ライフサイエンスコーパス: channel opener

1 chemia or pinacidil (ATP-sensitive potassium channel opener).

2 (KATP channel blockers), and diazoxide (KATP channel opener).

3 nd without diazoxide, a mitochondrial K(ATP) channel opener.

4 = 158%) was identified as the optimal maxi-K channel opener.

5 was mimicked by pinacidil, which is a K(ATP) channel opener.

6 micromol/L; n=6), an ATP-sensitive potassium channel opener.

7 own that retigabine acts as a KCNQ potassium channel opener.

8 blocks can be prevented by retigabine, a Kv7 channel opener.

9 Ca(2+) channels and was effective as a K(+) channel opener.

10 was relaxed by pinacidil, a selective K(ATP) channel opener.

11 2+) channels but was not effective as a K(+) channel opener.

12 sine triphosphate-sensitive potassium (KATP) channel opener.

13 ed as an orally bioavailable KCNQ2 potassium channel opener.

14 n banding, with tolerance improved by K(ATP) channel openers.

15 d adenosine triphosphate-sensitive potassium channel openers.

16 action with sulfonylurea drugs and potassium channel openers.

17 omycin mimicked the effects of the potassium channel openers.

18 hannels may mediate the protection from KATP channel openers.

19 PGI2 or PGF2, all of which are putative KATP channel openers.

20 rteries to synthetic ATP-sensitive K+ (KATP) channel openers.

21 , resulting in a diminished response to KATP channel openers.

22 ccount in considering the pharmacology of K+ channel openers.

23 ho substituent retain activity as maxi-K ion channel openers.

24 of the mutant channels were rescued by KATP channel openers.

25 e presence of either valinomycin or the K(+) channel opener 1-EBIO.

26 f a novel iodinated 1,4-dihydropyridine KATP channel opener, [125I]A-312110 [(9R)-9-(4-fluoro-3-125io

27 es, yielded non-antiandrogen, KATP potassium channel openers (39, 41, and 64, respectively) that are

28 The K(ATP) channel openers, adenosine and levcromakalim, decreased

29 However, diazoxide (a K(+)-ATP channel opener) administered 1 h before FBS addition res

30 channel, however, remained sensitive to both channel opener and inhibitor, which indicated that Cys(1

31 h different ATP-sensitive potassium (K(ATP)) channel openers and blockers have implicated opening of

32 dings on the lack of specificity for several channel openers and blockers have questioned the actual

33 l arteries decreased the sensitivity to KATP channel openers and depolarized and constricted control

34 e agents were glyburide-reversible potassium channel openers and hyperpolarized human bladder cells a

35 he in vitro effects of established potassium channel openers and inhibitors (tolbutamide and glibencl

36 s required for KATP channel activation by K+ channel openers and nucleotides.

37 e the effects of ZD6169, an ATP-sensitive K+-channel opener, and capsaicin, an afferent neurotoxin, o

38 ically modulated by two drugs: ML297, a GIRK channel opener, and Tertiapin-Q (TQ), a GIRK channel blo

39 ected by ischemic preconditioning and K(ATP) channel openers, and it has been suggested that mitoK(AT

40 ith adenosine (200 mumol/L) or the potassium channel opener aprikalim (100 mumol/L), respectively.

41 Selective potassium channel openers are likely to represent novel therapies

42 ATP-sensitive K+ (KATP) channel openers are vasodilators that activate both plas

43 ded these results and showed that other K(+) channel openers as well as the K(+) ionophore valinomyci

44 Administration of three distinct M-channel openers at 0-6 h after ischemic injury significa

45 BK activity by chemical NS1619 or BMS191011 channel openers attenuated kidney fibrosis in these two

46 vasopressor effects to BAY K 8644, a calcium-channel opener, attenuated significantly vasodilator res

47 Coexposure to the calcium channel opener BayK, or the group I metabotropic glutama

48 ntiated (29-32%) by incubation with the Ca2+ channel opener BAYK8644 (1-10 microm).

