ライフサイエンスコーパス: diazoxide

1 bited WT-like sensitivity to ATP, MgADP, and diazoxide.

2 ved, however, with the K(ATP) channel opener diazoxide.

3 or, nifedipine, or by hyperpolarization with diazoxide.

4 cted by treating cells with sulfonylureas or diazoxide.

5 ) were PC for 30 minutes with 200 micromol/L diazoxide.

6 vely mimicked using the mKATP channel opener diazoxide.

7 nNOS in retinal cells after stimulation with diazoxide.

8 ked by injection of the mKATP channel opener diazoxide.

9 This was unchanged by the addition of diazoxide.

10 lling that was eliminated by the addition of diazoxide.

11 el and normal sensitivity to ATP, MgADP, and diazoxide.

12 ions with or without the KATP channel opener diazoxide.

13 te, proving the specificity of the action of diazoxide.

14 preceded by coinfusion of glibenclamide with diazoxide.

15 ated a 27% reduction in EGP (P = 0.002) with diazoxide.

16 de (NaCN), or the mitoK(ATP) channel opener, diazoxide.

17 whereas blebbing was produced by exposure to diazoxide.

18 min of KCl stimulation but were prevented by diazoxide.

19 of ATP-sensitive K+ channel openers such as diazoxide.

20 by inhibition of secretion by nimodipine and diazoxide.

21 of KCl in either the absence or presence of diazoxide.

22 n was isolated using 50 mmol/l potassium and diazoxide.

23 itoK(ATP) channels could not be activated by diazoxide.

24 nd do not respond to stimulation by MgADP or diazoxide.

25 ine augmented the cardioprotective effect of diazoxide.

26 l channels to cromakalim or pinacidil versus diazoxide.

27 rols responsiveness to the benzothiadiazine, diazoxide.

28 al lesion, they show clinical sensitivity to diazoxide.

29 hich IOP is lowered following treatment with diazoxide.

30 sensitive channel modulators tolbutamide and diazoxide.

31 e was facilitated by the KATP channel opener diazoxide.

32 and NAD(P)H oscillations were eliminated by diazoxide.

33 This was weakly potentiated by diazoxide (0.1 mm extracellular glucose) but insensitive

34 Diazoxide (10 mg/kg) or vehicle was injected intraperito

35 High doses of TAN-67 (10 mg/kg), diazoxide (10 mg/kg), and isoflurane (1 MAC) produced a

36 , p<0.01; 0.1, 10, 100 microM, p<0.001), and diazoxide (10 microM, p<0.01) increased growth.

37 in a concentration-dependent manner, whereas diazoxide (10 micromol/L), a selective mitoK(ATP) agonis

38 a combination of ryanodine and 4-AP reduced diazoxide (100 microM)-induced dilation in pressurized (

39 acological opening of mitoK(ATP) channels by diazoxide (100 micromol/L) preserved mitochondrial integ

40 ochondrial flavoprotein oxidation induced by diazoxide (100 micromol/L) was used to quantify mitochon

41 ated ischemia, the mitoK(ATP) channel opener diazoxide (100 micromol/L), but not P-1075, blunted cell

42 c inhibition, whereas the drug did not blunt diazoxide (100 micromol/L)-induced flavoprotein oxidatio

43 chondria are most effectively depolarized by diazoxide (-15%, tetramethylrhodamine [TMRM]), less so b

44 ydro-1,8-(2H,5H)-acridinedione (ZM244085) >> diazoxide (16.7 microM).

45 Insulin secretion was blocked with diazoxide (2.5-30 mg/kg/day).

46 at had been unresponsive to maximal doses of diazoxide (20 mg per kilogram of body weight per day) an

47 ally, the ATP-sensitive K(+) channel agonist diazoxide (200 micromol/l) inhibited GKA50-induced insul

48 The K(+) channels opener diazoxide (200-500 microM) increased channel opening pro

49 -3.6% versus 47.1+/-3.8% with MPG; P<0.001), diazoxide (22.1+/-2.7% versus 56.3+/-3.8% with MPG; P<0.

