ライフサイエンスコーパス: nicardipine

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 Channel blockage by nicardipine, a DHP antagonist, inhibited axonal remodeli

24 influx through L-type calcium channels with nicardipine also blocked retraction.

25 Other dihydropyridines, nicardipine and Bay K8644, had similar augmenting effect

26 annels which are antagonized and agonized by nicardipine and Bay K8644, respectively and receptor-ope

27 Nicardipine and CaV1.2AS decreased Ca(2+) and cytokine r

28 and tested the effect of the Cav1 inhibitors nicardipine and Cav1.2AS on their functions.

29 Using measured volumes for nicardipine and miconazole aggregate particles (2.1 x 10

30 or two compounds that form large aggregates, nicardipine and miconazole, we measured particle numbers

31 Both nicardipine and nifedipine stimulated the ATPase activit

32 d observed that 1,4-dihydropyridines such as nicardipine and nifedipine, which are clinically used as

33 In rod cells, L-type channel antagonists nicardipine and verapamil inhibited not only the outgrow

34 gliclazide were inhibited by thapsigargin or nicardipine and were significantly potentiated by 8-pCPT

35 nd glutathione), vasodilators (adenosine and nicardipine), and possibly energy substrates (fructose,

36 n in myocytes and was abolished by 10 microM nicardipine, and an outward current carried exclusively

37 w 100 microM: clotrimazole, benzyl benzoate, nicardipine, and delavirdine.

38 dropyridines such as amlodipine, isradipine, nicardipine, and felodipine also appear to be effective

39 itivity to blockade by omega-conotoxin GVIA, nicardipine, and omega-conotoxin MVIIC: N-, L-, and P/Q-

40 te reference sample, except for fluticasone, nicardipine, and sorafenib which suffer from severe matr

41 Nicardipine, atropine, TTX, or hexamethonium (100 microM

42 The PKC inhibitors Go6976 and Gf109203x or nicardipine blocked increases in pT38 and pT696.

43 Verapamil, diltiazem, and nicardipine, but not nifedipine or isradipine, can signi

44 ersisted upon 3-5 min exposure to 1-5 microM nicardipine, but were abolished after 10-15 min exposure

45 Continuous intravenous nicardipine (CIVN), prescribed for posttransplant hypert

46 ek or more with high doses (50 mg/kg/day) of nicardipine, clotrimazole, or pregnenolone 16alpha-carbo

47 The effects of pretreatment with nicardipine (dihydropyridine Ca2+ channel antagonist), B

48 s with and without calcium channel blockade (nicardipine) during blood pressure fluctuations (oscilla

49 Nicardipine, in a dose that reduced significantly vasopr

50 TP stimulation, blocking these channels with nicardipine increases habituation.

51 s for 24 hrs after initiation of intravenous nicardipine infusion.

52 The nicardipine-insensitive current was activated by small d

53 In separate experiments, the effects of nicardipine; N omega-I-nitro-L-arginine methyl ester, an

54 diazoxide, hydralazine, labetalol, esmolol, nicardipine, nifedipine, enalaprilat, and minoxidil.

55 dipine, delavirdine, etravirine, felodipine, nicardipine, nilotinib, and sorafenib) or low micromolar

56 Clevidipine, felodipine, nicardipine, nilvadipine, and nimodipine have the same 1

57 induced by PKC activation were inhibited by nicardipine or Cav1.2AS in TH2 cells.

58 ive proportions of omega-conotoxin GVIA- and nicardipine-sensitive N- ( approximately 40 %) and L- (

59 smissions similarly in both age groups while nicardipine showed no effect.

60 The Rho kinase inhibitor, but not nicardipine, significantly blocked rod axonal retraction

61 However, the Ca(2+) channel blockers nicardipine, SKF96365, diltiazem, and verapamil had no e

62 Several compounds, including verapamil, nicardipine, tetraphenylphosphonium, and prazosin, stimu

63 After nicardipine, there was a shift in the potential at which

64 Addition of 10 microM nicardipine to cells resulted in a slowing of the molsid

65 e recently demonstrated that microsomes from nicardipine-treated rats will form cytochrome P450 3A (C

66 n down' during dialysis and was resistant to nicardipine (up to 10(-6) M).

67 hemorrhage who were treated with intravenous nicardipine using mean arterial pressure goals defined b

68 bide-a, from ABCG2-overexpressing cells, and nicardipine was more potent in inhibiting this transport

69 -agatoxin (Aga) IVA, and the dihydropyridine nicardipine were studied on synaptic transmission in the

70 sitive neurons equally as did treatment with nicardipine, which blocks voltage-gated calcium channels

71 There is growing experience with IV nicardipine, which is becoming a viable alternative to s

72 Patients were treated with intravenous nicardipine within 24 hrs of symptom onset to reduce and