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1 nd 40-min hypoxic dilations before and after iberiotoxin).
2 +/-1 vs. 10+/-1 and 19+/-1% before and after iberiotoxin).
3 ium chloride, 70 nM charybdotoxin, or 100 nM iberiotoxin).
4 ilation (36+/-1 vs. 14+/-2% before and after iberiotoxin).
5 ontrol and moderate hypoxia before and after iberiotoxin).
6  and externally by a Ca(V) 1.3 antagonist or iberiotoxin.
7 as well as by the specific K(Ca) 1.1 blocker iberiotoxin.
8 d intact muscle strips, an effect blocked by iberiotoxin.
9  are unchanged by the Kca channel antagonist iberiotoxin.
10 ries and by 158 +/- 12 nM in the presence of iberiotoxin.
11 rons isolated from embryos were unchanged by iberiotoxin.
12 and U50488H all were similarly attenuated by iberiotoxin.
13  cAMP analogue, 8-bromo cAMP, was blunted by iberiotoxin.
14 ation was also inhibited by BaCl2 but not by iberiotoxin.
15 ntracellular BaCl2 or by 10 nM extracellular iberiotoxin.
16 loxyphenyl)hexanoic acid, sulfaphenazole, or iberiotoxin.
17 onents sensitive to apamin, clotrimazole and iberiotoxin.
18  calcium-activated potassium channel blocker iberiotoxin.
19 es when exposed to the MaxiK channel blocker iberiotoxin.
20 -type hSlo channels were sensitive to 100 nM iberiotoxin.
21 onductance Ca(2+)-dependent K+ channels with iberiotoxin (0.1 microM) and apamin (1 microM), respecti
22 e pharmacological block of K(Ca) channels by iberiotoxin (0.1 to 100 nmol/L) dose-dependently constri
23 ive BKCa channel blocker paxilline (100 nm), iberiotoxin (10 mum), Ca(2+) free solutions and divalent
24 ed by the Ca2+-dependent K+ channel blockers iberiotoxin (10 nM) and charybdotoxin (10 nM).
25  attenuated by the Kca+2 channel antagonist, iberiotoxin (10(-7) M) (7 +/- 1, 11 +/- 1 and 16 +/- 1 v
26                                              Iberiotoxin (10(-7) M) attenuated hypoxic dilation but h
27                                              Iberiotoxin (100 nM) and apamin (50 nM), toxins known to
28  8-pCPT-AM-activated STOCs were sensitive to iberiotoxin (100 nM) and to ryanodine (30 muM).
29 conductance K(+) (BK(Ca)) channel opening as iberiotoxin (100 nM) significantly reduced the ability o
30 channels (TEA (1 mM), paxilline (10 muM) and iberiotoxin (100 nM)).
31                                              Iberiotoxin (100 nM), a blocker of KCa channels, under t
32 ensitive Ca2+ release (RyR) channel blocker; iberiotoxin (100 nM), a large-conductance Ca2+-activated
33 s also 56% blocked by the BK channel blocker iberiotoxin (100 nM).
34  but, unlike BK channels, are insensitive to iberiotoxin (100 nmol/L).
35 -sensitive potassium channel inhibitor), and iberiotoxin (100 nmol/L, calcium-activated potassium cha
36  two Ca(2+)-activated K(+) channel blockers (iberiotoxin, 100 nm and apamin, 1 mum).
37  and the Ca2+-dependent K+ channel inhibitor iberiotoxin (20 nM) failed to depolarize these cells fur
38 ckers with a combination of apamin 1 microM, iberiotoxin 200 nM, and clotrimazole 500 nM; 3) blocking
39 rs tetraethylammonium ions (TEA(+); 1 mM) or iberiotoxin (200 nM).
40 uring local perifusion with KCa antagonists, iberiotoxin (5 microm) had no effect, but charybdotoxin
41  were minimally affected by apamin (100 nM), iberiotoxin (50 nM), or ketoconazole (10 microM).
42 potassium channel (BK(Ca) channel) inhibitor iberiotoxin (50 nM).
