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1 (KATP channel blockers), and diazoxide (KATP channel opener).
2 nd without diazoxide, a mitochondrial K(ATP) channel opener.
3 = 158%) was identified as the optimal maxi-K channel opener.
4 was mimicked by pinacidil, which is a K(ATP) channel opener.
5 micromol/L; n=6), an ATP-sensitive potassium channel opener.
6 own that retigabine acts as a KCNQ potassium channel opener.
7 blocks can be prevented by retigabine, a Kv7 channel opener.
8  Ca(2+) channels and was effective as a K(+) channel opener.
9 was relaxed by pinacidil, a selective K(ATP) channel opener.
10 2+) channels but was not effective as a K(+) channel opener.
11 sine triphosphate-sensitive potassium (KATP) channel opener.
12 ed as an orally bioavailable KCNQ2 potassium channel opener.
13 n banding, with tolerance improved by K(ATP) channel openers.
14 d adenosine triphosphate-sensitive potassium channel openers.
15 action with sulfonylurea drugs and potassium channel openers.
16 omycin mimicked the effects of the potassium channel openers.
17 hannels may mediate the protection from KATP channel openers.
18 PGI2 or PGF2, all of which are putative KATP channel openers.
19 rteries to synthetic ATP-sensitive K+ (KATP) channel openers.
20 , resulting in a diminished response to KATP channel openers.
21 ccount in considering the pharmacology of K+ channel openers.
22  of the mutant channels were rescued by KATP channel openers.
23 ho substituent retain activity as maxi-K ion channel openers.
24 e presence of either valinomycin or the K(+) channel opener 1-EBIO.
25 f a novel iodinated 1,4-dihydropyridine KATP channel opener, [125I]A-312110 [(9R)-9-(4-fluoro-3-125io
26 es, yielded non-antiandrogen, KATP potassium channel openers (39, 41, and 64, respectively) that are
27                                   The K(ATP) channel openers, adenosine and levcromakalim, decreased
28               However, diazoxide (a K(+)-ATP channel opener) administered 1 h before FBS addition res
29 channel, however, remained sensitive to both channel opener and inhibitor, which indicated that Cys(1
30 h different ATP-sensitive potassium (K(ATP)) channel openers and blockers have implicated opening of
31 dings on the lack of specificity for several channel openers and blockers have questioned the actual
32 l arteries decreased the sensitivity to KATP channel openers and depolarized and constricted control
33 e agents were glyburide-reversible potassium channel openers and hyperpolarized human bladder cells a
34 he in vitro effects of established potassium channel openers and inhibitors (tolbutamide and glibencl
35 s required for KATP channel activation by K+ channel openers and nucleotides.
36 e the effects of ZD6169, an ATP-sensitive K+-channel opener, and capsaicin, an afferent neurotoxin, o
37 ected by ischemic preconditioning and K(ATP) channel openers, and it has been suggested that mitoK(AT
38 ith adenosine (200 mumol/L) or the potassium channel opener aprikalim (100 mumol/L), respectively.
39                          Selective potassium channel openers are likely to represent novel therapies
40                      ATP-sensitive K+ (KATP) channel openers are vasodilators that activate both plas
41 ded these results and showed that other K(+) channel openers as well as the K(+) ionophore valinomyci
42           Administration of three distinct M-channel openers at 0-6 h after ischemic injury significa
43 vasopressor effects to BAY K 8644, a calcium-channel opener, attenuated significantly vasodilator res
44                    Coexposure to the calcium channel opener BayK, or the group I metabotropic glutama
45 ntiated (29-32%) by incubation with the Ca2+ channel opener BAYK8644 (1-10 microm).
46                                   The K(ATP) channel opener bimakalim (1 micromol/L) increased postis
47 by the mitochondrial ATP-sensitive potassium channel opener BMS-191095.
48  rats were pretreated with pinacidil (K+(ATP)channel opener), bradykinin, methacholine, or morphine b
49 inje system that was prevented with a K(ATP) channel opener but not a calcium channel blocker and the
50  (10 micromol/L), an ATP-sensitive potassium channel opener, caused a significant (P<0.001) shortenin
51                                           K+ channel openers completely reversed ATP inhibition of K+
52 sphate and dipeptide derivatives of the KATP channel opener cromakalim and evaluated their IOP loweri
53 re to the K+ ionophore valinomycin or the K+-channel opener cromakalim induced apoptosis.
54 ists glibenclamide and U-37883A and the KATP channel opener cromakalim suggested that venular, unlike
55 side or the ATP-sensitive potassium (K(ATP)) channel opener cromakalim.
