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1 d in Ca2+-free medium and largely blocked by nicardipine.
2 12-induced CCK secretion was also blocked by nicardipine.
3 lished by the L-type Ca2+ channel antagonist nicardipine.
4                                              Nicardipine (1 microM) blocked only half of the voltage-
5 nd was not inhibited by the Ca2+ antagonists nicardipine (1 microM) or D600 (10 microM).
6 h muscle relaxants isoproterenol (1 microM), nicardipine (1 microM) or papavarine (10 microM), and by
7 y TTX (1 microM) and completely abolished by nicardipine (1 microM).
8 1-1 microM) also affected the fast EPSP, but nicardipine (1-10 microM) was ineffective.
9 Ps, but both omega-agatoxin IVA (100 nM) and nicardipine (1-10 microM) were ineffective.
10 tagonism of L-type VGCCs with nimodipine and nicardipine (10 microM each).
11 +-free medium or the Ca2+-channel antagonist nicardipine (10 microM) blocked the CS-induced [Ca2+]i i
12 age-operated Ca2+ channel (VOCC) antagonists nicardipine (10 microM), nimodipine (10 microM) or omega
13                         Furthermore, whereas nicardipine, 12, displaced radioligand from the Na(+)-in
14                                        (R,S)-Nicardipine, 12, displayed Ki values of 19.6 and 63.8 mi
15 nitial drug was labetalol (48%), followed by nicardipine (15%), hydralazine (15%), and sodium nitropr
16                                              Nicardipine (2 microm) eliminated the Ca(2+) transient g
17 (1 mM) blocked intracellular Ca2+ waves, and nicardipine (2 microM) reduced their frequency and inten
18 (1 muM) or the L-type Ca(2+) channel blocker nicardipine (2 muM) and was potentiated by 8-pCPT-2'-O-M
19  subjected to the combined pretreatment with nicardipine (5 mg/kg) and MK-301 (10 mg/kg) indicates th
20                                              Nicardipine (5 mg/kg) reduces the accumulation of PAF, t
21 s is completely inhibited by pretreatment of nicardipine (5 mg/kg).
22  L-type Ca(2+) currents and was inhibited by nicardipine (5 x 10(-7) M).
23                                              Nicardipine, a Ca(v)1 channel antagonist, markedly reduc
24                          Channel blockage by nicardipine, a DHP antagonist, inhibited axonal remodeli
25  influx through L-type calcium channels with nicardipine also blocked retraction.
26                      Other dihydropyridines, nicardipine and Bay K8644, had similar augmenting effect
27 annels which are antagonized and agonized by nicardipine and Bay K8644, respectively and receptor-ope
28                                              Nicardipine and CaV1.2AS decreased Ca(2+) and cytokine r
29 and tested the effect of the Cav1 inhibitors nicardipine and Cav1.2AS on their functions.
30                   Using measured volumes for nicardipine and miconazole aggregate particles (2.1 x 10
31 or two compounds that form large aggregates, nicardipine and miconazole, we measured particle numbers
32                                         Both nicardipine and nifedipine stimulated the ATPase activit
33 d observed that 1,4-dihydropyridines such as nicardipine and nifedipine, which are clinically used as
34     In rod cells, L-type channel antagonists nicardipine and verapamil inhibited not only the outgrow
35 gliclazide were inhibited by thapsigargin or nicardipine and were significantly potentiated by 8-pCPT
36 nd glutathione), vasodilators (adenosine and nicardipine), and possibly energy substrates (fructose,
37 n in myocytes and was abolished by 10 microM nicardipine, and an outward current carried exclusively
38 w 100 microM: clotrimazole, benzyl benzoate, nicardipine, and delavirdine.