43 0(-6) M) was attenuated by glibenclamide and iberiotoxin (8+/-1 and 17+/-1 vs. 4+/-1 and 9+/-1% befor
44        The dilation was largely abolished by iberiotoxin, a BK(Ca) channel blocker.
45 gly, by charybdotoxin (ChTX; 100 nM) but not iberiotoxin, a charybdotoxin analogue, which blocks the
46                                              Iberiotoxin, a KCa channel blocker, reduced H(2)S-induce
47                                              Iberiotoxin, a MaxiK blocker, antagonizes the relaxation
48  contractions had a decreased sensitivity to iberiotoxin, a selective BK channel inhibitor, in DSM st
49 umor capillaries, and could be attenuated by iberiotoxin, a selective inhibitor for calcium-dependent
50 ellular K+ with Cs+ or by the application of iberiotoxin, a selective inhibitor of large-conductance,
51  Per1::GFP neurons under voltage clamp using iberiotoxin, a specific BK channel blocker.
52                         Both were blocked by iberiotoxin, a specific blocker of large-conductance K(C
53               Coadministration of L-NAME and iberiotoxin almost abolished the vasodilation induced by
54                                      Because iberiotoxin also inhibited abn-cbd-induced relaxation of
55 V that was abolished by KT5823, or by 100 nM iberiotoxin (an inhibitor of BKCa channels).
56                                              Iberiotoxin, an inhibitor of BK channels, increased the
57                                 In contrast, iberiotoxin and apamin did not block the effects of apic
58 lammonium; similar results were evident with iberiotoxin and charybdotoxin block.
59                                  In oocytes, iberiotoxin and charybdotoxin, peptidyl scorpion toxins,
60  and inhibited by the BK channel inhibitors, iberiotoxin and charybdotoxin.
61       Specific inhibitors of these channels, iberiotoxin and paxilline, blocked oxidase-induced 86Rb+
62     In contrast, the BK(Ca) channel blockers iberiotoxin and paxilline, the phosphoinositide 3-kinase
63 ic K(Ca) current of E13 LMNs is inhibited by iberiotoxin and resistant to apamin.
64                                              Iberiotoxin and ryanodine, a ryanodine receptor channel
65  by the BK Ca2+-activated K+ channel blocker iberiotoxin and unaffected by apamin, indicating selecti
66 r pressures, and reduced vasoconstriction to iberiotoxin and vasodilation to NS1619, BK channel inhib
67 ce calcium-activated potassium channels with iberiotoxin, and is abolished by blocking small conducta
68 t human KSper is inhibited by charybdotoxin, iberiotoxin, and paxilline, while mouse KSper is insensi
69  a pharmacological inhibitor of BK channels, iberiotoxin, and small-conductance Ca(2+)-activated K(+)
70 of endothelial integrity, prevented by 55 nM iberiotoxin, and unmodified by 0.8 mM 4-aminopyridine, i
71  were mediated by inhibition of Ca-activated iberiotoxin- and apamin-sensitive K channels, but only i
72 ed by external TEA but not by charybdotoxin, iberiotoxin, apamin, or 4-aminopyridine.
73 um as a LRET donor and a fluorophore-labeled iberiotoxin as the LRET acceptor for measurements of dis
74          BKCa channel blockers paxilline and iberiotoxin, as well as Ca(2+) free solutions and divale
75 rosoyasaponin-I-induced activation, and (iv) iberiotoxin blockade.
76 ls is subunit specific, as paxilline but not iberiotoxin blocked mGluR-LTD.
77                                              Iberiotoxin broadened action potentials (APs), indicatin
78 dependent and sensitive to charybdotoxin and iberiotoxin but not to apamin, suggesting that they were
79 educed by 1 mM 4-aminopyridine and/or 100 nM iberiotoxin but unaffected by 10 nM dendrotoxin-K.
