ライフサイエンスコーパス: diltiazem

1 nuated by calphostin C and La(3+) but not by diltiazem.

2 for DHP block, are not involved in block by diltiazem.

3 (1A) background also increase sensitivity to diltiazem.

4 P and PA block as well as residues unique to diltiazem.

5 zothiazepine L-type calcium channel blocker, diltiazem.

6 he light-sensitive conductance such as l-cis-diltiazem.

7 )-free conditions and markedly attenuated by diltiazem.

8 e taking nifedipine, 181 amlodipine, and 186 diltiazem.

9 2+)] or blocking L-type Ca(2+) channels with diltiazem.

10 l and approximately-30-fold more potent than diltiazem.

11 rts and compared with those of adenosine and diltiazem.

12 usly identified a new metabolite of the drug diltiazem.

13 2-aminoethoxydiphenyl borate, verapamil, and diltiazem.

14 ntly by application of nimodipine but not of diltiazem.

15 441 cells in the presence of CFTRinh-172 and diltiazem.

16 activity, substantially higher than that of diltiazem.

17 1 microM U-46619 were partially inhibited by diltiazem.

18 e to glucose that was partially inhibited by diltiazem.

19 and decreased sensitivity to block by l-cis-diltiazem.

20 by a complete loss of use-dependent block by diltiazem.

21 rast, the Ca2+channel blockers nifedipine or diltiazem (1 microm) had a negligible effect on conducti

22 ected by the L-type Ca2+ channel antagonists diltiazem (10 and 30 mum) or nifedipine (3 mum).

23 inhibit sarcoplasmic reticulum Ca2+ release; diltiazem (10 mg/kg given over first 6 hrs postburn); or

24 Blocking L-type calcium channels by diltiazem (10 microm) significantly attenuated ghrelin-m

25 channels with nifedipine (0.1 micromol/L) or diltiazem (10 micromol/L) abolished this effect.

26 nwhile, concomitant infusion of opioids with diltiazem (10 or 100 nmol/microliter/h) inhibited the wi

27 ersus 20 mg; metoprolol: 80 mg versus 72 mg; diltiazem: 212 mg versus 180 mg, and verapamil: 276 mg v

28 l person-quarters were atorvastatin (27.6%), diltiazem (22.7%), digoxin (22.5%), and amiodarone (21.1

29 antly different from controls in response to diltiazem (-22+/-5% in both groups) and exogenous NO don

30 0.0+/-15.5, atenolol: 75.9+/-11.7, digoxin + diltiazem: 67.3+/-14.1 and digoxin + atenolol: 65.0+/-9.

31 s of VR (bpm) were - digoxin: 78.9 +/- 16.3, diltiazem: 80.0+/-15.5, atenolol: 75.9+/-11.7, digoxin +

32 Verapamil (a phenylalkylamine) and diltiazem (a benzothiazepine) were imperfectly selective

33 also measured in adult rats pretreated with diltiazem, a Ca(2+) channel antagonist.

34 somatosensory cortices, which was blocked by diltiazem, a Ca2+ channel antagonist.

35 ycin, an inhibitor of protein synthesis, and diltiazem, a calcium-channel blocker, were both ineffect

36 Diltiazem, a commonly prescribed ventricular rate-contro

37 rotoxin and 8-br-cGMP were reversed by L-cis-diltiazem, a cyclic nucleotide-gated channel inhibitor,

38 which blocks all calcium channels, and l-cis-diltiazem, a potent antagonist of cGMP-gated channels, s

39 channel conformation and use dependence for diltiazem, a specific benzothiazepine calcium channel in

40 channels, we perfused a group of hearts with diltiazem, a specific L-type calcium channel blocker, to

41 Ca(2+) load, and occurred in the presence of diltiazem, a voltage-dependent Ca(2+) channel blocker.

42 s met inclusion criteria, with verapamil and diltiazem accounting for 27 of 40 (67.5%) and 13 of 40 (

43 The results suggest that diltiazem acts by causing open-channel block of the 5-HT

44 randomized to amlodipine 10 mg once daily or diltiazem (Adizem XL) 300 mg once daily in a 14-week dou

45 II) compared the efficacy of amlodipine and diltiazem (Adizem XL) and the combination of amlodipine/

46 Both monotherapy with amlodipine and diltiazem (Adizem XL) were effective on symptoms and amb

47 ipine and isosorbide 5-mononitrate 100 mg to diltiazem (Adizem XL).

