ライフサイエンスコーパス: nimodipine

1 ndent intrinsic firing, which was blocked by nimodipine.

2 logically were also reduced significantly by nimodipine.

3 in MVIIC but was reduced > 70% by micromolar nimodipine.

4 s blocked by the selective L-type antagonist nimodipine.

5 olished by the L-type Ca(2+) channel blocker nimodipine.

6 eversed by the L-type Ca(2+) channel blocker nimodipine.

7 ation, including leflunomide, flutamide, and nimodipine.

8 presence of the L-type channel blocker (R,S)-nimodipine.

9 stablished L-type calcium channel antagonist nimodipine.

10 y the potent L-type Ca2+ channel inhibitor, *nimodipine.

11 scillations were usually blocked by 2 microm nimodipine.

12 ttenuated by the L-type Ca2+ channel blocker nimodipine.

13 micked by the L-type calcium channel blocker nimodipine (1 micro;M) as well as by protein kinase C (P

14 or the addition of the Ca2+ channel blocker nimodipine (1 microM) inhibited store refilling, as asse

15 locked by the L-type Ca2+ channel antagonist nimodipine (1 microM).

16 Ca(2+) channel blockers Cd(2+) (200 muM) or nimodipine (1 muM), and potentiated by FPL-64176 (1 muM)

17 ated current was isolated in the presence of nimodipine (1 mum), which was subtracted from the total

18 Further, in cultured Kupffer cells, nimodipine (1 mumol/L) largely prevented the elevation i

19 Nimodipine (10 mg/kg, sc) increased the magnitude of lig

20 In the experimental group, nimodipine (10 mg/kg/d) was added to the diet and was sh

21 Nimodipine (10 micrograms/kg) also blocked the swift inc

22 (VOCC) antagonists nicardipine (10 microM), nimodipine (10 microM) or omega-grammotoxin SIA (1 micro

23 when L-type Ca2+ channels were blocked with nimodipine (10 microm) or when cAMP-dependent protein ki

24 cations of the L-type Ca(2+) channel blocker nimodipine (10 microm).

25 presence of an L-type Ca2+ channel blocker, nimodipine (10 microm).

26 In the presence of nimodipine, 10 microM tamoxifen still abolished pressure

27 Nimodipine (100 microM), an L-type voltage-sensitive cal

28 Nimodipine (50 nmol/L), a blocker of L-type voltage-sens

29 sia were randomly assigned to receive either nimodipine (60 mg orally every 4 hours) or intravenous m

30 ients in the analysis (all treated with oral nimodipine), 93 (33%) developed symptomatic vasospasm wi

31 charide (LPS) (LPS, 200 +/- 11 nmol/L; LPS + nimodipine, 94 +/- 31 nmol/L; P < .05).

32 Coadministration of artemether and nimodipine, a calcium channel blocker used to treat post

33 Nimodipine, a DHP-type blocker of L-type Ca2+ channels,

34 Nimodipine, a dihydropyridine (DHP) antagonist, suppress

35 cases, this Ca(2+) signal was eliminated by nimodipine, a selective L-type voltage-gated Ca(2+)-chan

36 In contrast, nimodipine, a voltage-dependent Ca(2+) channel inhibitor

37 Blockade of L-type calcium channels with nimodipine abolished the induction of LTD and reduced th

38 adenylate cyclase activator, indicating that nimodipine acts through the alpha2 receptor-G(alphai)-co

39 t with the L-type calcium channel antagonist nimodipine affects the responsiveness of the circadian p

40 )-cAMPS), an L-type Ca2+ channel antagonist (nimodipine), an antagonist of the sarco(endo)plasmic ret

41 Nimodipine, an L-type calcium channel blocker has been s

42 Nimodipine, an L-type channel antagonist, partly inhibit

43 Conversely, nimodipine, an L-VGCC antagonist, protected older but no

44 [Ca2+]i were blocked to a similar extent by nimodipine and cadmium and augmented by Bay K 8644.

45 fractions and by inhibition of secretion by nimodipine and diazoxide.

46 Moreover, in the presence of nimodipine and high glucose, acetylcholine still elevate

47 by selective antagonism of L-type VGCCs with nimodipine and nicardipine (10 microM each).

48 MK801, nimodipine and nickel all abolished both stimulus-evoked

49 The L-type Ca2+ channel blockers nimodipine and nifedipine (both 10 microm) reduced spine

50 The L-type calcium channel blockers nimodipine and nifedipine abolished the plateau potentia

51 hibited by the L-type Ca2+ channel blockers, nimodipine and nifedipine.

