ライフサイエンスコーパス: verapamil

1 or no effect (haloperidol, moxifloxacin, and verapamil).

2 ipine, felodipine, nifedipine, diltiazem, or verapamil).

3 Q-sensitive) P. falciparum by agents such as verapamil.

4 and in vivo in diabetic mice receiving oral verapamil.

5 oline, bradykinin, sodium nitroprusside, and verapamil.

6 more effective intracellularly than neutral verapamil.

7 bited by the chloroquine resistance-reverser verapamil.

8 poprotein (HDL) to the drugs propranolol and verapamil.

9 bited by the human ABCB1 and ABCC1 modulator verapamil.

10 rectional (45)Ca(2+) entry by nifedipine and verapamil.

11 fibrosis can be attenuated by treatment with verapamil.

12 Finally, we treated mice with verapamil.

13 Gating currents were unaffected by verapamil.

14 c pigments but no such effects were seen for verapamil.

15 t shows the SP phenotype and is sensitive to verapamil.

16 he absence and 180 microM in the presence of verapamil.

17 an be reversed by the channel-blocking agent verapamil.

18 the absence of transport substrates such as verapamil.

19 ent mice with the calcium channel antagonist verapamil.

20 ents, before and after infusion of 0.1 mg/kg verapamil.

21 up and received a saline infusion instead of verapamil.

22 a low-dose therapy regimen of Cilengtide and Verapamil.

23 lism reactions of amodiaquine, buspirone and verapamil.

24 accumulation of the P-glycoprotein substrate verapamil.

25 IP shRNA-transfected mice or those receiving verapamil.

26 nts still symptomatic after beta-blockade or verapamil.

27 d PET scan of 60-min duration with (R)-(11)C-verapamil.

28 with the P-glycoprotein substrate (R)-[(11)C]verapamil.

29 investigated the effect of carbamazepine and verapamil (0.005-10 mg/kg) on a range of plant responses

30 Verapamil (0.3 mg/kg) also inhibited TdP, but caused a 1

31 to induce hHcys, and TXNIP was inhibited by verapamil (1 mg/ml in drinking water) or by local microb

32 A combination of NS5806 (3-10 mumol/L) and verapamil (1 mumol/L) was used to pharmacologically mode

33 Propranolol (1.0 micromol/L) or verapamil (1.0 micromol/L) completely suppressed ectopic

34 revented by 0.5 mmol/L [Ca2+]o, 1 micromol/L verapamil, 1 micromol/L atropine, 10 micromol/L L-N5-(1-

35 odium nitroprusside (2 to 8 microg/min), and verapamil (10 to 100 microg/min) infusions 2 and 6 hours

36 S5806 (5 muM) and the Ca(2+)-channel blocker verapamil (2 muM) were used to pharmacologically mimic t

37 72 mg; diltiazem: 212 mg versus 180 mg, and verapamil: 276 mg versus 200 mg, respectively (p < 0.01

38 fter the intravenous administration of (11)C-verapamil (30-72 MBq/kg) before and during intravenous i

39 aterally with either artificial perilymph or verapamil (50 microg/ml).

40 urred between 6 AM and noon in both the COER verapamil (99/277) and atenolol or hydrochlorothiazide (

41 ions has been demonstrated by a synthesis of verapamil, a clinically used drug for the treatment of h

42 cancer cells, a 2-fold increase compared to verapamil, a first-generation chemosensitizer.

43 as having higher potency than compound 1 and verapamil, a first-generation P-gp modulator.

44 cin-resistant 4T1-R breast cancer cells with verapamil, a general inhibitor of P-glycoprotein, increa

45 blocking torsadogen used for intractable AF, verapamil, a non-torsadogenic MICE comparator and beprid

46 significantly reduced brain accumulation of verapamil, a P-glycoprotein substrate.

