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1 rular changes compared to diabetic mice with nitrendipine.
2  in the absence or presence of 10 micromol/l nitrendipine.
3 influx through L-type channels is blocked by nitrendipine.
4 n the presence of the Ca(2+)-channel blocker nitrendipine.
5 tagonists such as nifedipine, nimodipine, or nitrendipine.
6 was also blocked by the Ca2+ channel blocker nitrendipine.
7 at was sensitive to both omega-CgTX GVIA and nitrendipine.
8  combined application of omega-CgTX GVIA and nitrendipine.
9 he classical l-type calcium channel blocker, nitrendipine.
10 4513; and the L-type Ca2+ channel antagonist nitrendipine.
11 oM), an N-type Ca2+ channel blocker, whereas nitrendipine (1.5 microM), an inhibitor of L-type Ca2+ c
12 extracellular Ca2+, addition of 1 mM Mg2+ or nitrendipine (10 microM) to the saline had no effect.
13 -type voltage-gated Ca2+ channel antagonists nitrendipine (2-5 microM) or nifedipine (10 microM).
14 led that 23% of the current was sensitive to nitrendipine, 35% to omega-conotoxin GVIA, and between 1
15 icroM) and by the calcium channel antagonist nitrendipine (500 nM).
16 ndent on extracellular Ca2+ and inhibited by nitrendipine, a Ca2+ channel blocker, or 2',5'-dideoxyad
17  change occurs even when the medium contains nitrendipine, a voltage-gated calcium channel blocker, b
18                 Radioligand binding with [3H]nitrendipine also revealed a significant increase in the
19 nvolves Ca(2+) influx, as it is inhibited by nitrendipine, an inhibitor of L-type voltage-gated chann
20                                 In contrast, nitrendipine, an L-type Ca(2+) channel blocker terminate
21 refinement and LTD magnitude is depressed by nitrendipine, an L-type Ca(2+) channel blocker.
22     These arrhythmias could be terminated by nitrendipine, an l-type calcium channel blocker, but not
23                           Furthermore, [(3)H]nitrendipine and bodipy-Fl-dihydropyridine accumulation
24             They resist the dihydropyridines nitrendipine and PN200-110, but 1-10 micrometer mibefrad
25                           In the presence of nitrendipine and thapsigargin, glucose failed to stimula
26                 The potential was blocked by nitrendipine and/or APV and facilitated by bicuculline,
27 agents (SKF 96365, miconazole, clotrimazole, nitrendipine, and trifluoperazine) that in the absence o
28 rsts that are suppressed by the LTCC blocker nitrendipine but not by the Na(+) current blocker tetrod
29 lin secretion, reduced by both diazoxide and nitrendipine but was immune to inhibition by mannoheptul
30   Diazepam, allopregnanolone, Ro15-4513, and nitrendipine had no effect or enhanced tremor, whereas M
31          Mannoheptulose, 2-deoxyglucose, and nitrendipine inhibit glucose-stimulated insulin release
32  omega-CgTX GVIA (N-type) and 30% blocked by nitrendipine (L-type).
33 nally, motility was blocked by verapamil and nitrendipine, molecules known to block voltage-gated cal
34 own to interfere with normal Ca2+ transport (nitrendipine, nisoldipine, Bay K 8644, A 23187) do not s
35 in release, even in the presence of 5 microM nitrendipine or 150 microM diazoxide.
36  flupirtine had no significant effect on [3H]nitrendipine or [3H]diltiazem binding to cortical membra
37 a2+ concentration ([Ca2+]i) was inhibited by nitrendipine or diazoxide or by severe Ca2+ deprivation.
38 dihydropyridines nimodipine, nifedipine, and nitrendipine, the benzothiazepine diltiazem, and the phe
39               In the absence and presence of nitrendipine, there were 6.1 +/- 0.7 and 6.3 +/- 0.6 gra

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