50 ns, the selective mitoK(ATP) channel agonist diazoxide (25-50 microM) potently reduced mitochondrial

51 Diazoxide (250 microm), an activator of KATP channels, p

52 her 1) vehicle, 2) the K(ATP) channel opener diazoxide, 3) the K(ATP) channel closer glybenclamide, 4

53 Although diazoxide (5 microM) alone did not change FAS activity i

54 1.0 minutes, control versus NaCN, P<0.05) or diazoxide (5.5+/-1.4 versus 2.0+/-0.8 minutes, control v

55 Direct addition of diazoxide (50 microM) to isolated mitochondria also inhi

56 The mitoK(ATP) channel opener, diazoxide (50 microM), caused a similar increase in matr

57 dom-sequence, double-blind administration of diazoxide (6.0 mg/kg) or placebo at -30 and 1 min, inges

58 d in 12 T1D subjects with prior ingestion of diazoxide (7 mg/kg) or placebo.

59 In hearts treated with diazoxide (80 micromol/L), a significant improvement in

60 However, diazoxide (a K(+)-ATP channel opener) administered 1 h b

61 inism that is unresponsive to treatment with diazoxide, a channel agonist.

62 the young adult rat, exposure to 300 microM diazoxide, a K(ATP) channel agonist, significantly hyper

63 years, and 15 of 16 were well controlled on diazoxide, a KATP channel agonist.

64 mic PC or 5-minute exposure to 10 micromol/L diazoxide, a mito K(ATP) channel opener, reduced infarct

65 Chemical preconditioning with diazoxide, a mitochondrial ATP-sensitive potassium chann

66 oflurane, together or alone with and without diazoxide, a mitochondrial K(ATP) channel opener.

67 By contrast, diazoxide, a potassium channel opener that also binds SU

68 Responsive cells also hyperpolarized with diazoxide, a selective opener for K(ATP) channels contai

69 Diazoxide, a selective opener of the mitochondrial ATP-s

70 In other groups, rats were pretreated with diazoxide, a specific opener of the mitoK(ATP) channel (

71 Diazoxide, a sulfonylurea receptor 1 (SUR1)selective KAT

72 s is reported to require ATP hydrolysis, but diazoxide, a SUR1-selective agonist, concentration-depen

73 chemia assays, coapplication of MCC-134 with diazoxide abolished the cardioprotective effect of diazo

74 ) the SUR activator ("KATP channel opener"), diazoxide, activated the NCCa-ATP channel, whereas pinac

75 nockdown of ROMK inhibits the ATP-sensitive, diazoxide-activated component of mitochondrial thallium

76 While we have previously shown that diazoxide administration induces acute preconditioning a

77 With diazoxide administration, insulin (P = 0.0016) and C-pep

78 Diazoxide also attenuated the decrease in contractility

79 Diazoxide also failed to suppress EGP in diabetic rats.

80 due to the influx of extracellular Ca2+, and diazoxide, an activator of KATP channels, resulted in pa

81 pL activity was unaffected by treatment with diazoxide, an inhibitor of insulin exocytosis that does

82 sensitive K+ channel (mitoKATP) sensitive to diazoxide and 5-hydroxydecanoate (5-HD) represents an at

83 ive potassium channel (KATP channel) openers diazoxide and 7-chloro-3-isopropylamino-4H-1,2,4-benzoth

84 We confirmed previous findings that diazoxide and activators of PKG or protein kinase C (PKC

85 mula mixed meal (Ensure Plus) at 0 min after diazoxide and after placebo and, on a separate occasion,

86 ucose infused to prevent hypoglycemia) after diazoxide and after placebo in 11 healthy young adults.

87 eight-state model describes linkage between diazoxide and ATP(4-) binding; diazoxide markedly increa

88 nclamide and the specific mitoK(ATP) openers diazoxide and BMS-191095.

89 ntly, combination of the KATP channel opener diazoxide and carbamazepine led to enhanced mutant chann

90 s hyperinsulinism was easily controlled with diazoxide and chlorothiazide.

