ライフサイエンスコーパス: nifedipine

1 ity (isoproterenol, Y27632, pilocarpine, and nifedipine).

2 nel antagonists (1 mm diltiazem or 20 microm nifedipine).

3 ked by the L-type calcium channel inhibitor, nifedipine).

4 , or by the L-type Ca(2+) channel antagonist nifedipine.

5 ndogenous I(Ca,L), which was suppressed with nifedipine.

6 234), but not isoproterenol, pilocarpine, or nifedipine.

7 se in [Ca(2+)](i) was partially inhibited by nifedipine.

8 micromol/L), as well as the I(Ca,L) blocker nifedipine.

9 ivating inward current that was abolished by nifedipine.

10 odulated by the Ca(V)1Ca(2+) channel-blocker nifedipine.

11 ere not inhibited by neuronal antagonists or nifedipine.

12 and was mimicked by Bay K8644 and blocked by nifedipine.

13 ains of action potentials in the presence of nifedipine.

14 44, and depressed or eliminated by cobalt or nifedipine.

15 s, although both were inhibited by 10 microM nifedipine.

16 erpolarizing currents and was not blocked by nifedipine.

17 nts were rare and smaller in the presence of nifedipine.

18 ts and Ca2+ transients were fully blocked by nifedipine.

19 but was unaffected by addition of 10 microM nifedipine.

20 n sham or AVP dogs treated with saralasin or nifedipine.

21 was mimicked by the calcium channel blocker, nifedipine.

22 change mimicking STM that was suppressed by nifedipine.

23 eincubation with 4.1 microm STX or 20 microm nifedipine.

24 romol/l of the L-type Ca(2+)-channel blocker nifedipine.

25 pacemaker) currents that were not blocked by nifedipine.

26 TX) or by the L-type Ca2+ channel antagonist nifedipine.

27 itivity to the l-type Ca(2+) channel blocker nifedipine.

28 oltage-dependent calcium channels (L-VDCCs), nifedipine.

29 Cav1.3/Cav1.2 selectivity in comparison with nifedipine.

30 l conditions to the facilitation observed in nifedipine.

31 of control in the presence of 20 nmol l(-1) nifedipine.

32 Inhibition of CaV1.2 channels with nifedipine (0.1 micromol/L) or diltiazem (10 micromol/L)

33 Nifedipine (1 mg kg-1, I.V.) reduced the peak magnitude

34 itivity to the L-type Ca(2+) channel blocker nifedipine (1 microm) (100 +/- 29%).

35 th capsaicin (10 microM), were unaffected by nifedipine (1 microM) and did not require the mucosa or

36 Nifedipine (1 microm) had no effect, suggesting that the

37 ha,beta-methylene ATP (1 microM), but not by nifedipine (1 microM) or prazosin (100 nM), suggesting t

38 In the presence of nifedipine (1 microm), an ongoing discharge of excitator

39 shed by the L-type Ca(2+) channel antagonist nifedipine (1 microm).

40 Blocking Ca2+ influx with nifedipine (1 muM) or levcromakalim (10 muM) had no effe

41 In the presence of nifedipine (1-2 microm) to paralyse the muscle, simultan

42 ring colonic MMC activity in the presence of nifedipine (1-2 microm).

43 NO release was reduced (18-24%) by nifedipine (10 microm) and potentiated (29-32%) by incub

44 ence of the L-type Ca(2+) channel inhibitor, nifedipine (10 microM), partially inhibited 17beta-estra

45 I(Na) was insensitive to nifedipine (10 microM).

46 Nifedipine (10-6 M) and indomethacin (10-5 M) were inclu

47 Of the 12 patients who tolerated a trial of nifedipine,10 (83%) reported decreased or resolved nippl

48 production similar to high concentration of nifedipine (100 muM).

49 were randomly assigned to receive 10 mg oral nifedipine, 200 mg oral labetalol (hourly, in both of wh

50 is: 298 (33%) women were assigned to receive nifedipine, 295 (33%) women were assigned to receive lab

51 nel antagonists diltiazem (10 and 30 mum) or nifedipine (3 mum).