80                                              Iberiotoxin, but not apamin, inhibited STOC activity in
81 served in the presence of the BK antagonist, iberiotoxin, but persisted in the presence of KATP and S
82                                              Iberiotoxin did not affect the resting potential but inh
83               Inhibition of BK channels with iberiotoxin did not alter the fEPSPs in inflamed tissue,
84                                  Analysis of iberiotoxin difference currents also demonstrated that B
85                                              Iberiotoxin enhanced myogenic tone in both groups but mo
86                                              Iberiotoxin extended the duration of ventral root bursts
87               Coadministration of L-NNA with iberiotoxin further decremented hypoxic pial dilation an
88 by >= 0.1 mM barium (Ba2+) and unaffected by iberiotoxin, glibenclamide, apamin, 3,4-DAP and ouabain.
89 n of calcium-activated potassium channels by iberiotoxin had no effect on this dilation.
90                                              Iberiotoxin had no further effect on whole-cell K+ curre
91                 The K(ca) channel antagonist iberiotoxin had no influence on pial dilation during 5 m
92                                              Iberiotoxin (IbTX or alpha-KTx 1.3), a selective, high-a
93                                 Substituting iberiotoxin (IbTX) for CbTX greatly diminished inhibitio
94 mino acids comprising the alpha/beta turn in iberiotoxin (IbTX) replaced the corresponding seven amin
95  that generates NO, were reduced by > 50% by iberiotoxin (IBTX), an inhibitor of Ca(2+)-dependent K+
96    The pore blockers charybdotoxin (CTx) and iberiotoxin (IbTx), at nanomolar concentrations, have be
97 rostone isopropyl and M1 activated sustained iberiotoxin (IbTX)-sensitive, AL-8810 (FP receptor antag
98 ted in a 30-50% increase in the amplitude of iberiotoxin (IBTX)-sensitive, whole-cell K(+) current.
99 ve Ca(2+)-dependent K+ channel (KCa) blocker iberiotoxin (IbTx, 100 nm) reduced IK in glomus cells fr
100  presence and absence of the BKCa inhibitor, iberiotoxin (IBTX; 0.1 microM).
101 osal bumetanide (NKCC1 inhibitor) or mucosal iberiotoxin (IbTX; BK channel blocker), but not TRAM-34
102 hetized rats: (I) KCa channel-inhibited (via iberiotoxin); (II) KATP channel-inhibited (via glibencla
103 re inhibited by 4-AP, TEA, charybdotoxin and iberiotoxin implicating functional K(v) and BK(Ca) chann
104 Slo-/- mice and by blocking BK channels with iberiotoxin in the Slo+/+ strips.
105                                              Iberiotoxin increased the amplitude and frequency of pha
106               Blockade of BK channels (using iberiotoxin) increased action potential amplitude and en
107 > old coronary arteries (explained by larger iberiotoxin-induced contraction and decreased dynamic ra
108 tivated a K+-selective, apamin-sensitive and iberiotoxin-insensitive current, detected as a tail curr
109        Our findings suggest that apamin- and iberiotoxin-insensitive K(Ca) channels are subject to di
110                            Glibenclamide and iberiotoxin, K(ATP) and K(ca) channel antagonists, atten
111  387 +/- 34 nM), but is resistant to apamin, iberiotoxin, kaliotoxin, scyllatoxin (Kd > 1 microM), an
112                            Glibenclamide and iberiotoxin, KATP and Kca channel antagonists, attenuate
113 % of the outward current was also blocked by iberiotoxin (Kd = 36 nM).
114  response to 8-pCPT-AM that was sensitive to iberiotoxin (n = 5).
115 harybdotoxin (NPo, 37% of control), or 10 nM iberiotoxin (NPo, 5% of control), whereas neurohypophysi
116 n contractions were similar to the effect of iberiotoxin on control mice.
117                                              Iberiotoxin or 1 mM tetraethylammonium (TEA+) constricte
118 ng outward currents, which were abolished by iberiotoxin or by chelation of intracellular calcium.
119 t with Ca2(+)-activated K+ channel blockers, iberiotoxin or charybdotoxin, did not prevent potentiati
120  in VSMC that was prevented by coinfusion of iberiotoxin or of AG-1478.