91 itoKATP similar to KATP channel openers like diazoxide and cromakalim in heart, liver, and brain mito

92 Importantly, coapplication of diazoxide and CsA exhibited additive effects, improving

93 This response was inhibited by diazoxide and EGTA, indicating that beta-cell depolariza

94 brane potential with the KATP channel-opener diazoxide and KCl to fix Ca(2+) at an elevated level.

95 K(ATP) channel openers diazoxide and nicorandil are effective regulators of IOP

96 ith EGTA, or pharmacological inhibition with diazoxide and nifedipine, blocked the effects of glucose

97 abolished the effect of 10 microM minoxidil, diazoxide and NNC 55-0118; glibenclamide (10 microM) had

98 vestigated the molecular mechanisms by which diazoxide and pinacidil induce vasodilation by studying

99 ets of potassium channel openers (KCO; e.g., diazoxide and pinacidil).

100 ivity to glibenclamide, and responds to both diazoxide and pinacidil.

101 uglycemic pancreatic clamp studies following diazoxide and placebo administration.

102 basal secretion rates that were inhibited by diazoxide and restored by tolbutamide but were not furth

103 on currents that were largely insensitive to diazoxide and somatostatin.

104 When KATP channels were held open with diazoxide (and the plasma membrane partially depolarized

105 libenclamide before IRI, (5) IRI preceded by diazoxide, and (6) IRI preceded by coinfusion of glibenc

106 ort that the protection associated with IPC, diazoxide, and mitochondrial uncoupling requires transie

107 SUR1+SUR2A channels were sensitive to azide, diazoxide, and pinacidil, and their single-channel burst

108 II inhibitor, dilated arteries similarly to diazoxide, and this effect was attenuated by MnTMPyP and

109 suggest that the cardioprotective actions of diazoxide are mediated by generation of a pro-oxidant en

110 data highlight the dangers of using 5HD and diazoxide as specific modulators of mitoK(ATP) channels

111 pproximately 7 muM, is more efficacious than diazoxide at low micromolar concentrations, directly act

112 In rats, comparable doses of oral diazoxide attained appreciable concentrations in the cer

113 The mitoK(ATP) channel opener diazoxide attenuated the accumulation of [Ca(2+)](m) dur

114 reflow, hearts perfused with 100 micromol/L diazoxide before ischemia showed significantly improved

115 y of Q1178R for ATP(4-) and ATP(4-) augments diazoxide binding.

116 Atpenin also attenuated diazoxide-, but not pinacidil-induced vasodilation.

117 Similarly, with diazoxide, C-peptide concentrations were decreased (P =

118 K(ATP)) channel openers, e.g., minoxidil and diazoxide, can induce hair growth, their mechanisms requ

119 Diazoxide caused a twofold greater decrease in GABA leve

120 In the presence of KCl and diazoxide, cerulenin powerfully inhibited the augmentati

121 ion were also reversed by cyclosporine A and diazoxide, chemicals that regulate the pro- and anti-apo

122 ATP-sensitive K(+) channel agonist (opener) diazoxide, compared with placebo, results in higher plas

123 ocytes were unresponsive to the KATP agonist diazoxide, consistent with loss of KATP activity.

124 (m), in permeabilized myocytes revealed that diazoxide depolarized DeltaPsi(m) (by 12% at 10 micromol

125 In cultured cerebral endothelial cells, diazoxide depolarized the mitochondrial membrane, sugges

126 Glim on IP and on the protection afforded by diazoxide (Diaz), an opener of mitochondrial K(ATP) chan

127 nhibitor 5-hydroxydecanoate or the activator diazoxide did not affect dynamics of DeltaPsim.