47 likely MDR-mediated because cotreatment with verapamil, a P-gp inhibitor, partially reversed the sele

48 studied the dynamic biodistribution of (11)C-verapamil, a P-gp substrate, in the nonhuman primate Mac

49 -coupled NorM transporters in complexes with verapamil, a small-molecule pharmaceutical that inhibits

50 In the presence of verapamil, a substrate that activates ATP hydrolysis, th

51 We found that standard TB chemotherapy plus verapamil accelerates bacterial clearance in C3HeB/FeJ m

52 We propose that verapamil achieves its inhibitory effect via occlusion o

53 ease verapamil, we evaluated the activity of verapamil added to standard chemotherapy in both C3HeB/F

54 ese data demonstrate treatment shortening by verapamil adjunctive therapy in mice, and strongly suppo

55 Neither complementary fatty acid loading nor verapamil administered 1 h before (18)F-FDG injection co

56 ptor blockade, adenosine, nitroprusside, and verapamil against the aspirate-induced constriction were

57 Surprisingly, verapamil alone (1-300 microM) does not significantly af

58 Verapamil also gave similar behavior, with a K(a) of 6.0

59 Verapamil also improved transduction in human SCID (seve

60 Indomethacin and verapamil also inhibit the luminal Ca(2+) increase.

61 Verapamil also promoted beta-cell survival and improved

62 phate receptor-mediated calcium release, and verapamil, an inhibitor of L-type calcium channels, pref

63 ts in the absence but not in the presence of verapamil, an inhibitor of the export of monoacetyl diam

64 on with or without intracochlear infusion of verapamil, an L-type voltage-gated calcium channel antag

65 e voltage-gated Ca2+ channel (VGCC) blockers verapamil and (+)-cis-diltiazem significantly reduced th

66 Here, we show that low doses of verapamil and 2-deoxyglucose, to accentuate the cost of

67 y, 8241 participants received 180 mg of COER verapamil and 8361 received either 50 mg of atenolol or

68 changes were suppressed by pretreatment with verapamil and amlodipine.

69 ates calcein-AM, CellTrace RedOrange, BoDipy-verapamil and BoDipy-vinblastine, than any other cell in

70 was inhibited by the Ca(2+)-channel blocker verapamil and by the mitogen-activated protein kinase ki

71 (11)C-verapamil and compartmental analysis can estimate P-gp a

72 0-fold decrease in the apparent affinity for verapamil and cyclic peptide inhibitor QZ59-SSS was obse

73 progesterone), slightly overcoming those of verapamil and cyclosporin A.

74 of 40 patients met inclusion criteria, with verapamil and diltiazem accounting for 27 of 40 (67.5%)

75 The content of verapamil and its metabolites in plasma samples was dete

76 of local infusions of the L-VGCC antagonists verapamil and nifedipine on both within-session extincti

77 al nitroglycerin ointment, and intraarterial verapamil and nitroglycerin.

78 isease to reproduce the effects of the drugs verapamil and octreotide, and we show that the experimen

79 mice, and strongly support further study of verapamil and other efflux pump inhibitors in human TB.

80 At the CP, verapamil and probenecid (but not indomethacin) signific

81 with a detection limit of 8 and 25 fmol for verapamil and reserpine, respectively, and quantitation

82 macokinetic/pharmacodynamic relationships of verapamil and rifampin coadministration in mice.

83 Also, verapamil and TMB-8 were able to block the calcium respo

84 P-gp modulators verapamil and trans-flupenthixol and MDR1-targeted siRNA

85 n (by a factor of ~13, reaching 600 amol for verapamil), and extended dynamic range (6 orders of magn

86 th a labeled P-glycoprotein substrate, (11)C-verapamil, and (15)O-water to measure rCBF.

87 nated with adenosine, 2 of 2 terminated with verapamil, and 2 of 2 terminated with Valsalva.

88 ine the effects of propranolol, enalaprilat, verapamil, and caffeine on the vasodilatory properties o

89 Terfenadine, verapamil, and pinacidil each induced all-or-none repola

90 Norverapamil, R-verapamil, and potentially other derivatives present att

91 d type II cations (e.g., quinidine, quinine, verapamil, and rhodamine123) are also PMAT inhibitors.