121                               Application of iberiotoxin or paxilline, blockers of Maxi-K channels, m
122 nnel antagonist tetraethylammonium chloride, iberiotoxin, or 4-aminopyridine.
123  vessels elicited K(+) channel opening in an iberiotoxin- or PEG-CAT-sensitive fashion in cell-attach
124          When these channels were blocked by iberiotoxin outward current was significantly reduced in
125 H arteries, and this dilation was blocked by iberiotoxin, paxilline, and KCl preconstriction but not
126                       Tetraethylammonium and iberiotoxin, preferential KCa-channel inhibitors, attenu
127 e (5-HT) contractile efficacy was reduced by iberiotoxin pretreatment in young > old coronary arterie
128 )-activated K(+) (BK(Ca)) channel inhibitor, iberiotoxin, produced identical inhibition of resveratro
129 a(2+)-activated K(+) channel (charybdotoxin, iberiotoxin, quinine, and Ba(2+)) nor inhibitors of the
130 nd deactivation kinetics and a slower-gating iberiotoxin-resistant component.
131  tetraethylammonium-sensitive (IC50 = 9 mM), iberiotoxin-resistant, delayed rectifier K+ current and
132 -8), 10(-6) M in the absence and presence of iberiotoxin, respectively).
133 sion of gBK in Xenopus oocytes gives rise to iberiotoxin-sensitive (IbTX) currents, with an IC(50) fo
134 (Ca)) subtypes are decreased by axotomy, but iberiotoxin-sensitive and clotrimazole-sensitive current
135 lly, inhibition of CYP-epoxygenase abolished iberiotoxin-sensitive and flow-stimulated but not basal
136       Step depolarizations activated both an iberiotoxin-sensitive BK component with rapid activation
137 of outward K(+) current detected a prominent iberiotoxin-sensitive BK(Ca) current in SMCs that was ab
138 annels, including apamin-sensitive channels, iberiotoxin-sensitive channels, and channels that are in
139 t all BK current came from the faster-gating iberiotoxin-sensitive channels, even during bursts of ac
140 A or PP2, indicating that c-Src inhibits the Iberiotoxin-sensitive component, likely MaxiK channels.
141 all-sized control DRG neurons also expressed iberiotoxin-sensitive currents, which are reduced in bot
142 iments revealed a 4.7-fold higher density of iberiotoxin-sensitive K(Ca) channel current at physiolog
143 nctional studies demonstrated MYOCD-induced, iberiotoxin-sensitive potassium currents in porcine coro
144                                              Iberiotoxin-sensitive voltage- and [Ca2+]-activated K+ c
145  patch clamp recordings could not detect BK (iberiotoxin-sensitive) currents in cultured BAECs under
146  mV) cells, H(2)S increased the frequency of iberiotoxin-sensitive, Ca(2)(+) spark-induced transient
147 zation (7.9 +/- 3.9 mV) due to activation of iberiotoxin-sensitive, maxi-K(Ca) channels.
148         Inhibition by tetraethylammonium and iberiotoxin suggested that these currents represented ac
149 s (riluzole) and several potassium channels (iberiotoxin, TEA, 4-amino-pyridine), but blockers of cal
150 tes were more sensitive to the peptide toxin iberiotoxin than were hSlo + hSlobeta currents, and the
151 n/function in older myocytes, the ability of iberiotoxin to contract coronary rings was reduced appro
152 y effective blockers of BK current, although iberiotoxin was significantly more potent than charybdot
153 tion of outward current by MCD pretreatment, iberiotoxin was unable to produce any additional decreas
154 ge conductance channel was sensitive to TEA, iberiotoxin, was activated in excised inside-out patches
155                 The effects of ryanodine and iberiotoxin were not additive and were blocked by inhibi
156 tifying K+ currents, reversibly inhibited by iberiotoxin, were demonstrated in neutrophils and eosino
157 bout 53 % of IKCa was selectively blocked by iberiotoxin which had no effect on the delayed rectifier

 
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