128 Diazoxide did not alter cellular energetics, but rather

129 In contrast, diazoxide did not induce delayed preconditioning in isof

130 ive activator of expressed sK(ATP) channels, diazoxide did not open channels formed by Kir6.1/SUR2A,

131 Diazoxide did not reverse the glucagonostatic effect of

132 ation of ATP-sensitive potassium channels by diazoxide does not alter leptin inhibition of preproinsu

133 Data suggest diazoxide drives ROS generation by inducing a small mito

134 y was designed to investigate the effects of diazoxide (DZ) on mitochondrial structure, neurological

135 rted that attenuation of hyperinsulinemia by diazoxide (DZ), an inhibitor of glucose-mediated insulin

136 sitive potassium (KATP) channels by low-dose diazoxide (DZX) improves hypoglycemia-related complicati

137 the ATP-sensitive potassium channel opener, diazoxide (DZX) via an unknown mechanism.

138 patients, who were medically unresponsive to diazoxide (DZX), and nine of whom required a near-total

139 1); and pharmacological preconditioning with diazoxide (Dzx, 30 micromol/L) (22.1+/-2.7% versus 46.3+

140 mitochondrial membrane, suggesting a direct diazoxide effect on the endothelial mitochondria.

141 Treatment with diazoxide effectively blocked zinc secretion, as expecte

142 Diazoxide eliminated volume change due to mild hyposmoti

143 anesthetized with halothane, treatment with diazoxide exhibited a 35% reduction (48.3+/-3.0% to 31.3

144 Similar to diazoxide, exposure to 8-Br-cyclic GMP antagonized the P

145 Diazoxide failed to induce increased fluorescence of fla

146 By contrast, diazoxide failed to rescue any of the mutants.

147 Five minutes of diazoxide followed by a 30-minute washout still reduced

148 onditioned with 2 episodes of either NaCN or diazoxide followed by Tyrodes perfusion with membrane po

149 ic inhibition (induced by azide) plus a KCO (diazoxide for T1, pinacidil for T2).

150 The addition of glyburide inhibited diazoxide from increasing outflow facility.

151 y 5-hydroxydecanoate (5-HD) and activated by diazoxide has been implicated in ischaemic preconditioni

152 the potential for delayed preconditioning of diazoxide has not been examined.

153 The selective K(ATP) channel opener diazoxide hyperpolarized the RMP and attenuated neurotra

154 that the mitochondrial K-ATP channel opener diazoxide improves neurological function after spinal co

155 ement was reversed by subsequent exposure to diazoxide in a subpopulation of neurons.

156 Treatment with diazoxide in K(ir)6.2((-/-)) mice had no effect on IOP.

157 as well as for understanding of the role of diazoxide in preconditioning.

158 ty of NAC to block the protective effects of diazoxide in the perfused rat heart.

159 Hearts treated with diazoxide in the presence of 4 mmol/L NAC recovered 53%

160 Treatment with diazoxide in wild-type mice decreased IOP by 21.5 +/- 3.

161 croM pinacidil but only weakly by 100 microM diazoxide; in addition, they are blocked by 10 microM gl

162 In addition, diazoxide increased mitochondrial Ca(2+) in control cell

163 ure to the ATP-dependent K(+) channel opener diazoxide increases mitochondrial resistance to oxidativ

164 nsulin, 30 mm potassium chloride, or 0.25 mm diazoxide, indicating that insulin secretion and/or depo

165 rons revealed that the K(ATP) channel opener diazoxide induced an outward current that was antagonize

166 ents in adult rat myocytes demonstrated that diazoxide induced CsA-sensitive, low-conductance transie

167 Diazoxide induced moderate mitochondrial swelling and in

168 The maximum diazoxide-induced current was approximately twofold grea

169 However, MCC-134 inhibited diazoxide-induced flavoprotein oxidation in a dose-depen

170 In current clamp, estrogen enhanced the diazoxide-induced hyperpolarization to a similar degree.

171 The diazoxide-induced increase in ROS also was abrogated by

172 -Hydroxydecanoate was found to attenuate the diazoxide-induced increase in ROS generation.

173 ted in ischemic preconditioning, we examined diazoxide-induced ROS production in adult cardiomyocytes

174 induced vasodilation requires SUR2B, whereas diazoxide-induced vasodilation does not require SURs.