52 Tamsulosin 400 mug and nifedipine 30 mg are not effective at decreasing the nee

53 randomisation system to tamsulosin 400 mug, nifedipine 30 mg, or placebo taken daily for up to 4 wee

54 om Scn5a+/Delta and WT hearts confirmed that nifedipine (300 nm) completely suppressed the inward Ca2

55 LY294002 (20 micromol/L) and nifedipine (50 nmol/L) abolished Ca2+-induced spontaneou

56 atment with AACOCF3 (an inhibitor of cPLA2), nifedipine (a Ca(2+) channel blocker), or 3'-methyl-4'-n

57 Pretreatment of the muscles with nifedipine (a Ca2+ channel blocker) and gadolinium(III)

58 s sensitive to the antioxidant trolox and to nifedipine, a blocker of L-type voltage-dependent Ca(2+)

59 Nifedipine, a calcium channel blocker, most robustly ame

60 entified the accepted mechanism of action of nifedipine, a calcium-channel blocker clinically used in

61 In contrast, nifedipine, a CaV 1.2 inhibitor, markedly suppressed STO

62 cities, and whose initiation is prevented by nifedipine, a finding that in turn may have therapeutic

63 g fast inactivation and resistance to 20 mum nifedipine, a l-type Ca(2+) channel blocker, is sufficie

64 As a control experiment, nifedipine, a L-type voltage sensitive calcium channel (

65 type calcium channel blockers nimodipine and nifedipine abolished the plateau potential observed unde

66 UV flashes to reverse inhibition of I(Ca) by nifedipine accelerated replenishment.

67 mately 225 nM, and abolition of beating with nifedipine, acetylcholine or adenosine caused a fall in

68 duced by short- and long-term tacrolimus and nifedipine administration, alone or in combination, and

69 ced constrictions were sensitive to block by nifedipine after depletion of intracellular Ca(2+) store

70 injections of L-type Ca(2+) channel blocker nifedipine after stress resulted in a significantly lowe

71 ed preterm labor, maintenance tocolysis with nifedipine, after an initial course of tocolysis and cor

72 Nifedipine also ameliorated the motor defects of other m

73 Nifedipine also inhibited spontaneous action potentials

74 TTX and nifedipine also prevented the neuroprotection elicited b

75 olution and block of L-type Ca2+ channels by nifedipine also resulted in a cessation of spontaneous a

76 Nifedipine, amiloride and ethylisopropylamiloride were i

77 l lines and exposed them to 4 different CCBs-nifedipine, amlodipine, diltiazem, and verapamil-at thei

78 This Ca(2+) influx was blocked by nifedipine (an inhibitor of L-type voltage-gated Ca(2+)

79 Endocytosis of CHL1 is also reduced by nifedipine, an inhibitor of the L-type voltage-dependent

80 Nifedipine, an inhibitor of voltage-operated Ca(2+) chan

81 Nifedipine, an L-type Ca(2+) channel blocker, decreased

82 s novel effect of Gbeta5-RGS7 was blocked by nifedipine and 2-aminoethoxydiphenyl borate.

83 y 7, 2014, we randomly assigned 254 women to nifedipine and 256 to atosiban.

84 nt rates were 4.60 per 100 patient-years for nifedipine and 4.75 per 100 patient-years for placebo (0

85 mechanisms of action of the dihydropyridine nifedipine and an isosteric 4-phenyl-pyran.

86 Although nifedipine and Bay K 8644 occupy the same fenestration s

87 However AHP is not blocked by nifedipine and is insensitive to [Cl-]o.

88 fic inhibitors of LCCs and reverse-mode NCX, nifedipine and KB-R7943, respectively.

89 e primary outcome did not differ between the nifedipine and labetalol groups (249 [84%] women vs 228

90 so we could silence endogenous Ca(V)1.2 with nifedipine and maintain peak I(Ca) at control levels in

91 By contrast, nifedipine and nimodipine only partially reduced airway

92 ype voltage-gated Ca(2+) channel inhibitors (nifedipine and nimodipine) on airway contraction and Ca(

93 systemic injections of two LVGCC inhibitors, nifedipine and nimodipine, which both effectively cross

94 tetrodotoxin, calcium currents sensitive to nifedipine and omega-conotoxin GVIA, and sustained as we

95 nding that GLP-1 release was blocked both by nifedipine and omega-conotoxin MVIIC.

