBD2 is not essential for glibenclamide binding, and that interactions between Kir

141 re-forming subunit (Kir) and a sulfonylurea (glibenclamide)-binding protein, a member of the ATP bind

142 We conclude that the glibenclamide-binding site includes amino acid residues

143 Glibenclamide block was also reduced in beta-cells expre

144 Pretreatment of monolayers with NPPB and glibenclamide blocked the PGE2 and cAMP-mediated increas

145 ) activation was modulated by intra-arterial glibenclamide (blocker) and diazoxide (opener).

146 owever, STa-stimulated DBS was unaffected by glibenclamide but inhibited by DIDS.

147 tly activated by GTPgammaS, was inhibited by glibenclamide but not by DIDS, thus exhibiting known pha

148 MP-stimulated Isc component was sensitive to glibenclamide but not to DIDS, suggesting that a cystic

149 ; in addition, they are blocked by 10 microM glibenclamide, but are insensitive to 500 microM 5-hydro

150 imulated DBS were significantly inhibited by glibenclamide, but not by 4,4'-diisothiocyanato-stilbene

151 The K(ATP) channel inhibitor glibenclamide caused membrane depolarization (9 mV) and

152 ted glibenclamide-induced insulin secretion, glibenclamide clearance from the blood, and glibenclamid

153 The fluorescent glibenclamides colocalize with Ins-C-GFP, a live-cell fl

154 te structural differences, carbamazepine and glibenclamide compete for binding to KATP channels, and

155 Our data demonstrate that high serum glibenclamide concentrations and an increased t(1/2) of

156 onse to glucose and decreased in response to glibenclamide, consistent with what is known about the e

157 Glibenclamide decreased GSH levels and glutathione perox

158 Addition of glibenclamide decreased internal pH (pHin), and addition

159 The channel inhibitor glibenclamide decreased the clonogenicity of HepG2 cells

160 Glibenclamide decreased the secretion and gene expressio

161 ) channel pathways were not involved because glibenclamide did not affect their anti-nociceptive acti

162 Glibenclamide did not alter the slope of the coronary ve

163 Adipocytes exhibited glibenclamide dose-responsive (0-20 microM) increases in

164 Ps, including cyclosporin A, rifampicin, and glibenclamide, each demonstrated concentration-dependent

165 genetic variability may therefore influence glibenclamide efficacy.

166 Glibenclamide exerted little effect on the I(sc) of nons

167 pressure whereas the K(ATP) channel blocker glibenclamide failed to produce a vasoconstrictive respo

168 vention by injecting NDM mice with high-dose glibenclamide for only 6 days, at the beginning of disea

169 The clearance of glibenclamide from the blood during the first hours afte

170 In diabetic dogs, however, glibenclamide further reduced myocardial O(2) delivery;

171 Glibenclamide (GBC), a sulfonylurea, was used as a confo

172 t: i) systemic K(ATP) channel inhibition via glibenclamide (GLI; 10 mg kg(-1) i.p.) would decrease ca

173 The sulfonylurea glibenclamide (Glib) abolishes the cardioprotective effe

174 TP-sensitive K(+) channel (K(ATP)) inhibitor glibenclamide (GLIB) or the mitochondrial K(ATP) (mitoK(

175 notropic antidiabetes compounds tolbutamide, glibenclamide, glimepiride, and nateglinide and identifi

176 SUR2 (cardiac, smooth muscle types), whereas glibenclamide, glimepiride, repaglinide, and meglitinide

177 ce of block of SUR1 by sulfonylureas such as glibenclamide (glyburide) in conditions as seemingly div

178 oglycaemic agents, principally metformin and glibenclamide (glyburide), are also used in some countri

179 ,2,4)-oxadiazole-[4,3-a]quinoxalin-1-one, or glibenclamide had no effect.