49 The K(ATP) channel opener bimakalim (1 micromol/L) increased postis

50 by the mitochondrial ATP-sensitive potassium channel opener BMS-191095.

51 rats were pretreated with pinacidil (K+(ATP)channel opener), bradykinin, methacholine, or morphine b

52 inje system that was prevented with a K(ATP) channel opener but not a calcium channel blocker and the

53 (10 micromol/L), an ATP-sensitive potassium channel opener, caused a significant (P<0.001) shortenin

54 K+ channel openers completely reversed ATP inhibition of K+

55 sphate and dipeptide derivatives of the KATP channel opener cromakalim and evaluated their IOP loweri

56 re to the K+ ionophore valinomycin or the K+-channel opener cromakalim induced apoptosis.

57 ists glibenclamide and U-37883A and the KATP channel opener cromakalim suggested that venular, unlike

58 side or the ATP-sensitive potassium (K(ATP)) channel opener cromakalim.

59 GTP (K1/2 = 232 microM) as well as by the K+ channel openers cromakalim (20 microM) and diazoxide (10

60 The potassium channel openers cromakalim and BMS-180448 were competiti

61 are not antagonized by the ATP-sensitive K+ channel openers cromakalim, pinacidil, or diazoxide.

62 At all stages of Ca2+ uptake, the potassium channel openers depolarized the mitochondrial membrane t

63 The mitoKATP channel opener diazoxide (100 micromol/L) partially oxid

64 model of simulated ischemia, the mitoK(ATP) channel opener diazoxide (100 micromol/L), but not P-107

65 Importantly, combination of the KATP channel opener diazoxide and carbamazepine led to enhanc

66 The mitoK(ATP) channel opener diazoxide attenuated the accumulation of

67 The selective K(ATP) channel opener diazoxide hyperpolarized the RMP and atte

68 the first time that the mitochondrial K-ATP channel opener diazoxide improves neurological function

69 ioning or exposure to the ATP-dependent K(+) channel opener diazoxide increases mitochondrial resista

70 rotein-GnRH neurons revealed that the K(ATP) channel opener diazoxide induced an outward current that

71 The KATP channel opener diazoxide is used clinically to treat int

72 ondrial ATP-sensitive potassium (mitoK(ATP)) channel opener diazoxide markedly decreased the likeliho

73 rfusion with the ATP-sensitive K(+) (K(ATP)) channel opener diazoxide mimicked the effect of reduced

74 We investigated the effects of mitoK(ATP) channel opener diazoxide on BBB functions during ischemi

75 Kir6.1 currents were unaffected by the K+ channel opener diazoxide or by dialysis with 0.3 mM ATPi

76 The ATP-sensitive K(+) (K(ATP)) channel opener diazoxide or the l-type calcium channel b

77 Application of the K(ATP) channel opener diazoxide or the ob gene product leptin m

78 njection of either 1) vehicle, 2) the K(ATP) channel opener diazoxide, 3) the K(ATP) channel closer g

79 Neither MgADP, nor the K+ channel opener diazoxide, enhanced Kir6.2/SUR1bDelta33,

80 inism (CHI) cases unresponsive to the K(ATP) channel opener diazoxide, the mainstay medical therapy f

81 ureas, which stimulate secretion, and the K+ channel opener diazoxide, which inhibits insulin release

82 or carbamazepine was facilitated by the KATP channel opener diazoxide.

83 ried response to activation by the potassium channel opener diazoxide.

84 ation was observed, however, with the K(ATP) channel opener diazoxide.

85 ould be effectively mimicked using the mKATP channel opener diazoxide.

86 fectively mimicked by injection of the mKATP channel opener diazoxide.

87 and 0.6T) solutions with or without the KATP channel opener diazoxide.