175 Rather, diazoxide-induced vasodilation involves ETCII inhibition

176 s 10% of that in SUR2(+/+) arteries, whereas diazoxide-induced vasodilation was similar in SUR2(+/+)

177 Ca2+ spark and KCa channel blockers reduced diazoxide-induced vasodilations by >60%, but did not alt

178 kinase C antagonist, given either to bracket diazoxide infusion or just before the index ischemia.

179 ), bracketing either 5-minute PC ischemia or diazoxide infusion, blocked protection (24+/-3 and 28+/-

180 ATP) channels, as the KATP channel activator diazoxide inhibited the effects of glucose and sucralose

181 rotein kinase C-dependent, the protection by diazoxide involves tyrosine kinase.

182 Rats were treated with 6, 20 or 40 mg/kg diazoxide ip for 3 days then exposed to global cerebral

183 IPC and diazoxide IPC-mimicking significantly enhanced mitochond

184 ed by 5-HD (36+/-3%, 33+/-2%, 37+/-2%; NaCN, diazoxide, IPC, respectively).

185 channel complexes to tolbutamide, MgADP and diazoxide is disturbed.

186 linemic hypoglycemia that is unresponsive to diazoxide is subtotal pancreatectomy.

187 Diazoxide is the prototypical opener of mitochondrial AT

188 The KATP channel opener diazoxide is used clinically to treat intractable hypogl

189 d glibenclamide (KATP channel blockers), and diazoxide (KATP channel opener).

190 sitive potassium (mitoK(ATP)) channel opener diazoxide markedly decreased the likelihood that cells w

191 nkage between diazoxide and ATP(4-) binding; diazoxide markedly increases the affinity of Q1178R for

192 We, therefore, conclude that diazoxide-mediated preconditioning against apoptosis inv

193 ection in infancy and is often responsive to diazoxide medical therapy, without the need for surgical

194 e ATP-sensitive K(+) (K(ATP)) channel opener diazoxide mimicked the effect of reduced glucose, while

195 ned hearts, whereas the KATP channel agonist diazoxide mimicked these effects in nonpreconditioned he

196 Glibenclamide abolishes and diazoxide mimics endothelial IPC in humans.

197 However, 5-hydroxydecanoate and diazoxide- mitochondrial K(ATP) channel modulators-did n

198 ice were treated with K(ATP) channel openers diazoxide (n = 10) and nicorandil (n = 10) for 14 days.

199 mia and reperfusion (1 hour) with or without diazoxide (n = 6 in each group) by clamping and releasin

200 and treated with the K(ATP) channel openers diazoxide, nicorandil, and P1075 or the K(ATP) channel c

201 Diazoxide not only decreased the number of cells undergo

202 ted the effects of mitoK(ATP) channel opener diazoxide on BBB functions during ischemia/reperfusion i

203 We also determined the direct effects of diazoxide on FAS in 3T3-L1 adipocytes.

204 ubunits, attenuated the inhibitory effect of diazoxide on I(CRAC)-mediated calcium influx and cell pr

205 The effect of diazoxide on IOP in anesthetized Brown Norway rats was m

206 As with diazoxide, only a subpopulation of sensory neurons were

207 icular myocytes, we found that pinacidil and diazoxide open mitoK(ATP) channels, but P-1075 does not.

208 y intra-arterial glibenclamide (blocker) and diazoxide (opener).

209 The cardioprotection afforded by diazoxide or by preconditioning was prevented by the mit

210 Blocking insulin secretion with diazoxide or insulin action with insulin receptor antibo

211 reduced in hearts preconditioned with NaCN, diazoxide or IPC (18+/-3%, 26+/-3%, 21+/-2%, respectivel

212 d (5-HD) prior to preconditioning with NaCN, diazoxide or IPC.

213 The combination of TAN-67 and diazoxide or isoflurane and diazoxide resulted in a mark

214 channels but severely impaired responses to diazoxide or MgADP.