180 th T-wave impacts, the animals that received glibenclamide had significantly fewer occurrences of ven

181 Block of SUR 1 with sulfonylurea such as glibenclamide has been shown to be highly effective in r

182 TP-dependent potassium (K-ATP) channels with glibenclamide (i.c.v.) abolished salvage only in the SHR

183 Glibenclamide impaired critical speed proportionally mor

184 DA release was prevented by the sulfonylurea glibenclamide, implicating ATP-sensitive K+ (KATP) chann

185 d by diphenylamine carboxylic acid (DPC) and glibenclamide in ADPKD cells but blocked only by DPC in

186 igh-affinity sensitivity to the KATP blocker glibenclamide in both intact cells and excised patches.

187 In this study, we tested glibenclamide in both severe and moderate models of neon

188 To study the metabolism of glibenclamide in Hnf-1alpha(-/-) animals, we analyzed li

189 ation of residues predicted to interact with glibenclamide in our model led to reduced sensitivity to

190 e demonstrate that the half-life (t(1/2)) of glibenclamide in the blood is increased in Hnf-1alpha(-/

191 de concentrations and an increased t(1/2) of glibenclamide in the blood of Hnf-1alpha(-/-) mice are c

192 ther group of NDM mice was initiated on oral glibenclamide (in the drinking water), and the dose was

193 on, whereas increasing metabolic demand with glibenclamide increased oxygen consumption but not cytoc

194 d sodium nitroprusside were not inhibited by glibenclamide, indicating that cAMP- and cGMP-induced di

195 cogenetic mechanism(s), we have investigated glibenclamide-induced insulin secretion, glibenclamide c

196 diabetic Hnf-1alpha(-/-) mice have a robust glibenclamide-induced insulin secretory response.

197 Glibenclamide inhibited basal and stimulated J(lyz), but

198 Basolateral application of glibenclamide inhibited I(sc) to a greater extent.

199 xis, revealing a possible mechanism by which glibenclamide inhibits channel activity.

200 imals, we analyzed liver extracts from [(3)H]glibenclamide-injected animals by reverse-phase chromato

201 nhibitors, charybdotoxin and apamin, inhibit glibenclamide-insensitive, H(2)S-induced vasorelaxation.

202 the structure shows for the first time that glibenclamide is lodged in the transmembrane bundle of t

203 Glibenclamide (KATP blocker) and pinacidil (KATP opener)

204 blocker), the sulfonylureas tolbutamide and glibenclamide (KATP channel blockers), and diazoxide (KA

205 rrent activation were attenuated by 5-HD and glibenclamide, KATP channel blockers.

206 Tolbutamide and glibenclamide, KATP+-channel blockers, microinjected int

207 mg/dL to normal values, ca. 87 mg/dL, unlike glibenclamide, leading to subnormal values (i.e., 63 mg/

208 s encoding Kir6.1 or SUR2, and suggests that glibenclamide may be an appropriate therapeutic agent.

209 glibenclamide clearance from the blood, and glibenclamide metabolism in wild-type and Hnf-1alpha-def

210 nf-1alpha(-/-) mice, suggesting that hepatic glibenclamide metabolism was not impaired in animals wit

211 le perfusion with the K(ATP) channel blocker glibenclamide mimicked the effects of increased glucose.

212 Cl(-)>> Asp(-)) and sensitivity to block by glibenclamide, niflumic acid, DIDS and extracellular ATP

213 , our data show a link between the effect of glibenclamide on GSH and PMN functions in response to B.

214 The effect of glibenclamide on the growth of cysts formed within a col

215 determinant of the insulinotropic effect of glibenclamide on the tissue level.

216 icular perfusion of sulfonylurea (120 ng/min glibenclamide or 2.7 microg/min tolbutamide) suppressed

217 , paxilline, and KCl preconstriction but not glibenclamide or 3-isobutyl-1-methylxanthine.

218 hane was not changed in animals treated with glibenclamide or 5-HD or DPCPX.

