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1 +/-1 vs. 10+/-1 and 19+/-1% before and after iberiotoxin).
2 ium chloride, 70 nM charybdotoxin, or 100 nM iberiotoxin).
3 ilation (36+/-1 vs. 14+/-2% before and after iberiotoxin).
4 ontrol and moderate hypoxia before and after iberiotoxin).
5 nd 40-min hypoxic dilations before and after iberiotoxin).
6 d intact muscle strips, an effect blocked by iberiotoxin.
7  are unchanged by the Kca channel antagonist iberiotoxin.
8 ries and by 158 +/- 12 nM in the presence of iberiotoxin.
9 rons isolated from embryos were unchanged by iberiotoxin.
10 and U50488H all were similarly attenuated by iberiotoxin.
11  cAMP analogue, 8-bromo cAMP, was blunted by iberiotoxin.
12 ation was also inhibited by BaCl2 but not by iberiotoxin.
13 ntracellular BaCl2 or by 10 nM extracellular iberiotoxin.
14 loxyphenyl)hexanoic acid, sulfaphenazole, or iberiotoxin.
15 onents sensitive to apamin, clotrimazole and iberiotoxin.
16  calcium-activated potassium channel blocker iberiotoxin.
17 es when exposed to the MaxiK channel blocker iberiotoxin.
18 -type hSlo channels were sensitive to 100 nM iberiotoxin.
19 onductance Ca(2+)-dependent K+ channels with iberiotoxin (0.1 microM) and apamin (1 microM), respecti
20 e pharmacological block of K(Ca) channels by iberiotoxin (0.1 to 100 nmol/L) dose-dependently constri
21 ive BKCa channel blocker paxilline (100 nm), iberiotoxin (10 mum), Ca(2+) free solutions and divalent
22 ed by the Ca2+-dependent K+ channel blockers iberiotoxin (10 nM) and charybdotoxin (10 nM).
23  attenuated by the Kca+2 channel antagonist, iberiotoxin (10(-7) M) (7 +/- 1, 11 +/- 1 and 16 +/- 1 v
24                                              Iberiotoxin (10(-7) M) attenuated hypoxic dilation but h
25                                              Iberiotoxin (100 nM) and apamin (50 nM), toxins known to
26  8-pCPT-AM-activated STOCs were sensitive to iberiotoxin (100 nM) and to ryanodine (30 muM).
27 conductance K(+) (BK(Ca)) channel opening as iberiotoxin (100 nM) significantly reduced the ability o
28 channels (TEA (1 mM), paxilline (10 muM) and iberiotoxin (100 nM)).
29                                              Iberiotoxin (100 nM), a blocker of KCa channels, under t
30 ensitive Ca2+ release (RyR) channel blocker; iberiotoxin (100 nM), a large-conductance Ca2+-activated
31 s also 56% blocked by the BK channel blocker iberiotoxin (100 nM).
32  but, unlike BK channels, are insensitive to iberiotoxin (100 nmol/L).
33 -sensitive potassium channel inhibitor), and iberiotoxin (100 nmol/L, calcium-activated potassium cha
34  two Ca(2+)-activated K(+) channel blockers (iberiotoxin, 100 nm and apamin, 1 mum).
35  and the Ca2+-dependent K+ channel inhibitor iberiotoxin (20 nM) failed to depolarize these cells fur
36 ckers with a combination of apamin 1 microM, iberiotoxin 200 nM, and clotrimazole 500 nM; 3) blocking
37 rs tetraethylammonium ions (TEA(+); 1 mM) or iberiotoxin (200 nM).
38 uring local perifusion with KCa antagonists, iberiotoxin (5 microm) had no effect, but charybdotoxin
39  were minimally affected by apamin (100 nM), iberiotoxin (50 nM), or ketoconazole (10 microM).
40 potassium channel (BK(Ca) channel) inhibitor iberiotoxin (50 nM).
41 0(-6) M) was attenuated by glibenclamide and iberiotoxin (8+/-1 and 17+/-1 vs. 4+/-1 and 9+/-1% befor
42        The dilation was largely abolished by iberiotoxin, a BK(Ca) channel blocker.
43 gly, by charybdotoxin (ChTX; 100 nM) but not iberiotoxin, a charybdotoxin analogue, which blocks the
44                                              Iberiotoxin, a KCa channel blocker, reduced H(2)S-induce
45                                              Iberiotoxin, a MaxiK blocker, antagonizes the relaxation
46  contractions had a decreased sensitivity to iberiotoxin, a selective BK channel inhibitor, in DSM st
47 umor capillaries, and could be attenuated by iberiotoxin, a selective inhibitor for calcium-dependent
48 ellular K+ with Cs+ or by the application of iberiotoxin, a selective inhibitor of large-conductance,
49  Per1::GFP neurons under voltage clamp using iberiotoxin, a specific BK channel blocker.
50                         Both were blocked by iberiotoxin, a specific blocker of large-conductance K(C
51               Coadministration of L-NAME and iberiotoxin almost abolished the vasodilation induced by
52                                      Because iberiotoxin also inhibited abn-cbd-induced relaxation of
53 V that was abolished by KT5823, or by 100 nM iberiotoxin (an inhibitor of BKCa channels).
54                                              Iberiotoxin, an inhibitor of BK channels, increased the
55                                 In contrast, iberiotoxin and apamin did not block the effects of apic
56 lammonium; similar results were evident with iberiotoxin and charybdotoxin block.