48 d the combination of amlodipine/atenolol and diltiazem (Adizem XL)/isosorbide 5-mononitrate on exerci

49 urther, with amlodipine/atenolol superior to diltiazem (Adizem XL)/isosorbide 5-mononitrate.

50 ent use of atorvastatin; digoxin; verapamil; diltiazem; amiodarone; fluconazole; ketoconazole, itraco

51 Thus, unlike nifedipine and diltiazem, amlodipine releases NO from blood vessels.

52 Conversely, diltiazem, an inhibitor of the mitochondrial Na(+)/Ca(2+

53 To investigate the effects of diltiazem, an L-type Ca2+ channel blocker, on naloxone-p

54 kinase II [CaMKII]) via the AC3I peptide and diltiazem, an L-type calcium channel antagonist.

55 ic acid, blocked by Ba2+, and insensitive to diltiazem; an inwardly rectifying K+ current; and a nons

56 ron binding nor affected its displacement by diltiazem and (+)-verapamil.

57 icare beneficiaries, of whom 53 275 received diltiazem and 150 880 received metoprolol.

58 The VGCC antagonist diltiazem and agonist (-)BayK 8644 were used to manipula

59 at specifically targeted Ca2+ slow channels (diltiazem and amlodipine).

60 ning the prevalence of overgrowth induced by diltiazem and amlodipine, with estimates of 74% and 3.3%

61 l hazards regression compared survival among diltiazem and beta-blocker users, controlling for patien

62 Topical diltiazem and BTA are promising agents in the treatment

63 tes in the short term, though after 3 months diltiazem and BTA resulted in equal healing rates.

64 As to date diltiazem and BTA were never compared in a solid randomi

65 Thus, diltiazem and chemical analogs of diltiazem represent a

66 of Ca2+ transport was slightly inhibited by diltiazem and greatly inhibited by ruthenium red.

67 These results indicate that both diltiazem and lisinopril are safe for treatment of hyper

68 In vivo tests showed that diltiazem and M2 each stimulated growth hormone release

69 e voltage-dependent calcium channel blockers diltiazem and nifedipine.

70 channel knockdown with short hairpin RNA and diltiazem and nimodipine, voltage-dependent Ca(2+) chann

71 hibitors of voltage-dependent Ca2+ channels (diltiazem and nisoldipine) or to the same extent by remo

72 Reductions in MVO2 in response to diltiazem and nitroglycerin were not altered by inhibiti

73 on agents such as warfarin, bisphosphonates, diltiazem and others, which are primarily aimed at treat

74 Diltiazem and selective knockdown of TRPV6 or CaV1.3 cha

75 iazepin-4-one, which is the bicyclic core of diltiazem and structurally related drugs.

76 Binding affinities of diltiazem and these metabolites to GHSR1a receptors foll

77 to the synthesis of fluorinated analogues of diltiazem and tiazesim, both therapeutic agents.

78 Switches to diltiazem and verapamil have been described; however, th

79 that the inhibition of [3H]mCPBG binding by diltiazem and verapamil is mediated by a site that is di

80 her short-acting calcium antagonists such as diltiazem and verapamil may have associated adverse effe

81 ype calcium channel antagonists, nifedipine, diltiazem and verapamil on Ang II-induced drinking behav

82 Diltiazem and verapamil pretreatment had no significant

83 Diltiazem and verapamil traverse the central cavity of t

84 er, the nondihydropyridine blockers, such as diltiazem and verapamil, had no effect on the CaSR-media

85 5 transmembrane segment (HHT-5411) with both diltiazem and verapamil.

86 egions of IVS5 in the use-dependent block by diltiazem and verapamil.

87 age-dependent Ca2+ channel (VDCC) inhibitor, diltiazem and with P2X receptor blockade.

