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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
23 attenuated by the Kca+2 channel antagonist, iberiotoxin (10(-7) M) (7 +/- 1, 11 +/- 1 and 16 +/- 1 v
27 conductance K(+) (BK(Ca)) channel opening as iberiotoxin (100 nM) significantly reduced the ability o
30 ensitive Ca2+ release (RyR) channel blocker; iberiotoxin (100 nM), a large-conductance Ca2+-activated
33 -sensitive potassium channel inhibitor), and iberiotoxin (100 nmol/L, calcium-activated potassium cha
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
38 uring local perifusion with KCa antagonists, iberiotoxin (5 microm) had no effect, but charybdotoxin
41 0(-6) M) was attenuated by glibenclamide and iberiotoxin (8+/-1 and 17+/-1 vs. 4+/-1 and 9+/-1% befor
43 gly, by charybdotoxin (ChTX; 100 nM) but not iberiotoxin, a charybdotoxin analogue, which blocks the
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,
60 In contrast, the BK(Ca) channel blockers iberiotoxin and paxilline, the phosphoinositide 3-kinase
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
70 um as a LRET donor and a fluorophore-labeled iberiotoxin as the LRET acceptor for measurements of dis
74 dependent and sensitive to charybdotoxin and iberiotoxin but not to apamin, suggesting that they were
77 served in the presence of the BK antagonist, iberiotoxin, but persisted in the presence of KATP and S
84 by >= 0.1 mM barium (Ba2+) and unaffected by iberiotoxin, glibenclamide, apamin, 3,4-DAP and ouabain.
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
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
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
106 387 +/- 34 nM), but is resistant to apamin, iberiotoxin, kaliotoxin, scyllatoxin (Kd > 1 microM), an
110 harybdotoxin (NPo, 37% of control), or 10 nM iberiotoxin (NPo, 5% of control), whereas neurohypophysi
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
118 vessels elicited K(+) channel opening in an iberiotoxin- or PEG-CAT-sensitive fashion in cell-attach
120 H arteries, and this dilation was blocked by iberiotoxin, paxilline, and KCl preconstriction but not
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
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
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
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
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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