57                                  In oocytes, iberiotoxin and charybdotoxin, peptidyl scorpion toxins,
58  and inhibited by the BK channel inhibitors, iberiotoxin and charybdotoxin.
59       Specific inhibitors of these channels, iberiotoxin and paxilline, blocked oxidase-induced 86Rb+
60     In contrast, the BK(Ca) channel blockers iberiotoxin and paxilline, the phosphoinositide 3-kinase
61 ic K(Ca) current of E13 LMNs is inhibited by iberiotoxin and resistant to apamin.
62                                              Iberiotoxin and ryanodine, a ryanodine receptor channel
63  by the BK Ca2+-activated K+ channel blocker iberiotoxin and unaffected by apamin, indicating selecti
64 r pressures, and reduced vasoconstriction to iberiotoxin and vasodilation to NS1619, BK channel inhib
65 ce calcium-activated potassium channels with iberiotoxin, and is abolished by blocking small conducta
66 t human KSper is inhibited by charybdotoxin, iberiotoxin, and paxilline, while mouse KSper is insensi
67 of endothelial integrity, prevented by 55 nM iberiotoxin, and unmodified by 0.8 mM 4-aminopyridine, i
68  were mediated by inhibition of Ca-activated iberiotoxin- and apamin-sensitive K channels, but only i
69 ed by external TEA but not by charybdotoxin, iberiotoxin, apamin, or 4-aminopyridine.
70 um as a LRET donor and a fluorophore-labeled iberiotoxin as the LRET acceptor for measurements of dis
71          BKCa channel blockers paxilline and iberiotoxin, as well as Ca(2+) free solutions and divale
72 rosoyasaponin-I-induced activation, and (iv) iberiotoxin blockade.
73                                              Iberiotoxin broadened action potentials (APs), indicatin
74 dependent and sensitive to charybdotoxin and iberiotoxin but not to apamin, suggesting that they were
75 educed by 1 mM 4-aminopyridine and/or 100 nM iberiotoxin but unaffected by 10 nM dendrotoxin-K.
76                                              Iberiotoxin, but not apamin, inhibited STOC activity in
77 served in the presence of the BK antagonist, iberiotoxin, but persisted in the presence of KATP and S
78                                              Iberiotoxin did not affect the resting potential but inh
79               Inhibition of BK channels with iberiotoxin did not alter the fEPSPs in inflamed tissue,
80                                  Analysis of iberiotoxin difference currents also demonstrated that B
81                                              Iberiotoxin enhanced myogenic tone in both groups but mo
82                                              Iberiotoxin extended the duration of ventral root bursts
83               Coadministration of L-NNA with iberiotoxin further decremented hypoxic pial dilation an
84 by >= 0.1 mM barium (Ba2+) and unaffected by iberiotoxin, glibenclamide, apamin, 3,4-DAP and ouabain.
85 n of calcium-activated potassium channels by iberiotoxin had no effect on this dilation.
86                                              Iberiotoxin had no further effect on whole-cell K+ curre
87                 The K(ca) channel antagonist iberiotoxin had no influence on pial dilation during 5 m
88                                              Iberiotoxin (IbTX or alpha-KTx 1.3), a selective, high-a
89                                 Substituting iberiotoxin (IbTX) for CbTX greatly diminished inhibitio
90 mino acids comprising the alpha/beta turn in iberiotoxin (IbTX) replaced the corresponding seven amin
91  that generates NO, were reduced by > 50% by iberiotoxin (IBTX), an inhibitor of Ca(2+)-dependent K+
92    The pore blockers charybdotoxin (CTx) and iberiotoxin (IbTx), at nanomolar concentrations, have be
93 rostone isopropyl and M1 activated sustained iberiotoxin (IbTX)-sensitive, AL-8810 (FP receptor antag
94 ted in a 30-50% increase in the amplitude of iberiotoxin (IBTX)-sensitive, whole-cell K(+) current.
95 ve Ca(2+)-dependent K+ channel (KCa) blocker iberiotoxin (IbTx, 100 nm) reduced IK in glomus cells fr
96  presence and absence of the BKCa inhibitor, iberiotoxin (IBTX; 0.1 microM).