88 (nimodipine, Bay K 8644), benzothiazepines (diltiazem) and acetonitrile derivatives (verapamil, D600

89 mizole, dofetilide, ibutilide, bepridil, and diltiazem) and compared the outcomes to in vitro optical

90 whether other bronchodilators (terbutaline, diltiazem, and aminophylline) relax bronchiolus to a gre

91 of the calcium channel blockers nifedipine, diltiazem, and amlodipine or the ACE inhibitors enalapri

92 crolide antibiotics, antifungals, verapamil, diltiazem, and isoniazid.

93 Verapamil, diltiazem, and nicardipine, but not nifedipine or isradi

94 We studied the effects of verapamil, diltiazem, and nifedipine on HERG K+ channels that encod

95 ype Ca2+ channel blockers such as verapamil, diltiazem, and nifedipine, or the nonselective Ca2+,Na+

96 or As subunit, (+)-verapamil, (-)-verapamil, diltiazem, and nimodipine caused reversible and concentr

97 sporter substrate inhibitors like quinidine, diltiazem, and ritonavir also enhanced transduction 2- t

98 channel antagonists, nifedipine, verapamil, diltiazem, and the agonist, Bay K 8644, even at relative

99 ipine, and nitrendipine, the benzothiazepine diltiazem, and the phenylalkylamine verapamil all preven

100 ise and while at rest: atenolol, metoprolol, diltiazem, and verapamil (drugs listed alphabetically by

101 (2+) channel blockers nicardipine, SKF96365, diltiazem, and verapamil had no effect at appropriate do

102 h archetypal antagonistic drugs, nifedipine, diltiazem, and verapamil, at resolutions of 2.9 angstrom

103 to 4 different CCBs-nifedipine, amlodipine, diltiazem, and verapamil-at their physiological serum co

104 to 0.1 microM PGF(2alpha) was insensitive to diltiazem, and was abolished in Ca2+-free physiological

105 On postnatal days 26 and 27, diltiazem- and saline-treated mice had only one row of r

106 ceptor activation to the clinical actions of diltiazem are discussed in the context of the known bene

107 ardiology, such as nifedipine, verapamil and diltiazem, are selective for L-type Ca2+ channels, the r

108 This study indicates that digoxin and diltiazem, as single agents at the doses tested, are lea

109 cleotide-gated (CNG) channel inhibitor l-cis-diltiazem, as well as the chelation of intracellular Ca(

110 olate, cyclosporine, prednisone, furosemide, diltiazem, aspirin, simvastatin, an angiotensin receptor

111 ydrochlorothiazide, atenolol, clonidine, and diltiazem at 1 year and with all treatments at 2 years.

112 ere more efficacious and/or more potent than diltiazem at GHSR1a receptors, with a rank order of agon

113 For ventricular rate control, verapamil, diltiazem, atenolol, and metoprolol were qualitatively s

114 ignificant effect on [3H]nitrendipine or [3H]diltiazem binding to cortical membranes.

115 dues (I1150, M1160, and I1460) contribute to diltiazem block but have not been shown to affect DHP or

116 nding site that mediates the potentiation of diltiazem block of both closed and inactivated Cav1.2 ch

117 Diltiazem block of Cav1.2 is frequency-dependent and pot

118 Potentiation of diltiazem block of closed Cav1.2 channels in Ca2+ was ab

119 one of the mutations affected the potency of diltiazem block of closed channels (0.05 Hz stimulation)

120 srupts Ca2+ dependent inactivation, enhanced diltiazem block of closed channels in Ba2+.

121 ude that, in Ba2+, E1419 slows recovery from diltiazem block of depolarized Cav1.2 channels, but in C

122 these L-type-specific amino acid residues in diltiazem block, and also indicated that Y1152 of alpha(

123 th DHP and PA block, does not play a role in diltiazem block.

124 7A, is not required for Ca2+ potentiation of diltiazem block.

125 Diltiazem blocked a mutant P/Q-type channel containing n

126 es in apo, cGMP-bound, cAMP-bound, and L-cis-Diltiazem-blocked states.