88 d-type C57BL/6 mice were treated with K(ATP) channel openers diazoxide (n = 10) and nicorandil (n = 1

89 K(ATP) channel openers diazoxide and nicorandil are effective r

90 Treatment with the K(+)(ATP) channel openers diazoxide or pinacidil 48 h prior to let

91 on organ culture and treated with the K(ATP) channel openers diazoxide, nicorandil, and P1075 or the

92 erence ATP-sensitive potassium channel (KATP channel) openers diazoxide and 7-chloro-3-isopropylamino

93 we clamped membrane potential with the KATP channel-opener diazoxide and KCl to fix Ca(2+) at an ele

94 The K(+) channels opener diazoxide (200-500 microM) increased cha

95 s study evaluated the hypothesis that a KATP channel opener (diazoxide) would benefit volume homeosta

96 well times; and (4) the SUR activator ("KATP channel opener"), diazoxide, activated the NCCa-ATP chan

97 The mitoK(ATP) channel opener, diazoxide (50 microM), caused a similar

98 is prevented by the ATP-sensitive potassium channel opener, diazoxide (DZX) via an unknown mechanism

99 ells with the mitochondrial ATP-sensitive K+ channel opener, diazoxide, preconditions cells to subseq

100 or, sodium cyanide (NaCN), or the mitoK(ATP) channel opener, diazoxide.

101 n the N terminus of Kir6.2 and SUR1, whereas channel openers did not, suggesting the inhibitors enhan

102 Application of a K(ATP) channel opener drug improved survival in the endotoxic W

103 ls, ZF channels are insensitive to potassium channel opener drugs (pinacidil, minoxidil) in both cham

104 rafish channels are insensitive to potassium channel opener drugs (pinacidil, minoxidil) in both cham

105 endowing sensitivity to sulphonylurea and K+ channel opener drugs, and the potentiatory action of MgA

106 Although ATP-sensitive potassium (K(ATP)) channel openers, e.g., minoxidil and diazoxide, can indu

107 phagocytic vacuole, whereas NS1619, a BK(Ca) channel opener, enhanced both.

108 Kv7 (KCNQ) potassium channel openers (enhancers) decrease neuropathic pain in

109 Potassium channel openers exhibited a rank order of potency of P10

110 rrent study assessed the effects of the KCNQ channel opener ezogabine (also known as retigabine) on r

111 nerated force in response to KCl, the L-type channel opener FPL64176, or the SMC agonists 5-HT and ET

112 ATP-sensitive potassium (KATP) channel openers have emerged as potential therapeutics f

113 (ATP) channel inhibitor and a surface K(ATP) channel opener in native cardiac cells.

114 of depression, we report that KCNQ-type K(+) channel openers, including FDA-approved drug retigabine

115 K(ATP) channel openers increased outflow facility in human ante

116 ent addition of arachidonic acid (10 mum), a channel opener, increased the open probability of methio

117 ERP shortening by an ATP-sensitive potassium channel opener increases ventricular vulnerability to re

118 e authors sought to determine whether K(ATP) channel openers influence outflow facility in human ante

119 5'-triphosphate-sensitive potassium (K(ATP)) channel openers is described.

120 njury by ischemic preconditioning and K(ATP) channel openers is known to involve the mitochondrial AT

121 Binding of channel openers is reported to require ATP hydrolysis, b

122 f 2 to the synthesis of ABT-598, a potassium channel opener, is demonstrated.

123 c potential of the SUR-1-selective potassium channel opener (KCO), NN414, to amplify counterregulator

124 eptor for the cardioprotective effects of K+ channel openers (KCO) and for the blocking of cardioprot

125 e metabolic sensors and targets of potassium channel openers (KCO; e.g., diazoxide and pinacidil).

126 ihypertensive ATP-sensitive potassium (KATP) channel openers (KCOs) activate plasma membrane KATP cha

127 I]A-312110 by structurally diverse potassium channel openers (KCOs) indicated a similar rank order of

128 A novel series of benzylamine, potassium channel openers (KCOs) is presented as part of our progr

129 ) smooth muscle cell K(ATP) channels to K(+) channel openers (KCOs) is the basis for the selective pr

130 Potassium channel openers (KCOs) such as diazoxide and levochromak

131 entifying novel, bladder-selective potassium channel openers (KCOs) targeted for urge urinary inconti

132 (K(ATP) channels) are the target for K(ATP)-channel openers (KCOs), such as pinacidil and P1075.