92 nitroimidazole antifungal agents, diltiazem, verapamil, and troleandomycin; each doubles, at least, t

93 -generation calcium channel blockers such as verapamil are a widely used class of antihypertensive dr

94 Nitroprusside and verapamil are more potent than adenosine to attenuate th

95 TCC) blockers, represented by amlodipine and verapamil, are widely used antihypertensive drugs that a

96 rvative human bioequivalent doses, we tested verapamil as an adjunctive drug together with standard T

97 We used (11)C-verapamil as the prototypic P-gp substrate and cyclospor

98 the fraction of current blocked by 30 microM verapamil at 0.05 Hz stimulation.

99 ocking activity yet were similarly active as verapamil at inhibiting macrophage-induced drug toleranc

100 orrespondingly, TXNIP shRNA transfection and verapamil attenuated hHcys-induced proteinuria, albuminu

101 esponse to adenosine A(2A)-agonists, whereas verapamil attenuated this vasodilation through inhibitio

102 al did not demonstrate equivalence of a COER verapamil-based antihypertensive regimen compared with a

103 tely 172 d) underwent PET imaging with (11)C-verapamil before and during infusion (6, 12, or 24 mg/kg

104 ials, although all data were consistent with verapamil binding in the pore.

105 domain III may contribute to a high affinity verapamil binding site accessed during 1-Hz stimulation

106 In contrast, the phenylalkylamine Br-verapamil binds in the central cavity of the pore on the

107 ll significantly reduced frequency-dependent verapamil block (1-Hz stimulation) in both Ba(2+) and Ca

108 n mutations abolished Ca(2+) potentiation of verapamil block at 0.05 Hz.

109 Verapamil block of Ca(v)1.2 is frequency-dependent and p

110 le sites may be required for potentiation of verapamil block of closed channels.

111 ), but little is known about state-dependent verapamil block of T channels.

112 Verapamil blocked currents at micromolar concentrations

113 At clinically relevant concentrations, verapamil blocked hCav1.2 and hERG, as did vanoxerine an

114 Verapamil blocked this response, indicating an extracell

115 In T-type calcium channels, verapamil blocks with micromolar affinity and has modest

116 ntanoic acid, succinimidyl ester (bodipy-FL)-verapamil, bodipy-FL-vinblastine, calcein-AM, bodipy-FL-

117 al MDR susbtrates such as calcein-AM, bodipy-verapamil, bodipy-vinblastine, and mitoxantrone.

118 smethoxyverapamil (D888), is comparable with verapamil both in affinity and in state-dependence.

119 apamil radioactivity extraction ratio ((11)C-verapamil brain distributional clearance, K1/rCBF).

120 Dynamic (11)C-verapamil brain or fetal liver (reporter of placental P-

121 uivalent levels matched to those of standard verapamil, but lower than those of extended release vera

122 on of P-glycoprotein substrates morphine and verapamil, but not the tight junction marker, sucrose; t

123 anic cations carnitine, diphenhydramine, and verapamil, but penicillin and other organic anions faile

124 We determined that a dose adjustment of verapamil by 1.5-fold is required to compensate for conc

125 l control conferred by this newly identified verapamil-calcineurin-NFY signaling cascade was not limi

126 CQR including reduced drug accumulation and verapamil chemosensitization.

127 titive inhibitors, such as cyclosporin A and verapamil, cis-(Z)-flupentixol does not interfere with s

128 ethanol/water as solvent for the analysis of verapamil, citalopram, amitriptyline, lidocaine, and sun

129 es (diltiazem) and acetonitrile derivatives (verapamil, D600) and the insensitivity to non-L-type cal

130 Dynamic (11)C-verapamil data were assessed by a 2-tissue-compartment (

131 Verapamil decreased spatial dispersion of refractoriness

132 ha2-agonists, apical uptake was inhibited by verapamil, desipramine, and quinidine, but not by MPP+ (

133 ClC-2 inhibitor Cd2+, and the MDR-1 blocker verapamil did not affect EAA release or VRAC currents.

134 Verapamil did not affect nsPEF-induced Ca2+ transients,

135 The P-glycoprotein blocker verapamil did not interfere with (18)F-FBnTP cellular up

136 for resistance to GA overexpressed P-gp, but verapamil did not reverse the resistance.