215 hibited 30% by inhibitors of calcium influx (diazoxide or nimodipine), whereas a protein synthesis in

216 Treatment with the K(+)(ATP) channel openers diazoxide or pinacidil 48 h prior to lethal ischemia pro

217 e ATP-sensitive K(+) (K(ATP)) channel opener diazoxide or the l-type calcium channel blocker nifedipi

218 ced by high concentrations of tolbutamide or diazoxide, or disruption of K(ATP) channels (Sur1(-/-) m

219 was not seen in the presence of nifedipine, diazoxide, or tolbutamide or if K(ATP) channel knockout

220 morphological abnormalities were observed in diazoxide- or nicorandil-treated eyes.

221 1.4 versus 2.0+/-0.8 minutes, control versus diazoxide, P<0.05).

222 Bracketing diazoxide perfusion with N:-(2-mercaptopropionyl) glycin

223 tetraphenylphosphonium cation) and openers (diazoxide, pinacidil, chromakalim, minoxidil, testostero

224 the K(ATP) channel closer glybenclamide, 4) diazoxide plus the GABA(A) receptor agonist muscimol, or

225 is was decreased by approximately 50% in the diazoxide preconditioned hearts compared with control I/

226 tochondrial ATP-sensitive K+ channel opener, diazoxide, preconditions cells to subsequent injuries an

227 Diazoxide pretreatment also significantly inhibited the

228 We have found that diazoxide pretreatment inhibited etoposide-induced apopt

229 We have studied the effect of diazoxide pretreatment on mitochondrial morphology and f

230 administered either on the first day before diazoxide pretreatment or 10 minutes before I/R on the s

231 ation in the cortex was also decreased after diazoxide pretreatment.

232 Diazoxide prevented DeltaPsi depolarization in a concent

233 Diazoxide prevented endothelial dysfunction after IRI (P

234 activity strongly regulated Deltapsi(m), and diazoxide prevented MPT by inhibiting the driving force

235 tide or forskolin reversed the inhibition by diazoxide, probably through mobilization of intracellula

236 These findings support the concept that diazoxide produces delayed preconditioning via mitoK(ATP

237 rpose of this study was to determine whether diazoxide promotes delayed preconditioning following 90

238 mone T3 up-regulated mitoIK, ATP, conferring diazoxide protective effect on T3-treated hESC-VCMs.

239 preconditioning of cerebral endothelium with diazoxide protects the BBB against ischemic stress.

240 The effects of adenosine and diazoxide reflected mitochondrial K(ATP) channel activat

241 m dominant mutations of SUR1 associated with diazoxide-responsive disease.

242 t K(ATP) mutations have been associated with diazoxide-responsive disease.

243 ine SUR1 mutations associated with dominant, diazoxide-responsive hyperinsulinism.

244 al birth weight, late onset of hypoglycemia, diazoxide responsiveness, and protein-sensitive hypoglyc

245 Diazoxide resulted in a 37% increase in plasma levels of

246 on of TAN-67 and diazoxide or isoflurane and diazoxide resulted in a marked reduction in IS compared

247 idation in SUR2KO cells, indicating that the diazoxide-sensitive mitoK(ATP) channel activity was asso

248 the cell surface have normal ATP, MgADP, and diazoxide sensitivities, demonstrating that SUR1 harbori

249 Cells treated with 50 micromol/L diazoxide showed a 173% increase in ROS production relat

250 , we found that, similar to preconditioning, diazoxide significantly attenuated ischemia-induced intr

251 Since diazoxide significantly enhanced [3H]thymidine incorpora

252 In vivo, diazoxide significantly lowered IOP in Brown Norway rats

253 with pharmacological agents (tolbutamide and diazoxide) suggested a possible role for changes in thes

254 along with the effects of pretreatment with diazoxide, suggested that glucose signaling is mediated

255 RESULTS-As expected, diazoxide suppressed glucose infusion rates and increase

256 Diazoxide suppressed IS and tolbutamide antagonized the

257 Two of the three infants are still requiring diazoxide therapy at 8 and 18 months, whereas one of the

258 Diazoxide therapy often fails in the treatment of CHI an

259 rinsulinism, and all three patients required diazoxide therapy to maintain normoglycemia.