56 GTP (K1/2 = 232 microM) as well as by the K+ channel openers cromakalim (20 microM) and diazoxide (10
57                                The potassium channel openers cromakalim and BMS-180448 were competiti
58  are not antagonized by the ATP-sensitive K+ channel openers cromakalim, pinacidil, or diazoxide.
59  At all stages of Ca2+ uptake, the potassium channel openers depolarized the mitochondrial membrane t
60                                 The mitoKATP channel opener diazoxide (100 micromol/L) partially oxid
61  model of simulated ischemia, the mitoK(ATP) channel opener diazoxide (100 micromol/L), but not P-107
62         Importantly, combination of the KATP channel opener diazoxide and carbamazepine led to enhanc
63                               The mitoK(ATP) channel opener diazoxide attenuated the accumulation of
64                         The selective K(ATP) channel opener diazoxide hyperpolarized the RMP and atte
65  the first time that the mitochondrial K-ATP channel opener diazoxide improves neurological function
66 ioning or exposure to the ATP-dependent K(+) channel opener diazoxide increases mitochondrial resista
67 rotein-GnRH neurons revealed that the K(ATP) channel opener diazoxide induced an outward current that
68                                     The KATP channel opener diazoxide is used clinically to treat int
69 ondrial ATP-sensitive potassium (mitoK(ATP)) channel opener diazoxide markedly decreased the likeliho
70 rfusion with the ATP-sensitive K(+) (K(ATP)) channel opener diazoxide mimicked the effect of reduced
71    We investigated the effects of mitoK(ATP) channel opener diazoxide on BBB functions during ischemi
72    Kir6.1 currents were unaffected by the K+ channel opener diazoxide or by dialysis with 0.3 mM ATPi
73              The ATP-sensitive K(+) (K(ATP)) channel opener diazoxide or the l-type calcium channel b
74                    Application of the K(ATP) channel opener diazoxide or the ob gene product leptin m
75 njection of either 1) vehicle, 2) the K(ATP) channel opener diazoxide, 3) the K(ATP) channel closer g
76                    Neither MgADP, nor the K+ channel opener diazoxide, enhanced Kir6.2/SUR1bDelta33,
77 ureas, which stimulate secretion, and the K+ channel opener diazoxide, which inhibits insulin release
78 ried response to activation by the potassium channel opener diazoxide.
79 ation was observed, however, with the K(ATP) channel opener diazoxide.
80 ould be effectively mimicked using the mKATP channel opener diazoxide.
81 fectively mimicked by injection of the mKATP channel opener diazoxide.
82 or carbamazepine was facilitated by the KATP channel opener diazoxide.
83 and 0.6T) solutions with or without the KATP channel opener diazoxide.
84 d-type C57BL/6 mice were treated with K(ATP) channel openers diazoxide (n = 10) and nicorandil (n = 1
85                                       K(ATP) channel openers diazoxide and nicorandil are effective r
86                 Treatment with the K(+)(ATP) channel openers diazoxide or pinacidil 48 h prior to let
87 on organ culture and treated with the K(ATP) channel openers diazoxide, nicorandil, and P1075 or the
88 erence ATP-sensitive potassium channel (KATP channel) openers diazoxide and 7-chloro-3-isopropylamino
89  we clamped membrane potential with the KATP channel-opener diazoxide and KCl to fix Ca(2+) at an ele
90                                     The K(+) channels opener diazoxide (200-500 microM) increased cha
91 s study evaluated the hypothesis that a KATP channel opener (diazoxide) would benefit volume homeosta
92 well times; and (4) the SUR activator ("KATP channel opener"), diazoxide, activated the NCCa-ATP chan
93                               The mitoK(ATP) channel opener, diazoxide (50 microM), caused a similar
94  is prevented by the ATP-sensitive potassium channel opener, diazoxide (DZX) via an unknown mechanism
95 ells with the mitochondrial ATP-sensitive K+ channel opener, diazoxide, preconditions cells to subseq
96 or, sodium cyanide (NaCN), or the mitoK(ATP) channel opener, diazoxide.
97 n the N terminus of Kir6.2 and SUR1, whereas channel openers did not, suggesting the inhibitors enhan
98                      Application of a K(ATP) channel opener drug improved survival in the endotoxic W
99 endowing sensitivity to sulphonylurea and K+ channel opener drugs, and the potentiatory action of MgA
100    Although ATP-sensitive potassium (K(ATP)) channel openers, e.g., minoxidil and diazoxide, can indu
101 phagocytic vacuole, whereas NS1619, a BK(Ca) channel opener, enhanced both.
102                         Kv7 (KCNQ) potassium channel openers (enhancers) decrease neuropathic pain in
103                                    Potassium channel openers exhibited a rank order of potency of P10
104 nerated force in response to KCl, the L-type channel opener FPL64176, or the SMC agonists 5-HT and ET
105               ATP-sensitive potassium (KATP) channel openers have emerged as potential therapeutics f
106 (ATP) channel inhibitor and a surface K(ATP) channel opener in native cardiac cells.