127 The benzothiazepine diltiazem blocks ionic current through L-type Ca(2+) cha

128 e-cell, voltage-clamp recordings showed that diltiazem blocks L-type Ca(2+) channels approximately 5-

129 alcium channels as nifedipine, verapamil and diltiazem, by calpain inhibitor I, or by the intracellul

130 application, as if the charged form of L-cis-diltiazem can only access the blocking site from the int

131 ranolol in city A, sildenafil in city B, and diltiazem, capecitabine, and sertraline in city D), with

132 Diphenhydramine, diltiazem, carbamazepine, and norfluoxetine were detecte

133 These experiments showed that diltiazem causes a rapid, reversible, block in the prese

134 aily regimens: 1) 0.25 mg digoxin, 2) 240 mg diltiazem-CD, 3) 50 mg atenolol, 4) 0.25 mg digoxin + 24

135 50 mg atenolol, 4) 0.25 mg digoxin + 240 mg diltiazem-CD, and 5) 0.25 mg digoxin + 50 mg atenolol; w

136 ter 1 year of treatment, whereas patients on diltiazem, clonidine, or prazosin do not.

137 e (concentration range, 10(-8) to 10(-4) M), diltiazem (concentration range, 3 x 10(-7) to 1 x 10(-4)

138 r patients were randomized to receive either diltiazem cream and placebo injection or BTA injection a

139 y different for concurrent use of verapamil; diltiazem; cyclosporine; ketoconazole, itraconazole, vor

140 Blood pressure reduction with once-daily diltiazem decreased urine albumin excretion (2967 +/- 78

141 Diltiazem did not reduce the cumulative occurrence of ca

142 D-cis-Diltiazem did not rescue photoreceptors of Pro23His rhod

143 antioxidant drug with sulfhydryl groups) and Diltiazem (DLT, L-type calcium channel blocker).

144 Risk for the primary outcome with initial diltiazem doses exceeding 120 mg/d was greater than that

145 s bleeding than metoprolol, particularly for diltiazem doses exceeding 120 mg/d.

146 d calcium channel blockers (verapamil ER and diltiazem ER) and that the dose of colchicine does not n

147 mycin, verapamil ER [extended release]), and diltiazem ER) on the pharmacokinetics of colchicine.

148 l and beta-blockers, digoxin, verapamil, and diltiazem, especially in elderly patients.

149 Diltiazem exposure increased the number of glutamatergic

150 Diltiazem failed to inhibit the activation of HSF.

151 by nondihydropyridine antagonists including diltiazem, flunarizine, or verapamil.

152 black men, from 50% for captopril to 97% for diltiazem for older black men, from 70% for hydrochlorot

153 from 84% for hydrochlorothiazide to 95% for diltiazem for older white men.

154 ine and 83%, 82%, and 83%, respectively, for diltiazem for patients with baseline DBP of 95-99 mm Hg)

155 was noted in 32 of 74 (43%) patients in the diltiazem group and 26 of 60 (43%) patients in the BTA g

156 was noted in 58 of 74 (78%) patients in the diltiazem group and 49 of 60 (82%) patients in the BTA g

157 rted and was noted in 15% of patients in the diltiazem group, and this difference was statistically s

158 Clonidine and diltiazem had consistent response rates regardless of re

159 D-cis-Diltiazem had no detectable effect on preservation of ph

160 Diltiazem-HCl arrested diastolic dysfunction progression

161 the mutation-specific response elicited with diltiazem highlights the necessity to understand mutatio

162 applied successfully in rd mice, with D-cis-diltiazem hydrochloride increased incrementally from 21

163 eatment with atenolol, captopril, clonidine, diltiazem, hydrochlorothiazide, or prazosin in a double-

164 eatment with atenolol, captopril, clonidine, diltiazem, hydrochlorothiazide, or prazosin in a double-

165 gh doses of verapamil (IC50 = 166 microM) or diltiazem (IC50 = 243 microM).

166 Neither nifedipine nor diltiazem increased nitrite production at any dose studi

167 This slow current was blocked by l-cis diltiazem, indicating that it was produced by ion flux t

168 s achieved in an average of 2 hrs, at a mean diltiazem infusion of 13.3 mg/hr.