52 Nimodipine and omega-conotoxin-GVIA reduced the ICa by a

53 results demonstrate that the interaction of nimodipine and other antagonists with the channel is mod

54 urrent was sensitive to blockade by Gd3+ and nimodipine and, to a lesser extent, by omega-conotoxin G

55 ced by the L-type Ca(2+) channel antagonist, nimodipine, and increased by the L-type Ca(2+) channel o

56 desartan, celecoxib, dasatinib, nilvadipine, nimodipine, and regorafenib).

57 Overall, nimodipine application seems to generate a favorable env

58 and a minor component was inhibited by (R,S)-nimodipine (approximately 8%).

59 ted risk ratio for eclampsia associated with nimodipine, as compared with magnesium sulfate, was 3.2

60 macological sensitivity to dihydropyridines (nimodipine, Bay K 8644), benzothiazepines (diltiazem) an

61 The IC(50) for nimodipine block of Ca(V)1.3alpha(1) L-type calcium chan

62 tion of the L-type Ca(2+) channel antagonist nimodipine blocked FSI.

63 Nimodipine blocks 90% of the Ca2+0-induced 5-HT release,

64 lso enhanced significantly by application of nimodipine but not of diltiazem.

65 Myogenic tone was abolished by 2 microM nimodipine, but Cl(-) efflux was unaffected.

66 Additionally, nimodipine can replace hyperpolarization, indicating tha

67 Nimodipine caused quantitatively greater reductions in t

68 (+)-verapamil, (-)-verapamil, diltiazem, and nimodipine caused reversible and concentration-dependent

69 to changes in L-type Ca2+ channel activity; nimodipine completely inhibited glucose-stimulated ISR a

70 of Gd3+, verapamil, omega-conotoxin GVIA, or nimodipine, consistent with Zn2+ entry through voltage-g

71 ing quantal content to 57.7 +/- 3.3 % of pre-nimodipine control levels.

72 f the ethanol, during the chronic treatment, nimodipine did not affect tolerance to the ataxic action

73 blockers of voltage-dependent Ca2+ channels (nimodipine, diltiazem), ryanodine and inhibitors of the

74 king calcium channels with either cadmium or nimodipine during depolarization abolished the rate incr

75 This nimodipine effect appears to be independent of its class

76 However, only the L-type VGCC antagonist nimodipine effectively antagonized the Ca(2+) oscillatio

77 monstrate a novel neural mechanism involving nimodipine enhancement of alpha2 signaling in RGCs.

78 ues only reached 101 +/- 9 U/L in rats given nimodipine + ethanol-values which were significantly low

79 thanol-fed and 144 +/- 38 mg/dL in ethanol + nimodipine-fed rats.

80 Magnesium sulfate is more effective than nimodipine for prophylaxis against seizures in women wit

81 differ significantly between groups, but the nimodipine group had a higher rate of postpartum seizure

82 n in the magnesium sulfate group than in the nimodipine group needed hydralazine to control blood pre

83 Nimodipine had no effect on body weight over a 4-week tr

84 e, felodipine, nicardipine, nilvadipine, and nimodipine have the same 1,4-dihydropyridine scaffold an

85 se play a role in murine CM pathogenesis and nimodipine holds potential as adjunctive therapy for CM.

86 Nimodipine, however, decreased the tolerance to the hypo

87 Treatment with oral nimodipine, hypervolemic therapy, and hypertensive thera

88 bited by the L-type Ca2+ channel antagonist, nimodipine; IC(50)=59 nM.

89 in febrile seizures, we tested the effect of nimodipine in an in vivo model of febrile seizures and f

90 olerance may be explained by dual actions of nimodipine in, firstly, decreasing the form of tolerance

91 argely inhibited by the Ca2+ channel blocker nimodipine, indicating that L-type voltage-gated Ca2+ ch

92 Administration of nimodipine induced vasodilation and increased pial blood

93 binding site and from the site through which nimodipine inhibits 5-HT3 receptor function.