107 of depression, we report that KCNQ-type K(+) channel openers, including FDA-approved drug retigabine
108                                       K(ATP) channel openers increased outflow facility in human ante
109 ent addition of arachidonic acid (10 mum), a channel opener, increased the open probability of methio
110 ERP shortening by an ATP-sensitive potassium channel opener increases ventricular vulnerability to re
111 e authors sought to determine whether K(ATP) channel openers influence outflow facility in human ante
112 5'-triphosphate-sensitive potassium (K(ATP)) channel openers is described.
113 njury by ischemic preconditioning and K(ATP) channel openers is known to involve the mitochondrial AT
114                                   Binding of channel openers is reported to require ATP hydrolysis, b
115 f 2 to the synthesis of ABT-598, a potassium channel opener, is demonstrated.
116 c potential of the SUR-1-selective potassium channel opener (KCO), NN414, to amplify counterregulator
117 eptor for the cardioprotective effects of K+ channel openers (KCO) and for the blocking of cardioprot
118 e metabolic sensors and targets of potassium channel openers (KCO; e.g., diazoxide and pinacidil).
119 ihypertensive ATP-sensitive potassium (KATP) channel openers (KCOs) activate plasma membrane KATP cha
120 I]A-312110 by structurally diverse potassium channel openers (KCOs) indicated a similar rank order of
121     A novel series of benzylamine, potassium channel openers (KCOs) is presented as part of our progr
122 ) smooth muscle cell K(ATP) channels to K(+) channel openers (KCOs) is the basis for the selective pr
123                                    Potassium channel openers (KCOs) such as diazoxide and levochromak
124 entifying novel, bladder-selective potassium channel openers (KCOs) targeted for urge urinary inconti
125  (K(ATP) channels) are the target for K(ATP)-channel openers (KCOs), such as pinacidil and P1075.
126 to nucleotides, sulfonylureas, and potassium channel openers, KCOs.
127  induces opening of mitoKATP similar to KATP channel openers like diazoxide and cromakalim in heart,
128                   Our data suggest that K(+) channel openers may be capable of abbreviating the long
129 ts the concept that bladder-selective K(ATP) channel openers may have utility in the treatment of ove
130                                         KCNQ channel openers merit further study as potential treatme
131                                       K(ATP) channel openers (minoxidil, cromakalim, and pinacidil) i
132 or adjunctive therapy with adenosine, K(ATP) channel openers, Na(+)/H(+) exchange inhibitors, and hyp
133  SMCs that was absent in ECs, and the BK(Ca) channel opener NS 1619 only enhanced K(+) current in the
134                           Addition of the BK channel opener NS11021 directly activated channels in co
135 line inhibited the oscillations, whereas the channel opener NS11021 increased the rate of these oscil
136 BK channel-mediated unitary currents, the BK channel opener NS1619 attenuated the effects of METH on
137 ereas the activation of BK channels with the channel opener NS1619 reversibly attenuated the mean amp
138 s in the response to charybdotoxin or the BK channel opener NS1619 were observed.
139     We here examined the action of potassium channel openers on mitochondrial Ca2+ homeostasis, as th
140  we investigated the protective effects of M-channel openers on stroke-induced brain injury in mouse
141   We also compared the potencies of these K+ channel openers on the plasma membrane KATP channel puri
142 f oral administration of ZD6169, a potassium channel opener, on neurally mediated plasma extravasatio
143 y examines the effects of nicorandil, a K(+) channel opener, on transmural dispersion of repolarizati
144                                           BK channel openers or BK channel gene transfer could be an
145 ure to pinacidil (2 to 5 micromol/L), a K(+) channel opener, or the combination of a Na(+) channel bl
146  current in control of neuronal discharge, M channel openers, or blockers, reduced or augmented the e
147 e utilized for drug development aimed at ion channel opener- or inhibitor-function.