137 d L-type Ca(2+) channels (LTCCs: nifedipine, verapamil, diltiazem) prevented the decrease in Ca(2+) t

138 certain macrolide antibiotics, antifungals, verapamil, diltiazem, and isoniazid.

139 embrane L-type Ca2+ channel blockers such as verapamil, diltiazem, and nifedipine, or the nonselectiv

140 For ventricular rate control, verapamil, diltiazem, atenolol, and metoprolol were qual

141 out concurrent use of atorvastatin; digoxin; verapamil; diltiazem; amiodarone; fluconazole; ketoconaz

142 ignificantly different for concurrent use of verapamil; diltiazem; cyclosporine; ketoconazole, itraco

143 activity at the human BBB using PET of (11)C-verapamil distribution into the brain in the absence and

144 We found a significant increase in (R)-(11)C-verapamil distribution to the retina during ABCB1 inhibi

145 We found a significant increase in (R)-(11)C-verapamil distribution to the retina during ABCB1 inhibi

146 Treatment of cells with verapamil does not affect ES-induced [Ca2+]i increases,

147 ter levels were achieved for propafenone and verapamil drugs.

148 t rest: atenolol, metoprolol, diltiazem, and verapamil (drugs listed alphabetically by class).

149 e (+E, 3.3x10(-8); -E, 1.9x10(-8) mol/L) and verapamil (+E, 8.3x10(-8); -E, 7.8x10(-8) mol/L), and th

150 le, ritonavir, clarithromycin, azithromycin, verapamil ER [extended release]), and diltiazem ER) on t

151 broadly prescribed calcium channel blockers (verapamil ER and diltiazem ER) and that the dose of colc

152 placers, including the single enantiomers of verapamil, fenoterol, and isoproterenol.

153 dazole (FMISO) for tissue hypoxia, and (11)C-verapamil for P-glycoprotein activity, in comparison wit

154 Colo-26 cells in the absence or presence of verapamil, for their dark and phototoxicity toward Colo-

155 blocked significantly more slowly by charged verapamil from the outside, with an increase in apparent

156 as more common with participants in the COER-verapamil group (n = 118) compared with the atenolol or

157 mm Hg for participants assigned to the COER verapamil group and by 13.5 and 7.1 mm Hg for partcipant

158 ase-related events that occurred in the COER verapamil group vs 365 in atenolol or hydrochlorothiazid

159 ockers nicardipine, SKF96365, diltiazem, and verapamil had no effect at appropriate doses.

160 ydropyridine blockers, such as diltiazem and verapamil, had no effect on the CaSR-mediated rise in [C

161 rpose of this study was to determine whether verapamil has rate-dependent effects on the atrial effec

162 2780 line) by continuous exposure to Ptx and verapamil, have point mutations in their major beta-tubu

163 transport is inhibited by the Pgp modulators verapamil (IC(50)=12.1 muM) and nifedipine, and also by

164 40% decrease in chloroquine with or without verapamil IC50 levels of pfcrt knockdown clones, relativ

165 odels for calcium chloride (EC50 1.8 mM) and verapamil (IC50 0.61 muM); isoproterenol elicited a posi

166 apply compartmental modeling to these human verapamil imaging studies.

167 We found the ABC transporter inhibitor verapamil improved transduction efficiency 2- to 6-fold

168 d clinical trials, all of which investigated verapamil in acute mania, and finding no evidence that i

169 re monitored during infusion of SEA-0400 and verapamil in anesthetized dogs.

170 100 nM for reserpine or better than 5 nM for verapamil in aqueous solution.

171 tion of closed channels blocked by 30 microM verapamil in Ba(2+) but did not affect frequency-depende

172 cridar and distribution volumes of (R)-(11)C-verapamil in different brain regions.