96 The complex effects of nifedipine and oxytocin exposure are simulated.

97 L-type Ca(2+) channel blocker nifedipine and phospholipase C inhibitor U73122 inhibite

98 Nifedipine and polyvinylpyrrolidone were dissolved in te

99 hibited the P450 3A4-catalyzed oxidations of nifedipine and quinidine, two prototypic substrates, in

100 of hydrogen bonding between the N-H group of nifedipine and the C=O group of PVP was observed and thi

101 ss and safety of the calcium-channel blocker nifedipine and the oxytocin inhibitor atosiban in women

102 on, we show that the calcium channel blocker nifedipine and the Rho-kinase inhibitor ROCKi significan

103 ished by the L-type Ca(2+) channel inhibitor nifedipine and the Src family kinase inhibitor PP2.

104 I(CaL) was blocked with nifedipine and then a hybrid patch clamp/mathematical-mo

105 inactivation and confer high sensitivity to nifedipine and to internal EGTA, are essentially involve

106 ucing frequencies of calcium transients with nifedipine and TTX reduced the incidence of differential

107 ved that the L-type calcium channel blockers nifedipine and verapamil effectively inhibited electrica

108 ns, or perfusion with the L-type antagonists nifedipine and verapamil strongly diminished the phloret

109 bition of unidirectional (45)Ca(2+) entry by nifedipine and verapamil.

110 Both nifedipine and Y-27632 prevented the depolarization-indu

111 ing AP recording, I(CaL) was inhibited (3 um nifedipine) and replaced by a dynamic clamp model curren

112 mine, labetalol), a calcium channel blocker (nifedipine), and splanchnic vasodilators (nitroglycerine

113 p modulators verapamil (IC(50)=12.1 muM) and nifedipine, and also by praziquantel, the current drug o

114 ergrowth induced by drugs such as phenytoin, nifedipine, and cyclosporin develops due to an increase

115 Medication with phenytoin, nifedipine, and cyclosporine-A often causes gingival ove

116 All three oral drugs-methyldopa, nifedipine, and labetalol-are viable initial options for

117 of the ET(A) receptor antagonist sitaxentan, nifedipine, and placebo on proteinuria, BP, arterial sti

118 Nifedipine- and cyclosporine A-induced gingival overgrow

119 resence of inflammation and little fibrosis, nifedipine- and especially phenytoin-induced lesions are

120 Nifedipine appears to be an effective medication for the

121 smooth muscle relaxant drugs tamsulosin and nifedipine assisted stone passage for people managed exp

122 eparations stopped beating in 100 micromol/L nifedipine at 1 day old, compared with 30 micromol/L at

123 Delta and WT hearts following perfusion with nifedipine at 1 nm, 10 nm, 100 nm, 300 nm and 1 microm n

124 was blocked by pretreating the animals with nifedipine at 2 mg/kg.

125 ective than betaxolol and much stronger than nifedipine at attenuating veratridine-induced influx of

126 X, reduction in external Na+, application of nifedipine at concentrations below 300 nM or substitutio

127 The L-type Ca(2+) channel blocker nifedipine attenuated cell death, suggesting excessive C

128 dependent calcium channels with diltiazem or nifedipine attenuated S1P-mediated vasoconstriction.

129 At 0 mV, the IC50 for nifedipine blockade of VICaR in the form of syntillas wa

130 harmacological inhibition with diazoxide and nifedipine, blocked the effects of glucose.

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

132 lar Ca2+ response to glucose was impaired by nifedipine but not by tetrodotoxin.

133 In secretion experiments, however, nifedipine, but not tetrodotoxin, omega-conotoxin GVIA o

134 Treatment with Nifedipine (Ca(2+) antagonist and vasodilator) prevented

135 In contrast nifedipine (Ca2+ channel block) and 2 mm Cs+ (HCN comple

136 n), L-type Ca channel (I(Ca,L)) antagonists (nifedipine, cadmium, verapamil), and agonists (Bay K 864

137 he control group indicates that a benefit of nifedipine cannot completely be excluded, its use for ma

138 hereas the equivalent marketed liquid filled nifedipine capsule took 3 times longer to reach 80% diss

139 w-omega-conotoxin GVIA (Cav2.2-selective) or nifedipine (Cav1.2-1.3-selective) [corrected].