219 d phase, 20 swine were randomized to receive glibenclamide or a control vehicle (in a double-blind fa

220 ented by high-dose sK(ATP) channel blockade (glibenclamide or HMR 1098) but not mitochondrial K(ATP)

221 Addition of either glibenclamide or pre-treatment of Calu-3 cells with the

222 Following SCI, block of SUR1 by glibenclamide or repaglinide or suppression of Abcc8, wh

223 ther the non-selective K(ATP) channel closer glibenclamide or the putatively selective mitochondrial

224 s could be significantly reduced with either glibenclamide or the specific inhibitor CFTR-inh172.

225 The halothane current was not sensitive to glibenclamide or thyrotropin-releasing hormone (TRH).

226 embrane conductance regulator (CFTR) blocker glibenclamide or vesicular release inhibitor brefeldin A

227 lfonylurea receptor (SUR) to increase (e.g., glibenclamide) or decrease (e.g., diazoxide) [Ca2+]i cau

228 KATP modulators (pinacidil and glibenclamide) or the specific Kir6.2-siRNA were injecte

229 L-NMMA, glibenclamide, or 5-hydroxydecanoic acid administered du

230 Addition of the Cl- channel blockers NPPB, glibenclamide, or bumetanide and experiments using Cl- f

231 TP-sensitive potassium (K(ATP)) channel with glibenclamide, or selectively transected the hepatic bra

232 When KATP channel antagonists, such as glibenclamide, or the mitochondrial selective inhibitor

233 ydroxydecanoate, tetraphenylphosphonium, and glibenclamide, PKG-selective inhibitor KT5823, and prote

234 nnel openers and inhibitors (tolbutamide and glibenclamide), plus a novel, selective Kir6.2/SUR1 open

235 titution at Arg-1150 significantly decreased glibenclamide potency.

236 re induction of ventricular fibrillation; c) glibenclamide pretreated alone 45 mins before induction

237 However, glibenclamide pretreatment had no effect on either renal

238 Also, glibenclamide prevented cell blebbing after ATP depletio

239 tly interact with Epac2 and that SUs such as glibenclamide promote Barr1/Epac2 complex formation, tri

240 ation of the sulfonylurea-receptor inhibitor glibenclamide promptly reversed these abnormalities.

241 We conclude that glibenclamide provided some long-term neuroprotective ef

242 Block of SUR1 with low-dose glibenclamide reduced cerebral edema, infarct volume and

243 Moreover, glibenclamide reduced cytokine production and migration

244 Recent evidence demonstrates that glibenclamide reduces pro-inflammatory cytokine producti

245 oduced an equally robust insulin response to glibenclamide regardless of whether their low basal FFA

246 n K(ATP) channel bound to pharmacochaperones glibenclamide, repaglinide, and carbamazepine.

247 NLRP3 inflammasome, and the NLRP3 inhibitor, glibenclamide, restored B lymphopoiesis and minimized in

248 stration of lemakalim with either glucose or glibenclamide resulted in alternation scores not signifi

249 (1 mM), all dopamine neurons responded with glibenclamide-reversible hyperpolarization.

250 Glibenclamide's effects on mitoKATP channels are difficu

251 ere acutely pretreated with chelerythrine or glibenclamide, selective blockers of PKC and K+(ATP) cha

252 r ATP levels (0.02-0.067 Hz), monitored from glibenclamide-sensitive changes in action potential dura

253 ndent on the activity of an apical NPPB- and glibenclamide-sensitive conductance.

254 cells to approximately -60 mV and increased glibenclamide-sensitive current by 2- to 4-fold.

255 nitroprusside (10 microM) did not activate a glibenclamide-sensitive current in cells held at -60 mV,

256 e-cell patch-clamp recordings demonstrated a glibenclamide-sensitive current in the presence of bariu

257 2+)-dependent protein phosphatase, type 2B), glibenclamide-sensitive currents were large and the rest

258 -cell line (MIN6)-which exhibits glucose and glibenclamide-sensitive insulin secretion-significantly

259 apparatus results in efflux of K(+) through glibenclamide-sensitive K(+) channels, which in turn sti

260 letion and substitution mutants and examined glibenclamide-sensitive K(+) currents in oocytes when co

261 r ROMK3, with rat SUR2B in oocytes generated glibenclamide-sensitive K(+) currents.