173 lly, APAP increased P-gp transport of BODIPY-verapamil in freshly isolated rat brain capillaries.

174 Addition of P-gp substrate verapamil increased CSF 125I-T4 recovery to 51.4+/-2.8%,

175 oreover, application of the P-gp antagonist, verapamil, increased Dox loading in HSF-1(-/-) cardiomyo

176 coadministration of low-dose Cilengitide and Verapamil increases tumor angiogenesis, leakiness, blood

177 during apoptosis, which was also blocked by verapamil, indicating an important role for calcium in t

178 fCRT also transports quinine, quinidine, and verapamil, indicating that the protein behaves as a mult

179 we found that a CCAAT element was mediating verapamil-induced transcriptional repression and identif

180 Thus, verapamil induces a calcineurin-NFY signaling pathway th

181 terally symmetric in chronically stimulated, verapamil-infused animals.

182 S(4)) were determined at baseline and during verapamil infusion.

183 Our finding that verapamil inhibits intracellular M. tuberculosis growth

184 ces among MATE transporters, and suggest how verapamil inhibits MATE-mediated multidrug efflux.

185 ndomethacin, 2-aminoethoxydiphenylborane, or verapamil inhibits repair of the damage and also inhibit

186 n occurs by a competitive mechanism, whereas verapamil inhibits transport by a non-competitive mechan

187 11)C were integrated over 0-9 min after each verapamil injection.

188 -gp increased blood-brain transfer (K(1)) of verapamil into the brain by 73% (range, 30%-118%; n = 12

189 Verapamil is a potent phenylalkylamine antihypertensive

190 Verapamil is a prototypical phenylalkylamine (PAA), and

191 As verapamil is a substrate for CYP3A4, which is induced by

192 layed rectifier potassium current (I(Kr)) by verapamil is frequency-dependent.

193 In addition to 'verapamil-like' chemosensitization to chloroquine and am

194 Verapamil markedly accelerated the rate of tight binding

195 contrast, the L-type calcium channel blocker verapamil markedly decreased S1P-induced HASM cell contr

196 harmacological therapy with beta-blockade or verapamil may realize meaningful symptom relief and low

197 Our data further suggest that this verapamil-mediated TXNIP repression is conferred by redu

198 le higher than therapeutic concentrations of verapamil (micromolar) were necessary to inhibit activit

199 PET scans with the ABCB1 substrate (R)-(11)C-verapamil on 5 healthy male volunteers without and with

200 PET scans with the ABCB1 substrate (R)-(11)C-verapamil on 5 healthy male volunteers without and with

201 This may result in variable effects of verapamil on the AERP, depending on the rate.

202 Na channels (SMC) in the presence of ISO and Verapamil only caused SR Ca release when block of I(Ca,L

203 more, reducing the wild-type VSMC [Ca2+]i by Verapamil or BAPTA-AM significantly increased cellular c

204 ions of the first generation P-gp inhibitors verapamil or cyclosporin, respectively.

205 patients with a discharge diagnosis of acute verapamil or diltiazem overdose at five university-affil

206 try that was inhibited with SKF96365 but not verapamil or KB-R7943.

207 Intra-BLA infusions of verapamil or nifedipine did not affect the expression of

208 h the P-glycoprotein inhibitors quinidine or verapamil) or warfarin (dose adjusted to maintain the in

209 odipine or isradipine, but not by diltiazem, verapamil, or cadmium.

210 Blocking Ca(2+) influx with verapamil, or inhibiting protein kinase A (PKA) with H89

211 etreatment with topical cyclosporin A (CsA), verapamil, or XR9576, modulators of P-glycoprotein (P-gp

212 or tariquidar followed by another (R)-[(11)C]verapamil PET scan 60 min later.