140 n IC50 of 0.37 muM for current inhibition by nifedipine, CaV1.1e is a potential drug target for the t

141 entry in liver sinusoids, whereas labetalol, nifedipine, CGRP, and glucagon were ineffective.

142 at 1 nm, 10 nm, 100 nm, 300 nm and 1 microm nifedipine concentrations.

143 gated L-type calcium channel (VGLCC) blocker nifedipine, consistent with the finding that allopregnan

144 was observed and this interaction inhibited nifedipine crystallisation.

145 voltage-gated calcium channels (VGCCs) with nifedipine decreases the number of GABA(A)Rs at synaptic

146 , but only the L-type Ca(2+) channel blocker nifedipine demonstrated cytoprotective effects comparabl

147 Nifedipine depressed (did not block) the Na2S2O4-induced

148 raphy and interventions in patients assigned nifedipine, despite an increase in peripheral revascular

149 deprivation was not seen in the presence of nifedipine, diazoxide, or tolbutamide or if K(ATP) chann

150 After 6 weeks of treatment, placebo and nifedipine did not affect plasma urate, ADMA, or urine E

151 Intra-BLA infusions of verapamil or nifedipine did not affect the expression of fear conditi

152 L-type voltage-gated calcium channel blocker nifedipine did not suppress calcium oscillations, the N-

153 DIR, but the L-type calcium channel blocker nifedipine did not.

154 310 patients allocated nifedipine died (1.64 per 100 patient-years) compared wi

155 complex with archetypal antagonistic drugs, nifedipine, diltiazem, and verapamil, at resolutions of

156 ium-channel blocker (amlodipine, felodipine, nifedipine, diltiazem, or verapamil).

157 while chronic intraperitoneal treatment with nifedipine during a period of synaptic consolidation enh

158 cium influx was occluded by cotreatment with nifedipine during glutamate application, suggesting that

159 duced in a concentration-dependent manner by nifedipine (ED50=159+/-54 nM) and Ni2+ (ED50=65+/-16 mic

160 Nifedipine either eliminated channel activity, had no ef

161 orted by experiments in which application of nifedipine eliminated Ca(i)2+ decrease at DeltaV+m sites

162 Furthermore, pretreatment with 1 muM nifedipine exerted a strong anti-arrhythmic effect in th

163 n of unidirectional (45)Ca(2+) absorption by nifedipine exerted similar effects.

164 The L-type Ca(2+) channel blocker nifedipine failed to ameliorate bifenthrin-triggered SCO

165 d more brain-penetrant dihydropyridines (eg, nifedipine, felodipine) on parkinsonism milestones as me

166 Nifedipine, flunarizine, and betaxolol all reduced the N

167 week control; 5) tacrolimus for 24 weeks; 6) nifedipine for 24 weeks; 7) tacrolimus and nifedipine fo

168 ) nifedipine for 24 weeks; 7) tacrolimus and nifedipine for 24 weeks; and 8) 24-week control.

169 eight groups: 1) tacrolimus for 8 weeks; 2) nifedipine for 8 weeks; 3) tacrolimus and nifedipine for

170 2) nifedipine for 8 weeks; 3) tacrolimus and nifedipine for 8 weeks; 4) 8-week control; 5) tacrolimus

171 coronary disease to double-blind addition of nifedipine GITS (gastrointestinal therapeutic system) 60

172 Nifedipine GITS is safe and reduces the need for coronar

173 Addition of nifedipine GITS to conventional treatment of angina pect

174 L-type Ca channels with the specific blocker nifedipine greatly reduced prolonged poststimulus firing

175 to 8.3]; p=0.73) and 304 (80%) of 379 in the nifedipine group (0.5% [-5.6 to 6.5]; p=0.88).