262 st isoprenaline (10 microM) also activated a glibenclamide-sensitive K+ current.

263 n Dsur alone is expressed in Xenopus oocytes glibenclamide-sensitive potassium channel activity occur

264 Our data reveal conservation of glibenclamide-sensitive potassium channels in Drosophila

265 induced a potent endothelium-independent and glibenclamide-sensitive vasodilation with membrane hyper

266 We report here that both ATP and glibenclamide sensitivities of the 30 pS K channel in TA

267 In vitro studies have shown that glibenclamide sensitivity is conferred upon Kir 1.1 K(+)

268 n between these two proteins is required for glibenclamide sensitivity of induced K(+) currents in oo

269 our results suggest that it does not confer glibenclamide sensitivity on ROMK2, as does the first ha

270 The latter is required to confer glibenclamide sensitivity to K(ATP) channels.

271 3 that blocks the ability of SUR2B to confer glibenclamide sensitivity to the expressed K(+) currents

272 6I substitutions had a significant effect on glibenclamide sensitivity.

273 e ATP-dependent K (K(ATP)) channel inhibitor glibenclamide specifically binds to mitochondria in both

274 The time course of the effect of glibenclamide suggests involvement of K(ATP) channels as

275 core offers the possibility of defining the glibenclamide/sulfonylurea binding pocket.

276 Vascular K(ATP) channel function (topical glibenclamide superfused onto hindlimb skeletal muscle)

277 nsitive K(+) channel (5-hydroxydecanoate and glibenclamide) suppressed swelling.

278 plausible blockers (ATP, 5-hydroxydecanoate, glibenclamide, tetraphenylphosphonium cation) and opener

279 d by pharmacological inhibition of K(ATP) by glibenclamide, The effects of hyperexcitable and underex

280 o block nitric oxide production, or 10(-5) M glibenclamide to block K(ATP) channel activity.

281 Binding of [3H]glibenclamide to membranes expressing SUR1 was abolished

282 Focal application of glucose or glibenclamide to neurogliaform cells mimics the excitati

283 Addition of glibenclamide to the media bathing the cysts inhibited t

284 0.6, 3.5 +/- 0.7 and 4.9 +/- 0.7 microm) or glibenclamide (to 0.4 +/- 0.3, 0.8 +/- 0.7 and 1.9 +/- 0

285 We found that PMNs from glibenclamide-treated diabetic individuals infected with

286 Calcium fluxes were unperturbed in glibenclamide-treated HepG2 cells and primary rat hepato

287 Glibenclamide treatment was associated with an equivalen

288 Glibenclamide uptake into hepatocytes was dramatically d

289 Glibenclamide was also found to inhibit the proliferatio

290 That glibenclamide was an effective K(+)-sparing diuretic in

291 rikes were compared with animals in which no glibenclamide was given.

292 Glibenclamide was K(+)-sparing in both genotypes with no

293 Oral glibenclamide was used to determine the dependence of RI

294 rain PKC was not activated by tolbutamide or glibenclamide, whether tested in the absence or presence

295 The dilation was blocked by 1 microm glibenclamide, which in that dose is a selective inhibit

296 oxide, and (6) IRI preceded by coinfusion of glibenclamide with diazoxide.

297 semble and that a SUR1 deletion mutant binds glibenclamide with high affinity.

298 selective and sensitive to levcromakalim and glibenclamide with unitary conductance of approximately

299 cantly enhances the insulinotropic effect of glibenclamide without affecting glucose-stimulated insul

300 ssed whether intravenous glyburide (RP-1127; glibenclamide) would safely reduce brain swelling, decre