213 and November, 2011, we completed (R)-[(11)C]verapamil PET studies in 14 pharmacoresistant patients,

214 ) to inhibit P-gp, a second set of water and verapamil PET studies was conducted, followed by (11)C-C

215 Molecular imaging with verapamil-PET identifies P-glycprotein overexpression as

216 Voxel-by-voxel, we calculated the (R)-[(11)C]verapamil plasma-to-brain transport rate constant, K1 (m

217 Gd(3+) and verapamil potentiated the HK-induced increase in [Ca(2+)

218 showed that inhibition of TXNIP by siRNA or verapamil prevented Hcys-induced TXNIP protein recruitme

219 Importantly, pretreatment with verapamil prevented scopolamine-induced behavioral respo

220 In addition, we found that verapamil prevented the release of [(3)H]arachidonic aci

221 ype, whereas the calcium channel antagonist, verapamil, prevented abnormal outcome in Kir6.2-KO.

222 Verapamil prolongs AERP at slow rates and shortens AERP

223 oprotein activity was expressed as the (11)C-verapamil radioactivity extraction ratio ((11)C-verapami

224 of P-gp function, the distribution of (11)C-verapamil radioactivity into these compartments is limit

225 Efflux pump inhibitors like verapamil reduce this tolerance.

226 The L-type Ca2+ channel blocker verapamil reduced SS Ca2+ spark frequency to 38% of cont

227 Moreover, verapamil reduced tolerance to bedaquiline and moxifloxa

228 nd human islets and that orally administered verapamil reduced TXNIP expression and beta-cell apoptos

229 nhibition of mycobacterial efflux pumps with verapamil reduces the bacterial drug tolerance and may e

230 tibody (UIC2) and a fluorescent drug (Bodipy-verapamil), respectively.

231 of 821.9 and 2.2 mg/kg for carbamazepine and verapamil, respectively.

232 SL-ATP to wild-type P-gp in the presence of verapamil resulted in reduction of the protein-bound spi

233 An L-type Ca(2+) channel blocker, verapamil, reversed some beneficial effects of GRK2KO.

234 preceding residue 76 modulate the degree of verapamil reversibility in CQ-resistant lines.

235 yrin IX in the digestive vacuole and loss of verapamil reversibility of CQ and quinine resistance.

236 have now proven that pfcrt mutations confer verapamil-reversible chloroquine resistance in vitro and

237 resistance transporter (PfCRT) can result in verapamil-reversible CQ resistance and altered susceptib

238 Verapamil's R isomer and its metabolite norverapamil hav

239 ogenase-positive cells as well as cells with verapamil-sensitive ability to efflux rhodamine 123.

240 east cancer-resistance protein 1-expressing, verapamil-sensitive SP of candidate cancer stem cells.

241 reast cancer-resistance protein 1-expressing verapamil-sensitive SPs in three of four human ovarian c

242 Verapamil significantly prolonged the AERP at BDCLs of 6

243 or 0.70, respectively) and trandolapril with verapamil SR (HRs 0.78 and 0.79) were associated with re

244 follow-up BP and addition of trandolapril to verapamil SR each were associated with reduced risk.

245 lease)/trandolapril in INVEST (INternational VErapamil SR Trandolapril STudy) were categorized into 3

246 the 22,576 participants in the International Verapamil SR-Trandolapril Study (INVEST).

247 ients and 1000 patients of the International Verapamil SR/Trandolapril Study (INVEST) Genetic Substud

248 is of either atenolol/hydrochlorothiazide or verapamil-SR (sustained release)/trandolapril in INVEST

249 ctivity of ABCG2, whereas both the basal and verapamil-stimulated ATPase activities of P-gp were inhi

250 -linking of mutant A259C/W803C inhibited its verapamil-stimulated ATPase activity mutant, but activit

251 Q2 was also an inhibitor of verapamil-stimulated ATPase activity.

252 n with the L-type antagonists nifedipine and verapamil strongly diminished the phloretin-sensitive ap

253 The presence of verapamil strongly magnified both effects.

254 activity and mitofusin 1 (Mfn1), because (i) verapamil suppressed both contraction and mitochondrial

255 In vivo, amlodipine and verapamil suppressed peritoneal macrophage recruitment i

256 tients were randomly assigned to either CAS (verapamil sustained release) or NCAS (atenolol).