133 to nucleotides, sulfonylureas, and potassium channel openers, KCOs.

134 induces opening of mitoKATP similar to KATP channel openers like diazoxide and cromakalim in heart,

135 Our data suggest that K(+) channel openers may be capable of abbreviating the long

136 overy of botanical KCNQ5-selective potassium channel openers may enable future targeted therapies for

137 ts the concept that bladder-selective K(ATP) channel openers may have utility in the treatment of ove

138 KCNQ channel openers merit further study as potential treatme

139 K(ATP) channel openers (minoxidil, cromakalim, and pinacidil) i

140 or adjunctive therapy with adenosine, K(ATP) channel openers, Na(+)/H(+) exchange inhibitors, and hyp

141 SMCs that was absent in ECs, and the BK(Ca) channel opener NS 1619 only enhanced K(+) current in the

142 the channel was stimulated by the potassium channel opener NS11021 and inhibited by hemin and paxill

143 Addition of the BK channel opener NS11021 directly activated channels in co

144 line inhibited the oscillations, whereas the channel opener NS11021 increased the rate of these oscil

145 BK channel-mediated unitary currents, the BK channel opener NS1619 attenuated the effects of METH on

146 ereas the activation of BK channels with the channel opener NS1619 reversibly attenuated the mean amp

147 s in the response to charybdotoxin or the BK channel opener NS1619 were observed.

148 We here examined the action of potassium channel openers on mitochondrial Ca2+ homeostasis, as th

149 we investigated the protective effects of M-channel openers on stroke-induced brain injury in mouse

150 We also compared the potencies of these K+ channel openers on the plasma membrane KATP channel puri

151 f oral administration of ZD6169, a potassium channel opener, on neurally mediated plasma extravasatio

152 y examines the effects of nicorandil, a K(+) channel opener, on transmural dispersion of repolarizati

153 Intracellular application of selective SK-channel openers or a genetic reintroduction of an N-term

154 BK channel openers or BK channel gene transfer could be an

155 ure to pinacidil (2 to 5 micromol/L), a K(+) channel opener, or the combination of a Na(+) channel bl

156 current in control of neuronal discharge, M channel openers, or blockers, reduced or augmented the e

157 e utilized for drug development aimed at ion channel opener- or inhibitor-function.

158 (ATP) channel blocker HMR1098 and the K(ATP) channel opener P-1075 on surfaceK(ATP) and mitoK(ATP) ch

159 tion of retigabine, a recently marketed KV 7 channel opener, partially reversed these effects for the

160 d activation of KATP channels by a potassium channel opener (PCO) would attenuate alterations in ioni

161 t adenosine triphosphate-sensitive potassium channel opener (PCO)-induced hyperpolarized arrest with

162 te-sensitive potassium channels by potassium channel openers (PCO) within the myocyte appears to conf

163 boratory has demonstrated that the potassium channel openers (PCOs) aprikalim and pinacidil are effec

164 Pretreatment with potassium channel openers (PCOs) has been shown to provide protect

165 KATP) and represent a new class of potassium channel openers (PCOs).

166 In these cells, the potassium channel opener pinacidil (10 micromol/L) did not prevent

167 The study was repeated with the K(ATP) channel opener pinacidil (n=6) and the calcium channel b

168 odilation of coronary arterioles to the KATP-channel opener pinacidil and to the endothelium-independ

169 native sarcKATP channels preactivated by the channel opener pinacidil in rabbit ventricular myocytes,

170 st, when given only at reperfusion, the K(+) channel opener pinacidil or the antioxidants 2-mercaptop

171 on, the effective concentration for the KATP channel opener pinacidil was 10-fold higher.

172 the hyperpolarizing ATP-sensitive potassium channel opener pinacidil, the protein kinase C activator

173 ) inhibited KATP current activated by the K+ channel opener pinacidil.

174 2+) channel blocker nisoldipine and the K(+) channel opener pinacidil.

175 dependent vasorelaxation induced by the KATP channel opener pinacidil.