176 s were reported in three participants in the nifedipine group (one had right loin pain, diarrhoea, an

177 vailable for 248 women and 297 babies in the nifedipine group and 255 women and 294 babies in the ato

178 y outcome occurred in 42 babies (14%) in the nifedipine group and in 45 (15%) in the atosiban group (

179 16 (5%) babies died in the nifedipine group and seven (2%) died in the atosiban gro

180 as significantly more common in women in the nifedipine group than in those in the methyldopa group (

181 11 (4%) women in the nifedipine group, ten (3%) women in the labetalol group,

182 six (1%) neonates (one [<1%] neonate in the nifedipine group, two [1%] neonates in the labetalol gro

183 Nifedipine had a depressing effect.

184 tone in PAs of chronic hypoxic animals, but nifedipine had minimal effects.

185 Nifedipine had no effect on the rate of myocardial infar

186 dropyridine Ca(2+) channel blockers, such as nifedipine, have been used for treatment of idiopathic p

187 and inhibited by the calcium channel blocker nifedipine in a dose-dependent manner.

188 o glucose was not significantly decreased by nifedipine in Ca(v)1.3/DHPi cells but was greatly reduce

189 Rosetta predicted receptor sites for nifedipine in the fenestration region and for the 4-phen

190 an lymphatic vessels are highly sensitive to nifedipine in vitro but that care must be taken when ext

191 re, we report that the dihydropyridines (eg, nifedipine) increase [Ca(2+)](cyt) by activating CaSR in

192 The Ca2+ channel blocker nifedipine increased the stability of VF frequencies and

193 These transients were blocked by TTX and nifedipine, indicating that they resulted from Ca2+ infl

194 oxin or alpha-amanitin but is insensitive to nifedipine, indicating that uncoupling is contingent upo

195 Perfusion of KCNE1-/- hearts with 1 mum nifedipine induced potentially anti-arrhythmic changes i

196 NA in IPAH-PASMC significantly inhibited the nifedipine-induced increase in [Ca(2+)](cyt), whereas ov

197 ession of CaSR in normal PASMC conferred the nifedipine-induced rise in [Ca(2+)](cyt).

198 Inhibition of LTCCs with felodipine or nifedipine induces progressive cortical cataract formati

199 The nifedipine-insensitive sustained rise in [Ca(2+)](i) and

200 Oxidation of the calcium-channel blocker nifedipine is measured using UV-Vis spectroscopy in-line

201 While nifedipine is thus not a pore blocker and might be stabi

202 In 10 microM nifedipine, KCl-elicited [Ca(2+)](i) elevation was retai

203 Pretreatment of muscle with nifedipine (L-type calcium channel antagonist) marginall

204 enzymes have been documented in phenytoin or nifedipine lesions.

205 ing fast inactivation and low sensitivity to nifedipine, mainly control the fast fusion of the readil

206 h slow inactivation and great sensitivity to nifedipine, mainly regulate the vesicular replenishment

207 In patients with threatened preterm labor, nifedipine-maintained tocolysis did not result in a stat

208 The nifedipine-mediated increase in [Ca(2+)](cyt) in IPAH-PA

209 her LTCC antagonists (diltiazem, nimodipine, nifedipine, methyoxyverapamil and isradipine) and for ot

210 Our preliminary data showed that nifedipine might be beneficial in preventing cocaine-ind

211 zoxide or the l-type calcium channel blocker nifedipine mimicked the effect of insulin, suggesting th

212 ve to tetrodotoxin (n=10) but was blocked by nifedipine (n=10) and cadmium (n=3).

213 idative metabolism of testosterone (TST) and nifedipine (NIF) was assessed by LC-MS/MS.

214 sts, including pregnenolone sulfate (PS) and nifedipine (Nif).

215 elective blockade of L-type Ca2+ channels by nifedipine not only significantly increased the threshol

216 single-cell imaging to study the effects of nifedipine on [Ca(2+)](i) signalling in human sperm.