39 dropyridines such as amlodipine, isradipine, nicardipine, and felodipine also appear to be effective
40 itivity to blockade by omega-conotoxin GVIA, nicardipine, and omega-conotoxin MVIIC: N-, L-, and P/Q-
41 te reference sample, except for fluticasone, nicardipine, and sorafenib which suffer from severe matr
42                                              Nicardipine, atropine, TTX, or hexamethonium (100 microM
43   The PKC inhibitors Go6976 and Gf109203x or nicardipine blocked increases in pT38 and pT696.
44                    Verapamil, diltiazem, and nicardipine, but not nifedipine or isradipine, can signi
45 ersisted upon 3-5 min exposure to 1-5 microM nicardipine, but were abolished after 10-15 min exposure
46                       Continuous intravenous nicardipine (CIVN), prescribed for posttransplant hypert
47 ek or more with high doses (50 mg/kg/day) of nicardipine, clotrimazole, or pregnenolone 16alpha-carbo
48             The effects of pretreatment with nicardipine (dihydropyridine Ca2+ channel antagonist), B
49 s with and without calcium channel blockade (nicardipine) during blood pressure fluctuations (oscilla
50 raoperatively receive 10 implants at 4 mg of nicardipine each plus standard of care (implant group) o
51 icles and pharmacokinetic (PK) parameters of nicardipine, for integration into the PK-Sim((R)) progra
52  clinical trial to investigate the effect of nicardipine implants on clinical outcome may be warrante
53                     The observed exposure of nicardipine in Child-Pugh A was found to be ~ 1.5-fold g
54 effectively elucidated the PK alterations of nicardipine in healthy and diseased populations, thus th
55 ble of accurately predicting the exposure of nicardipine in healthy individuals as well as hepatic an
56                                              Nicardipine, in a dose that reduced significantly vasopr
57 TP stimulation, blocking these channels with nicardipine increases habituation.
58 s for 24 hrs after initiation of intravenous nicardipine infusion.
59                                          The nicardipine-insensitive current was activated by small d
60                                              Nicardipine is a calcium channel blocker employed to man
61      In separate experiments, the effects of nicardipine; N omega-I-nitro-L-arginine methyl ester, an
62  diazoxide, hydralazine, labetalol, esmolol, nicardipine, nifedipine, enalaprilat, and minoxidil.
63 dipine, delavirdine, etravirine, felodipine, nicardipine, nilotinib, and sorafenib) or low micromolar
64                     Clevidipine, felodipine, nicardipine, nilvadipine, and nimodipine have the same 1
65  induced by PKC activation were inhibited by nicardipine or Cav1.2AS in TH2 cells.
66             These findings show that placing nicardipine release implants during microsurgical aneury
67 ive proportions of omega-conotoxin GVIA- and nicardipine-sensitive N- ( approximately 40 %) and L- (
68 smissions similarly in both age groups while nicardipine showed no effect.
69            The Rho kinase inhibitor, but not nicardipine, significantly blocked rod axonal retraction
70         However, the Ca(2+) channel blockers nicardipine, SKF96365, diltiazem, and verapamil had no e
71      Several compounds, including verapamil, nicardipine, tetraphenylphosphonium, and prazosin, stimu
72                                        After nicardipine, there was a shift in the potential at which
73                        Addition of 10 microM nicardipine to cells resulted in a slowing of the molsid
74 e recently demonstrated that microsomes from nicardipine-treated rats will form cytochrome P450 3A (C
75 n down' during dialysis and was resistant to nicardipine (up to 10(-6) M).
76 hemorrhage who were treated with intravenous nicardipine using mean arterial pressure goals defined b
77 bide-a, from ABCG2-overexpressing cells, and nicardipine was more potent in inhibiting this transport
78 -agatoxin (Aga) IVA, and the dihydropyridine nicardipine were studied on synaptic transmission in the
79 sitive neurons equally as did treatment with nicardipine, which blocks voltage-gated calcium channels
80          There is growing experience with IV nicardipine, which is becoming a viable alternative to s
81       Patients were treated with intravenous nicardipine within 24 hrs of symptom onset to reduce and