176 e and on vasodilations to the synthetic KATP channel openers pinacidil and levcromakalim.

177 eptides, we found that the effects of K(ATP) channel openers, PKG, or valinomycin were mediated by a

178 K(ATP) channel openers prevent detrimental myocyte swelling and

179 Thus, potassium channel openers prevent mitochondrial Ca2+ overload by r

180 sulfonylurea receptor 1 (SUR1)selective KATP-channel opener, prevented DA modulation by H2O2, glutama

181 her both metabolic inhibition and mitoK(ATP) channel openers protect both the whole organ and isolate

182 sensitive to the family of drugs known as K+ channel openers, raising the question whether mitochondr

183 re to 10 micromol/L diazoxide, a mito K(ATP) channel opener, reduced infarction to 3+/-1% and 8+/-1%,

184 These data indicate that KATP channel openers regulate arterial diameter via SUR-depen

185 signaling in distinct ways and that the KCNQ channel opener retigabine exerts rescuing effects.

186 In contrast, the Kv7 channel opener retigabine increased I(M) amplitude and I

187 g the KCNQ channel blocker XE991 or the KCNQ channel opener retigabine reverses the effects on consol

188 in the presence or absence of the specific M-channel opener retigabine, or agonists of bradykinin B2

189 lease was prevented by incubation with the M-channel opener retigabine.

190 emogenetically or by local infusion of the M-channel opener, retigabine.

191 modipine, and increased by the L-type Ca(2+) channel opener, S(-)-Bay K 8644.

192 Our results show that diazoxide, a KATP channel opener, selectively activates mitochondrial KATP

193 LNNA had little effect on the apparent KATP channel opener sensitivity, the membrane potential, and

194 Intrathecal injection of pinacidil, a KATP channel opener, significantly increased the tactile with

195 In the cell, channel openers stabilized posthydrolytic states promoti

196 trix volume with a range of ATP-sensitive K+ channel openers such as diazoxide.

197 Although KCNQ channel openers, such as retigabine, have emerged as ant

198 By contrast, diazoxide, a potassium channel opener that also binds SUR1, had no effect on su

199 Retigabine, an M-channel opener that does not open receptor-suppressed M-

200 nd 25 mumol/L pinacidil, and ATP-sensitive K channel opener that provides metabolic protection to the

201 elected caffeic acid derivatives as novel K+ channel openers that activate TREK-1 background K+ chann

202 When activated by K(ATP) channel openers, these channels increase outflow facilit

203 ffective CF therapies may require the use of channel openers to activate mutant CFTR channels at the

204 sted the efficacy of retigabine, a potassium channel opener, to suppress the loss of force induced by

205 However, the Na+ channel opener veratridine (10 and 50 microM) significan

206 ncreased energy utilization (addition of Na+ channel opener, veratridine, or ionophores, monensin and

207 lar Ca2+ loading irrespective of whether the channel opener was applied throughout the duration of hy

208 Dilation to NS1619 (KCa channel opener) was reduced in endothelial denuded arter

209 t evoked by pinacidil (100 microM), a K(ATP) channel opener, was significantly higher in E2-treated c

210 n response to levcromakalim (LEVC), a K(ATP) channel opener, was significantly shifted to the left in

211 Adenosine receptor agonists and a KATP channel opener were used to achieve early preconditionin

212 nvestigated by using adenosine and potassium-channel openers (which are thought to induce hyperpolari

213 pyrithione (ZnPy) is a newly identified KCNQ channel opener, which potently activates KCNQ2, KCNQ4, a

214 KATP channel openers, which bind to SUR, promoted ATPase acti

215 2, the prototype of a novel series of K(ATP) channel openers with unique selectivity for bladder smoo

216 the efficacy of flupirtine, a selective KCNQ channel opener, with phenobarbital and diazepam, two dru

217 channels, inhibited the effects of potassium channel openers, without preventing the action of valino

218 ine, Levetiracetam, and of a novel potassium channel opener (XEN1101) in two groups of healthy volunt