97 hetized rats: (I) KCa channel-inhibited (via iberiotoxin); (II) KATP channel-inhibited (via glibencla
98 re inhibited by 4-AP, TEA, charybdotoxin and iberiotoxin implicating functional K(v) and BK(Ca) chann
99 Slo-/- mice and by blocking BK channels with iberiotoxin in the Slo+/+ strips.
100                                              Iberiotoxin increased the amplitude and frequency of pha
101               Blockade of BK channels (using iberiotoxin) increased action potential amplitude and en
102 > old coronary arteries (explained by larger iberiotoxin-induced contraction and decreased dynamic ra
103 tivated a K+-selective, apamin-sensitive and iberiotoxin-insensitive current, detected as a tail curr
104        Our findings suggest that apamin- and iberiotoxin-insensitive K(Ca) channels are subject to di
105                            Glibenclamide and iberiotoxin, K(ATP) and K(ca) channel antagonists, atten
106  387 +/- 34 nM), but is resistant to apamin, iberiotoxin, kaliotoxin, scyllatoxin (Kd > 1 microM), an
107                            Glibenclamide and iberiotoxin, KATP and Kca channel antagonists, attenuate
108 % of the outward current was also blocked by iberiotoxin (Kd = 36 nM).
109  response to 8-pCPT-AM that was sensitive to iberiotoxin (n = 5).
110 harybdotoxin (NPo, 37% of control), or 10 nM iberiotoxin (NPo, 5% of control), whereas neurohypophysi
111 n contractions were similar to the effect of iberiotoxin on control mice.
112                                              Iberiotoxin or 1 mM tetraethylammonium (TEA+) constricte
113 ng outward currents, which were abolished by iberiotoxin or by chelation of intracellular calcium.
114 t with Ca2(+)-activated K+ channel blockers, iberiotoxin or charybdotoxin, did not prevent potentiati
115  in VSMC that was prevented by coinfusion of iberiotoxin or of AG-1478.
116                               Application of iberiotoxin or paxilline, blockers of Maxi-K channels, m
117 nnel antagonist tetraethylammonium chloride, iberiotoxin, or 4-aminopyridine.
118  vessels elicited K(+) channel opening in an iberiotoxin- or PEG-CAT-sensitive fashion in cell-attach
119          When these channels were blocked by iberiotoxin outward current was significantly reduced in
120 H arteries, and this dilation was blocked by iberiotoxin, paxilline, and KCl preconstriction but not
121                       Tetraethylammonium and iberiotoxin, preferential KCa-channel inhibitors, attenu
122 e (5-HT) contractile efficacy was reduced by iberiotoxin pretreatment in young > old coronary arterie
123 )-activated K(+) (BK(Ca)) channel inhibitor, iberiotoxin, produced identical inhibition of resveratro
124 a(2+)-activated K(+) channel (charybdotoxin, iberiotoxin, quinine, and Ba(2+)) nor inhibitors of the
125  tetraethylammonium-sensitive (IC50 = 9 mM), iberiotoxin-resistant, delayed rectifier K+ current and
126 -8), 10(-6) M in the absence and presence of iberiotoxin, respectively).
127 sion of gBK in Xenopus oocytes gives rise to iberiotoxin-sensitive (IbTX) currents, with an IC(50) fo
128 (Ca)) subtypes are decreased by axotomy, but iberiotoxin-sensitive and clotrimazole-sensitive current
129 lly, inhibition of CYP-epoxygenase abolished iberiotoxin-sensitive and flow-stimulated but not basal
130 of outward K(+) current detected a prominent iberiotoxin-sensitive BK(Ca) current in SMCs that was ab
131 annels, including apamin-sensitive channels, iberiotoxin-sensitive channels, and channels that are in
132 A or PP2, indicating that c-Src inhibits the Iberiotoxin-sensitive component, likely MaxiK channels.
133 all-sized control DRG neurons also expressed iberiotoxin-sensitive currents, which are reduced in bot
134 iments revealed a 4.7-fold higher density of iberiotoxin-sensitive K(Ca) channel current at physiolog
135 nctional studies demonstrated MYOCD-induced, iberiotoxin-sensitive potassium currents in porcine coro
136                                              Iberiotoxin-sensitive voltage- and [Ca2+]-activated K+ c
137  patch clamp recordings could not detect BK (iberiotoxin-sensitive) currents in cultured BAECs under
138  mV) cells, H(2)S increased the frequency of iberiotoxin-sensitive, Ca(2)(+) spark-induced transient
139 zation (7.9 +/- 3.9 mV) due to activation of iberiotoxin-sensitive, maxi-K(Ca) channels.
140         Inhibition by tetraethylammonium and iberiotoxin suggested that these currents represented ac
141 s (riluzole) and several potassium channels (iberiotoxin, TEA, 4-amino-pyridine), but blockers of cal
142 tes were more sensitive to the peptide toxin iberiotoxin than were hSlo + hSlobeta currents, and the
143 n/function in older myocytes, the ability of iberiotoxin to contract coronary rings was reduced appro
144 y effective blockers of BK current, although iberiotoxin was significantly more potent than charybdot
145 tion of outward current by MCD pretreatment, iberiotoxin was unable to produce any additional decreas
146 ge conductance channel was sensitive to TEA, iberiotoxin, was activated in excised inside-out patches
147                 The effects of ryanodine and iberiotoxin were not additive and were blocked by inhibi
148 tifying K+ currents, reversibly inhibited by iberiotoxin, were demonstrated in neutrophils and eosino
149 bout 53 % of IKCa was selectively blocked by iberiotoxin which had no effect on the delayed rectifier

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