260 ATP) channels and potentiates the ability of diazoxide to open these channels.

261 bitor bongkrekic acid mimicked the effect of diazoxide to suppress priming, except that its effects w

262 tively normal responses to glucose, leucine, diazoxide, tolbutamide, and extracellular CaCl2 omission

263 and SUR1 subunits, which correlated with the diazoxide/tolbutamide sensitivity.

264 = 11) which was significantly attenuated in diazoxide-treated rats (575 +/- 99, n = 9; 582 +/- 104,

265 Diazoxide treatment was effective in child 3 but ineffec

266 ved elevation in cytosolic calcium following diazoxide treatment.

267 a was translocated to the mitochondria after diazoxide treatment.

268 avenger, blocked protection, indicating that diazoxide triggers protection through free radicals.

269 extrapancreatic KATP channel activation with diazoxide under fixed hormonal conditions failed to supp

270 ministration of the K(ATP) channel activator diazoxide under fixed hormonal conditions substantially

271 3-acetate mimicked the protective effects of diazoxide, unless 5-hydroxydecanoate was present, indica

272 In 15 families with diazoxide-unresponsive diffuse hyperinsulism, we found 1

273 nly one K(ATP) mutation might have dominant, diazoxide-unresponsive disease.

274 at some dominant mutations of SUR1 can cause diazoxide-unresponsive hyperinsulinism.

275 for the mutation, was diagnosed with severe diazoxide-unresponsive hypersinsulinism at 2 weeks of ag

276 and they demonstrate that responsiveness to diazoxide varies with genotype in glucokinase hyperinsul

277 examined whether the KATP channel-activator diazoxide was able to amplify the CRR to hypoglycemia in

278 The KATP channel activator diazoxide was administered in a randomized, placebo-cont

279 analysis revealed that the response to oral diazoxide was blunted in participants with E23K polymorp

280 Under these conditions, 500 microM diazoxide was found to induce an outward current that wa

281 The antiproliferative action of diazoxide was mimicked by removal of extracellular calci

282 The protection by diazoxide was not blocked by 5 micromol/L chelerythrine,

283 se concentrations in the presence of KCl and diazoxide, was markedly inhibited in betaGlud1(-/-) isle

284 olishing Ca(2+) oscillations with 200 microM diazoxide, we observed that oscillations in NAD(P)H pers

285 cerebrospinal fluid, and the effects of oral diazoxide were abolished by i.c.v. administration of the

286 These effects of diazoxide were blocked by the mitoK(ATP) channel antagon

287 Both IPC and its mimicking by diazoxide were completely attenuated by the mKATP channe

288 Similar treatments with diazoxide were performed on K(ir)6.2((-/-)) mice (n = 10

289 These cytoprotective effects of diazoxide were reproduced by pinacidil, another mitoK(AT

290 ion, but genistein blocked the protection by diazoxide when administered shortly before the index isc

291 SNAP also enhanced the oxidative effects of diazoxide when both agents were applied together.

292 pulation of sensory neurons was sensitive to diazoxide whereas other neurons were unaffected.

293 ide abolished the cardioprotective effect of diazoxide, whereas MCC-134 alone did not alter cell deat

294 highly sensitive to metabolic inhibition and diazoxide, whereas SUR2 channels are sensitive to pinaci

295 % at 15 mmol/l glucose) and was abolished by diazoxide, which demonstrates the operation of the ATP-s

296 The benzothiadiazine diazoxide, which depolarized respiration-dependent mitoc

297 ponses to magnesium adenosine diphosphate or diazoxide, while dominant KCNJ11 mutations impaired chan

298 Bracketing preischemic exposure to diazoxide with 50 micromol/L genistein, a tyrosine kinas

299 d the hypothesis that a KATP channel opener (diazoxide) would benefit volume homeostasis by limiting

300 by a reduction in KATP channel conductance (diazoxide: young 5.1 +/- 0.2 nS; aged 3.5 +/- 0.5 nS, P