257 CAS group, 6391 patients (81.5%) were taking verapamil sustained release; 4934 (62.9%) were taking tr

258 CAD that were assigned randomly to either a verapamil sustained-release (SR)- or an atenolol-based s

259 ents from INVEST were randomly assigned to a verapamil sustained-release- or atenolol-based strategy;

260 Sav1866 displayed a Hoechst 33342, verapamil, tetraphenylphosphonium, and vinblastine-stimu

261 side population cells and can be blocked by verapamil, they do not express increased levels of the A

262 radiolabeled P-glycoprotein substrates, (3)H-verapamil (threefold increase), (3)H-loperamide (fivefol

263 ater to assess blood flow, followed by (11)C-verapamil to assess BBB P-gp activity.

264 We also found verapamil to be a partial mixed-type inhibitor of chloro

265 Group 4 received verapamil to evaluate the effect of calcium channel bloc

266 ations with the use of either terfenadine or verapamil to inhibit INa and ICa or pinacidil to activat

267 current agonist pinacidil or I(Ca,L) blocker verapamil to maintain AP duration (APD) near control lev

268 clinically approved calcium channel blocker verapamil to obese mice.

269 4.7 (1.4-15.9) times less likely to require verapamil to treat cardiovascular instability than those

270 wed potent inhibition (comparable to that of verapamil) toward the whole-cell drug efflux pump activi

271 The INternational VErapamil-trandolapril STudy (INVEST) compared outcomes

272 dary analysis of data from the International Verapamil-Trandolapril Study (INVEST), which was conduct

273 The verapamil-trandolapril-based strategy was as clinically

274 inhibition by CsA, indicated by a change in verapamil transport (K(1)).

275 o gain detailed insight into the kinetics of verapamil transport across the blood-brain barrier (BBB)

276 gle-Q-loop mutants are functional for Bodipy-verapamil transport.

277 Inhibition of P-gp unmasks verapamil trapping in brain tissue that requires a 2C mo

278 pinacidil-treated myocytes, but depressed in verapamil-treated myocytes.

279 Echocardiography of verapamil-treated, gamma-sarcoglycan-null mice showed an

280 Verapamil treatment eliminated evidence of vasospasm and

281 However, verapamil treatment significantly attenuated both cardia

282 ated by DLMC+US than those treated by DL, DL+verapamil under the same US treatment or DLMC without US

283 cases of cells treated by DLMC, DL+US or DL+verapamil+US.

284 ) were also mutated and assayed for block by verapamil using whole-cell voltage-clamp recordings in 1

285 of three drugs (promethazine, enalapril, and verapamil) using deuterated analogues of these drugs as

286 olarizations (EADs) and arrhythmias, whereas verapamil, vanoxerine and bepridil produced no proarrhyt

287 urnover ( k cat <or= 1-2 s (-1)) compared to verapamil (VER) ( k cat approximately 10 s (-1)).

288 three P-gp substrates used in these studies (verapamil, vinblastine, and digoxin) bind.

289 strate that many other substrates (including verapamil, vinblastine, and rifampicin) of the well stud

290 ransporter (PfCRT) are major determinants of verapamil (VP)-reversible CQ resistance (CQR).

291 cally relevant doses of chloroquine (CQ) and verapamil (VPL) and thereby present the first in vivo qu

292 also inspect how pH, the chemoreversal agent verapamil (VPL), and various amino acid mutations in PfC

293 0 times more effective reversal ability than verapamil (VRP) for TAX and VCR.

294 Permanently charged verapamil was more effective intracellularly than neutra

295 il, but lower than those of extended release verapamil, we evaluated the activity of verapamil added

296 holamine infusion, and response to adenosine/verapamil were evaluated.

297 al) distribution of lipophilic drugs such as verapamil will be limited by tissue blood flow.

298 e for 500 nM to 1.0 mM solutions (n = 11) of verapamil with R(2) = 0.988.

299 of analytes (e.g., approximately 800 zmol of verapamil) with a dynamic range spanning up to 4 orders

300 A lower dose of verapamil without effects on left ventricular pressure (