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 5.7-fold increase per 1 mg/kg body weight of glibenclamide).

4 1075 or the K(ATP) channel closer glyburide (glibenclamide).

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

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

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

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

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

10 oidosis patients in Thailand were prescribed glibenclamide.

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

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

13 s involved in the binding of tolbutamide and glibenclamide.

14 locked by the sulphonylureas tolbutamide and glibenclamide.

15 locked by the sulphonylureas tolbutamide and glibenclamide.

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

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

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

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

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

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

22 -sensitive potassium channels inhibitor), or glibenclamide.

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

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

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

26 y pretreatment with the KATP channel blocker glibenclamide.

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

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

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

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

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

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

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

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

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

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

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

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

39 -1.0 microm) and the K(ATP) channel blocker, glibenclamide (10 microm).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

55 Glibenclamide (50 microM) significantly blocked ICl,ATP

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

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

58 Glibenclamide, a KATP channel blocker, when present only

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

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

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

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

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

64 We sought to define effects of glibenclamide, a sulfonylurea known to block ATP-depende

65 Glibenclamide abolished IPC when given contemporaneously

66 5-Hydroxydecanoate and glibenclamide abolished PKGIalpha-mediated protection ag

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

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

69 Glibenclamide abolishes and diazoxide mimics endothelial

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

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

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

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

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

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

76 Glibenclamide also blocked Kir6.2/SUR1 and Kir6.2/SUR2A

77 Glibenclamide also blocked the formation of cysts when i

78 Meglitinide and glibenclamide also stimulated insulin release from perme

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

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

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

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

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

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

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

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

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

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

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

90 locked by the sulphonylureas tolbutamide and glibenclamide and by the photorelease of caged ATP withi

91 harmacological chaperoning mechanism wherein glibenclamide and carbamazepine stabilize the heteromeri

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

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

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

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

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

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

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

99 Glibenclamide and iberiotoxin, KATP and Kca channel anta

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

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

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

103 Glibenclamide and PTX attenuated the acidosis-induced ar

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

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

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

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

108 1H nuclear magnetic resonance spectroscopy, glibenclamide and tolbutamide, were found to incorporate

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

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

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

112 Tetraethylammonium, glibenclamide, and a high concentration of extraluminal

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

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

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

116 ificity of the sulfonylureas tolbutamide and glibenclamide, and the benzamido-derivative meglitinide,

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

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

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

120 orter proteins and ABC transporter inhibitor glibenclamide antagonizes secretion.

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

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

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

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

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

126 t intravenous bolus of arginine, leucine, or glibenclamide (as previously found using glucose as the

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

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

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

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

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

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

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

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

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

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

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

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

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

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

141 Glibenclamide block was also reduced in beta-cells expre

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

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

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

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

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

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

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

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

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

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

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

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

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

155 Glibenclamide decreased GSH levels and glutathione perox

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

157 The channel inhibitor glibenclamide decreased the clonogenicity of HepG2 cells

158 Glibenclamide decreased the secretion and gene expressio

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

160 Glibenclamide did not alter the slope of the coronary ve

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

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

163 genetic variability may therefore influence glibenclamide efficacy.

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

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

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

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

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

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

170 The sulfonylurea glibenclamide (Glib) abolishes the cardioprotective effe

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

172 + 60 minutes of Rep; (3) PC alone; (4) PC-IR-glibenclamide (GLIB): PC-IR + infusion of GLIB; (5) cont

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

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

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

176 ,2,4)-oxadiazole-[4,3-a]quinoxalin-1-one, or glibenclamide had no effect.

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

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

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

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

181 ED50 also increased in response to glibenclamide in a dose-related fashion (5.7-fold increa

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

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

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

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

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

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

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

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

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

191 Both L-NAME and glibenclamide increased systemic pressure and reduced co

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

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

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

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

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

197 ntrations of MgADP (100 micromol/l) enhanced glibenclamide inhibition of Kir6.2/SUR1 currents but red

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

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

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

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

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

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

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

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

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

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

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

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

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

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

212 as, we studied the effect of tolbutamide and glibenclamide on PKC activity.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

234 titution at Arg-1150 significantly decreased glibenclamide potency.

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

236 However, glibenclamide pretreatment had no effect on either renal

237 Also, glibenclamide prevented cell blebbing after ATP depletio

238 Glibenclamide produced an inverted-U dose-response curve

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

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

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

242 Moreover, glibenclamide reduced cytokine production and migration

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

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

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

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

247 (1 mM), all dopamine neurons responded with glibenclamide-reversible hyperpolarization.

248 Glibenclamide's effects on mitoKATP channels are difficu

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

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

251 ypes largely activated the Ca2+-independent, glibenclamide-sensitive Cl- current, whereas UTP activat

252 ed that the apical PGE2-activated, NPPB- and glibenclamide-sensitive conductance was Cl- dependent an

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 ATP- and glibenclamide-sensitive K+ channels were produced when b

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

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

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

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

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

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

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

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

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

272 3 that blocks the ability of SUR2B to confer glibenclamide sensitivity to the expressed K(+) currents

273 6I substitutions had a significant effect on glibenclamide sensitivity.

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

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

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

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

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

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

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

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

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

283 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

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

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

286 Glibenclamide treatment was associated with an equivalen

287 Glibenclamide uptake into hepatocytes was dramatically d

288 Glibenclamide was also found to inhibit the proliferatio

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

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

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

292 Oral glibenclamide was used to determine the dependence of RI

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

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

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

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

297 s, the Kir1.1a/CFTR channel was inhibited by glibenclamide with micromolar 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