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 l for tetraethylammonium, charybdotoxin, and nifedipine.

28 the dihydropyridine receptor (DHPR)-blocker nifedipine.

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

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

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

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

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

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

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

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

37 Nifedipine (1 microM) during refilling reduced the caffe

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

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

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

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

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

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

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

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

46 Brief exposure to nifedipine (10 microM) did not reduce the number of spon

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

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

49 reduced the amplitude by -35 +/-4 %, whereas nifedipine (10 microM; L-type) and omega-conotoxin MVIIC

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

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

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

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

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

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

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

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

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

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

60 Furthermore, pretreatment of cells with nifedipine, a calcium channel blocker, inhibited vanadiu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

81 oth oscillations were inhibited by 20 microM nifedipine, an L-type calcium channel antagonist, and 20

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 ompare the effectiveness of flunarizine with nifedipine and betaxolol at reducing the influx of calci

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

90 By contrast, nifedipine and nimodipine only partially reduced airway

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

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

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

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

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

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

97 Nifedipine and polyvinylpyrrolidone were dissolved in te

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

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

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

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

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

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

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

105 In addition, nifedipine and verapamil inhibited the expression of myo

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

107 In the presence of nifedipine and verapamil, myoblasts failed to form myotu

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

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

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

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

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

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

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

115 Nifedipine- and cyclosporine A-induced gingival overgrow

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

117 Nifedipine appears to be an effective medication for the

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

140 was observed and this interaction inhibited nifedipine crystallisation.

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

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

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

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

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

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

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

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

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

150 310 patients allocated nifedipine died (1.64 per 100 patient-years) compared wi

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

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

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

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

155 Nifedipine either eliminated channel activity, had no ef

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

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

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

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

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

161 Nifedipine, flunarizine, and betaxolol all reduced the N

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

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

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

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

166 ventricular (LV) mass reduction than does a nifedipine gastrointestinal treatment system by a progno

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

168 Nifedipine GITS is safe and reduces the need for coronar

169 Addition of nifedipine GITS to conventional treatment of angina pect

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

171 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).

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

173 minutes) in the NHEI group compared with the nifedipine group (P:=0.05).

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

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

176 16 (5%) babies died in the nifedipine group and seven (2%) died in the atosiban gro

177 ts in the NHEI group than in the control and nifedipine groups (P:=0.05).

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

179 Nifedipine had no effect on the rate of myocardial infar

180 Photodegraded nifedipine has been shown to increase uptake of nontrans

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

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

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

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

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

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

187 Photodegraded nifedipine increased iron uptake into keratinocytes 80-f

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

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

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

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

192 ues compared to controls, cyclosporin A-, or nifedipine-induced gingival overgrowth.

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

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

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

196 acellular electrical recordings demonstrated nifedipine-insensitive slow waves throughout the circula

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

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

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

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

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

202 enzymes have been documented in phenytoin or nifedipine lesions.

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

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

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

206 Photodegraded nifedipine may be a way delivering clinically significan

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

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

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

210 s undergoing therapy with phenytoin (n = 9), nifedipine (n = 4), cyclosporin A (n = 5), and control t

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

232 not microsomes from control, dexamethasone-, nifedipine-, or diltiazem-treated rats.

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

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

235 Nifedipine oxidation was inhibited when the cholesterol

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

237 faster despite all subjects achieving target nifedipine plasma concentrations.

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

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

240 (2+) entry, neither omega-conotoxin-GVIA nor nifedipine prevented ATP release.

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

242 Initial findings confirmed that nifedipine progressively dilated depolarization-induced

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

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

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

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

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

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

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

250 Nifedipine-resistant RRP exocytosis was poorly affected

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

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

253 ) channel blockers, omega-conotoxin GVIA and nifedipine, respectively, significantly inhibited the An

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

255 ransfected cells, the blocking of which with nifedipine restored apoptosis to the level of untransfec

256 Experiments with verapamil and nifedipine revealed that calcium influx is essential for

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

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

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

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

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

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

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

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

265 This nifedipine-sensitive current reversed at +29 +/- 2 mV, w

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

267 ic reticulum Ca2+-ATPase) also activated the nifedipine-sensitive sustained current.

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

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

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

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

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

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

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

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

276 ial K(+) depolarization or by application of nifedipine, suggesting that these RyR1 events are indepe

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

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

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

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

281 We investigated the ability of photodegraded nifedipine to stimulate iron transport and accumulation

282 Nifedipine to the site of stimulation (oral chamber) abo

283 Cell Ca2+ was then lowered by 1 microM nifedipine (to 135 +/- 22 nM), which reversed on washout

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

285 Moreover, acute nifedipine treatment potentiated neurotransmission at ne

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

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

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

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

290 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

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

292 Nifedipine was degraded to its nitroso derivative by exp

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

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

295 Responses to KCl and nifedipine were not different among groups.

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