94 L-type voltage-gated calcium channel blocker nimodipine interferes with the amnestic outcome.

95 Nimodipine is a calcium-channel blocker with specific ce

96 Our objective was to determine whether nimodipine is more effective than magnesium sulfate for

97 applied alone, but in the presence of (R,S)-nimodipine it reduced the current (approximately 40%), s

98 These results suggest that nimodipine may affect phase shifts of circadian activity

99 Nimodipine neither displaced [3H]granisetron binding nor

100 Specifically, the dihydropyridines nimodipine, nifedipine, and nitrendipine, the benzothiaz

101 Data for other LTCC antagonists (diltiazem, nimodipine, nifedipine, methyoxyverapamil and isradipine

102 g potentials (with firing stopped by TTX and nimodipine) of -55 to -50 mV, although input resistance

103 nists of high-threshold (HVA) Ca2+ channels, nimodipine, omega-Conotoxin GVIA, and Agatoxin IVA parti

104 ed Ca(2+) channel inhibitors (nifedipine and nimodipine) on airway contraction and Ca(2+) oscillation

105 By contrast, nifedipine and nimodipine only partially reduced airway contraction, Ca

106 tantially enhanced by background addition of nimodipine or isradipine, but not by diltiazem, verapami

107 cium channel antagonists such as nifedipine, nimodipine, or nitrendipine.

108 on (LLF-LTD) that is blocked by either AP-5, nimodipine, or Ro 25-6981 [R-(R,S)-alpha-(4-hydroxypheny

109 ree solution, by extracellular tetrodotoxin, nimodipine, or tetraethylammonium, or by intracellular d

110 hrough voltage-dependent Ca2+ channels using nimodipine partially blocked intact artery responses, bu

111 These results indicate that nimodipine prevents alcoholic hepatitis, possibly by inh

112 to determine whether a Ca2+ channel blocker, nimodipine, prevents early alcohol-induced liver injury

113 Nimodipine produced a slowing of pacemaking frequency.

114 omega-conotoxin GVIa and the L-type blocker nimodipine reduced mIPSC frequency.

115 The L-type Ca2+ channel inhibitor nimodipine reduced the frequency of Ca2+ oscillations at

116 The calcium channel antagonist, nimodipine, reduced significantly the antinociception in

117 modipine-sensitive, and Omega-conotoxin GVIA/nimodipine-resistant calcium currents, but it does not b

118 polarization and resultant activation of the nimodipine sensitive L- and conotoxin-sensitive N-type v

119 hreshold to activating a Ca2+ spike evoked a nimodipine-sensitive Ca2+ "hump" potential.

120 The voltage dependence of activation of the nimodipine-sensitive current could be fit with a single

121 Half-maximal activation of the nimodipine-sensitive current occurred at -30 mV, conside

122 d a non-inactivating, low-voltage-activated, nimodipine-sensitive current that was enhanced by the se

123 t Green revealed a depolarisation-activated, nimodipine-sensitive Zn2+ influx into cortical neurones

124 by allowing activation of sub-myelin L-type (nimodipine-sensitive) Ca(2+) channels.

125 increases in Omega-conotoxin GVIA-sensitive, nimodipine-sensitive, and Omega-conotoxin GVIA/nimodipin

126 ) (Ca(V)2.2), and pharmacological block with nimodipine showed an absence of alpha(1B) trafficking.

127 rons with the L-type Ca2+ channel antagonist nimodipine significantly enhanced survival.

128 ollowing 30 days treatment with LEMS plasma, nimodipine significantly reduced the remaining quantal c

129 was separated from the endogenous current by nimodipine subtraction.

130 n potentials and a relative insensitivity to nimodipine suggest the channels were of the alpha1D (CaV

131 ites than in the soma and were attenuated by nimodipine, suggesting a compartmentalization of Ca2+ si

132 channels, and was blocked by treatment with nimodipine, thapsigargin, or ryanodine, but not by the I

133 mega-conotoxin GVIA, omega-agatoxin IVA, and nimodipine to cultured cerebellar granule neurons from w

134 Nimodipine treatment attenuated clinical EAE and spinal

135 ted potassium current, and in current clamp, nimodipine usually depolarized cells and slowed firing o

136 own with short hairpin RNA and diltiazem and nimodipine, voltage-dependent Ca(2+) channel blockers, r

137 Under the depolarized condition, nimodipine was a more potent antagonist, inhibiting Ca2+

138 This effect of nimodipine was blocked by either a selective alpha2 anta

139 When nimodipine was given before the motor task learning and

140 The current blocked by nimodipine was greater in aged neurons, indicating that

141 dihydropyridine calcium channel antagonist, nimodipine, was found to decrease the extent of toleranc

142 The women who received nimodipine were more likely to have a seizure than those

143 y inhibitors of calcium influx (diazoxide or nimodipine), whereas a protein synthesis inhibitor (emet

144 ions of two LVGCC inhibitors, nifedipine and nimodipine, which both effectively cross the blood-brain

145 y high extracellular calcium, gadolinium, or nimodipine, which suggests that L-type calcium channels

146 ve channels blocked with the dihydropyridine nimodipine with virtual channels generated by dynamic cl