148 (ATP) channel blocker HMR1098 and the K(ATP) channel opener P-1075 on surfaceK(ATP) and mitoK(ATP) ch
149 tion of retigabine, a recently marketed KV 7 channel opener, partially reversed these effects for the
150 d activation of KATP channels by a potassium channel opener (PCO) would attenuate alterations in ioni
151 t adenosine triphosphate-sensitive potassium channel opener (PCO)-induced hyperpolarized arrest with
152 te-sensitive potassium channels by potassium channel openers (PCO) within the myocyte appears to conf
153 boratory has demonstrated that the potassium channel openers (PCOs) aprikalim and pinacidil are effec
154                  Pretreatment with potassium channel openers (PCOs) has been shown to provide protect
155 KATP) and represent a new class of potassium channel openers (PCOs).
156                In these cells, the potassium channel opener pinacidil (10 micromol/L) did not prevent
157       The study was repeated with the K(ATP) channel opener pinacidil (n=6) and the calcium channel b
158 odilation of coronary arterioles to the KATP-channel opener pinacidil and to the endothelium-independ
159 native sarcKATP channels preactivated by the channel opener pinacidil in rabbit ventricular myocytes,
160 st, when given only at reperfusion, the K(+) channel opener pinacidil or the antioxidants 2-mercaptop
161  the hyperpolarizing ATP-sensitive potassium channel opener pinacidil, the protein kinase C activator
162 ) inhibited KATP current activated by the K+ channel opener pinacidil.
163 2+) channel blocker nisoldipine and the K(+) channel opener pinacidil.
164 dependent vasorelaxation induced by the KATP channel opener pinacidil.
165 e and on vasodilations to the synthetic KATP channel openers pinacidil and levcromakalim.
166 eptides, we found that the effects of K(ATP) channel openers, PKG, or valinomycin were mediated by a
167                                       K(ATP) channel openers prevent detrimental myocyte swelling and
168                              Thus, potassium channel openers prevent mitochondrial Ca2+ overload by r
169 sulfonylurea receptor 1 (SUR1)selective KATP-channel opener, prevented DA modulation by H2O2, glutama
170 her both metabolic inhibition and mitoK(ATP) channel openers protect both the whole organ and isolate
171 sensitive to the family of drugs known as K+ channel openers, raising the question whether mitochondr
172 re to 10 micromol/L diazoxide, a mito K(ATP) channel opener, reduced infarction to 3+/-1% and 8+/-1%,
173                These data indicate that KATP channel openers regulate arterial diameter via SUR-depen
174                         In contrast, the Kv7 channel opener retigabine increased I(M) amplitude and I
175 g the KCNQ channel blocker XE991 or the KCNQ channel opener retigabine reverses the effects on consol
176 in the presence or absence of the specific M-channel opener retigabine, or agonists of bradykinin B2
177 lease was prevented by incubation with the M-channel opener retigabine.
178 emogenetically or by local infusion of the M-channel opener, retigabine.
179 modipine, and increased by the L-type Ca(2+) channel opener, S(-)-Bay K 8644.
180      Our results show that diazoxide, a KATP channel opener, selectively activates mitochondrial KATP
181  LNNA had little effect on the apparent KATP channel opener sensitivity, the membrane potential, and
182   Intrathecal injection of pinacidil, a KATP channel opener, significantly increased the tactile with
183                                 In the cell, channel openers stabilized posthydrolytic states promoti
184 trix volume with a range of ATP-sensitive K+ channel openers such as diazoxide.
185                                Although KCNQ channel openers, such as retigabine, have emerged as ant
186          By contrast, diazoxide, a potassium channel opener that also binds SUR1, had no effect on su
187                             Retigabine, an M-channel opener that does not open receptor-suppressed M-
188 nd 25 mumol/L pinacidil, and ATP-sensitive K channel opener that provides metabolic protection to the
189 elected caffeic acid derivatives as novel K+ channel openers that activate TREK-1 background K+ chann
190                     When activated by K(ATP) channel openers, these channels increase outflow facilit
191 ffective CF therapies may require the use of channel openers to activate mutant CFTR channels at the
192                             However, the Na+ channel opener veratridine (10 and 50 microM) significan
193 ncreased energy utilization (addition of Na+ channel opener, veratridine, or ionophores, monensin and
194 lar Ca2+ loading irrespective of whether the channel opener was applied throughout the duration of hy
195                      Dilation to NS1619 (KCa channel opener) was reduced in endothelial denuded arter
196 t evoked by pinacidil (100 microM), a K(ATP) channel opener, was significantly higher in E2-treated c
197 n response to levcromakalim (LEVC), a K(ATP) channel opener, was significantly shifted to the left in
198       Adenosine receptor agonists and a KATP channel opener were used to achieve early preconditionin
199 nvestigated by using adenosine and potassium-channel openers (which are thought to induce hyperpolari
200 pyrithione (ZnPy) is a newly identified KCNQ channel opener, which potently activates KCNQ2, KCNQ4, a
201                                         KATP channel openers, which bind to SUR, promoted ATPase acti
202 2, the prototype of a novel series of K(ATP) channel openers with unique selectivity for bladder smoo
203 the efficacy of flupirtine, a selective KCNQ channel opener, with phenobarbital and diazepam, two dru
204 channels, inhibited the effects of potassium channel openers, without preventing the action of valino

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