217 ions of the L-VGCC antagonists verapamil and nifedipine on both within-session extinction and fear ex

218 stigate the effect of the calcium antagonist nifedipine on long-term outcome in patients with stable

219 However, in 10 microM nifedipine, only Ca(v)1.3/DHPi cells maintained glucose-

220 atened preterm birth, 48 h of tocolysis with nifedipine or atosiban results in similar perinatal outc

221 cted by superfusion of Ca(2+)-free solution, nifedipine or Bay K 8644, excluding the direct involveme

222 ating rat islet beta-cell Ca(2+) influx with nifedipine or depolarization demonstrated that glucose-i

223 In contrast, the Ca2+channel blockers nifedipine or diltiazem (1 microm) had a negligible effe

224 -induced increase in pH(i) is not blocked by nifedipine or high K(+), whereas the FSP-induced pH(i) i

225 were randomly assigned (1:1) to either oral nifedipine or intravenous atosiban for 48 h.

226 itude of the nonlinear DD (ryanodine, BAPTA, nifedipine or isoproterenol) produced corresponding chan

227 Blockade of either L-type Ca2+ channels by nifedipine or N-type Ca2+ channels by omega-conotoxin GV

228 Pretreatment with nifedipine or the K(ATP) inhibitor glyburide prevented i

229 highest with dihydropyridines, particularly nifedipine (OR, 5.33 [95% CI, 3.39-8.38]; absolute risk

230 d by the voltage-gated Ca channel inhibitor, nifedipine, or by hyperpolarization with diazoxide.

231 principally as side-effects from phenytoin, nifedipine, or ciclosporin therapy in approximately half

232 STM dogs received placebo, nifedipine, or propranolol, and LTM dogs received placeb

233 inoculated animals were treated with trolox, nifedipine, or the adenosine receptor 2A antagonist KW60

234 l blockers such as verapamil, diltiazem, and nifedipine, or the nonselective Ca2+,Na+ channel blocker

235 gned 406 women to maintenance tocolysis with nifedipine orally (80 mg/d; n = 201) or placebo (n = 205

236 ed methoxyresorufin-O-demethylase (MROD) and nifedipine oxidase activities, respectively, and were 30

237 Nifedipine oxidation was inhibited when the cholesterol

238 placebo (p=0.78), or between tamsulosin and nifedipine (p=0.77).

239 faster despite all subjects achieving target nifedipine plasma concentrations.

240 PVP's high affinity for water and the nifedipine-polymer interaction lead to a significant dis

241 ined responses were significantly reduced in nifedipine pretreated cells.These findings are consisten

242 (2+) entry, neither omega-conotoxin-GVIA nor nifedipine prevented ATP release.

243 Moreover, coapplication of Z-VAD-FMK and nifedipine produced virtually complete neuroprotection.

244 Initial findings confirmed that nifedipine progressively dilated depolarization-induced

245 The freeze-dried capsule, 10%w/w nifedipine/PVP, had the highest dissolution rate constan

246 With nifedipine, rate of death and any cardiovascular event o

247 Although L-VOCC inhibitor nifedipine reduced basal tone and blocked vasoconstricti

248 Calcium channel blockade by nifedipine reduced primiR-199a2 promoter activity in MIN

249 numbers of cells showed that treatment with nifedipine reduced the duration but not the amplitude of

250 The calcium channel blocker nifedipine reduced, and the sarcoplasmic reticulum calci

251 Overnight incubations with nifedipine rescue Na(V) channel density, normal firing a

252 t incubation with the L-type channel blocker nifedipine rescued the normal AP firing of CCs, the dens

253 c sum of the amplitudes of the KB-R7943- and nifedipine-resistant components (deltaF(Tot)=deltaF(LCC)

254 e-resistant slow increase in [Ca(2+)](i) and nifedipine-resistant insulin secretion in response to gl

255 Nifedipine-resistant RRP exocytosis was poorly affected

256 g the II-III loop of Ca(v)1.3 demonstrated a nifedipine-resistant slow increase in [Ca(2+)](i) and ni

257 rfusion with 10 nm, 100 nm, 300 nm and 1 mum nifedipine, respectively (P < 0.05; n = 5), giving an ef

258 rfusion with 10 nm, 100 nm, 300 nm and 1 mum nifedipine, respectively.

259 As single drugs, nifedipine retard use resulted in a greater frequency of

260 y and safety of three oral drugs, labetalol, nifedipine retard, and methyldopa for the management of

261 of rabbit Ca(v) 1.1 bound to an achiral drug nifedipine reveals the general binding mode for DHP drug

262 cultured primary neurons and was blocked by nifedipine, ryanodine, and lack of extracellular Ca(2+)

263 ed sensitivity to the L-type calcium blocker nifedipine; SA node preparations stopped beating in 100

264 elerating protein activity, couples M3R to a nifedipine-sensitive Ca(2+) channel.

265 neurons of the VTA and substantia nigra via nifedipine-sensitive Ca(2+) channels.

266 m -80 mV to the range -40 to -10 mV evoked a nifedipine-sensitive Ca(2+) current that was followed by

267 rexpression recovered a wild-type density of nifedipine-sensitive Ca2+ currents with a slow activatio

268 lation rely on calcium entry via La(3+)- and nifedipine-sensitive calcium channels.

269 hannel opening by decreasing the activity of nifedipine-sensitive calcium channels.

270 onsistent with the occurrence of a discrete, nifedipine-sensitive component of the progesterone-induc

271 eases in its [Ca(2+)](i) via activation of a nifedipine-sensitive current.

272 on-induced activation of VGCCs resulted in a nifedipine-sensitive increase in endogenous smooth muscl

273 tal cells, consisting of a modulation of the nifedipine-sensitive, voltage-gated calcium current.

274 se-induced component was SGLT1-dependent and nifedipine-sensitive.

275 The L-type calcium channel blocker, nifedipine, significantly attenuated this afferent firin

276 ence of impermeable calcium channel blockers nifedipine, SKF96365, or LaCl3, inhibited PAR-1-induced

277 Both nicardipine and nifedipine stimulated the ATPase activity of ABCG2, and

278 ulated the ATPase activity of ABCG2, and the nifedipine-stimulated activity was inhibited by fumitrem

279 ced constrictions in MVs were blocked 80% by nifedipine suggesting restoration of Ca(2+) influx throu

280 Resting potentials can be restored by nifedipine, suggesting a tonic, depolarizing action of L

281 The block of this current by nifedipine suggests the direct involvement of Ca(v)1.3 C

282 I(CaL,D-C) -injection restored the nifedipine-suppressed AP plateau.

283 d (dis-inhibited) by rapidly photo-degrading nifedipine, the Ca(2+) channel blocker.

284 er channel, e.g. the calcium channel blocker nifedipine, the sodium channel blocker quinidine, etc.

285 lymphatics ex vivo were highly sensitive to nifedipine, this was not apparent in vivo when nifedipin

286 dihydropyridine Ca(2+) channel blockers (eg, nifedipine) to treat IPAH patients with upregulated CaSR

287 Moreover, acute nifedipine treatment potentiated neurotransmission at ne

288 not evident in our clinical trial comparing nifedipine treatment to placebo.

289 ogically in vitro and in vivo using glucose, nifedipine (VDCC blocker), the sulfonylureas tolbutamide

290 ne, S107) and L-type Ca(2+) channels (LTCCs: nifedipine, verapamil, diltiazem) prevented the decrease

291 In the presence of nifedipine, very few cells peaked "late" (>60 s after ap

292 oups: 11.9% (24/201; 95% CI, 7.5%-16.4%) for nifedipine vs 13.7% (28/205; 95% CI, 9.0%-18.4%) for pla

293 fedipine, this was not apparent in vivo when nifedipine was compared to placebo in a randomized, doub

294 Capsules containing 10 mg of nifedipine were amorphous and stable for over 3 months a

295 The effects of niflumic acid and nifedipine were non-additive.

296 1,4-dihydropyridines such as nicardipine and nifedipine, which are clinically used as antihypertensiv

297 mpared with the common antihypertensive drug nifedipine, which has 4.5-fold selectivity for the vascu

298 as blocked by the dihydropyridine antagonist nifedipine, which immobilizes the gating charge of DHPRs

299 peutic concentrations (nanomolar) of the CCB nifedipine while higher than therapeutic concentrations

300 resence of the L-type Ca(2+) channel blocker nifedipine, whilst antagonism of NMDA receptors did not