169 Intravenous bolus dose, when given, and diltiazem infusion rate and time necessary to achieve th

170 the half-maximal inhibitory concentration of diltiazem inhibition by approximately 10-fold, the state

171 oltage-gated calcium channels (VGCCs), since diltiazem inhibits calcium oscillations under all condit

172 c reticulum calcium release), verapamil, and diltiazem (L-type calcium channel inhibitors).

173 At the maximum dose, diltiazem (maximum relaxation, 95%+/-2% [proximal], 94%+

174 Diltiazem (mean dose, 392 +/- 27 mg/d) or nifedipine (me

175 of near unity suggests a single molecule of diltiazem mediates inhibition and, indeed, kinetic analy

176 the antagonist had no effect indicating that diltiazem mediates its effects by binding preferentially

177 are relatively selective for L- (verapamil, diltiazem, nifedipine) and N- (omega-conotoxin GVIA) typ

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

179 as undertaken to examine the effect of D-cis-diltiazem on photoreceptor structure and function in thi

180 To examine the effects of diltiazem on the open state of the receptor in more deta

181 tigate the action of one of these compounds, diltiazem, on the recombinant receptor expressed in huma

182 Patients received either 300 mg oral diltiazem once daily, or placebo, initiated within 36-96

183 X), or L-type Ca2+ channel antagonists (1 mm diltiazem or 20 microm nifedipine).

184 proximal and distal airways were noted with diltiazem or aminophylline in the entire dose range.

185 to determine the effectiveness and safety of diltiazem or lisinopril for treatment of hypertension af

186 ter trial of the effectiveness and safety of diltiazem or lisinopril in the treatment of hypertension

187 ivaroxaban use and also began treatment with diltiazem or metoprolol between January 1, 2012, and Nov

188 type voltage-dependent calcium channels with diltiazem or nifedipine attenuated S1P-mediated vasocons

189 to daily intraperitoneal injections of D-cis-diltiazem or saline between postnatal days 9 and 24.

190 Addition of diltiazem or verapamil had no significant effect on KCl

191 ver, rats pre-treated with i.c.v. 100 microg diltiazem or verapamil showed no change in Ang II-induce

192 type Ca(2+) channel blockers (isradipine and diltiazem) or knockdown of the Ca(V)1.3 channel abrogate

193 ent effects differed from those of prazosin, diltiazem, or clonidine.

194 blocker (amlodipine, felodipine, nifedipine, diltiazem, or verapamil).

195 We found no survival benefit of diltiazem over beta-blocker treatment for unstable angin

196 a discharge diagnosis of acute verapamil or diltiazem overdose at five university-affiliated teachin

197 tly lower than that on digoxin (p < 0.0001), diltiazem (p < 0.0002) and atenolol (p < 0.001).

198 44 placebo patients and 97 events in the 430 diltiazem patients (hazard ratio 0.79; 95% CI, 0.61-1.02

199 (2+) channels (LTCCs: nifedipine, verapamil, diltiazem) prevented the decrease in Ca(2+) transients i

200 In contrast, diltiazem produced only state-dependent block of alpha1C

201 Diltiazem rapidly (<2 min) and reversibly decreased the

202 Extracellular application of L-cis-diltiazem rapidly and reversibly suppressed the photocur

203 L-cis-Diltiazem reduced the light-activated conductance withou

204 Diltiazem reduces non-fatal reinfarction and refractory

205 Thus, diltiazem and chemical analogs of diltiazem represent a new class of GHSR1a receptor agoni

206 The diltiazem-resistant components of both of these response

207 ation of the L-type Ca(2+) channel inhibitor diltiazem restores normal levels of these sarcoplasmic r

208 voltage-dependent Ca2+ channels (nimodipine, diltiazem), ryanodine and inhibitors of the SR calcium A

209 e enterotoxin and 8-br-cGMP induced an L-cis-diltiazem-sensitive conductance, promoting Ca(2+) influx

210 hannel (VGCC) blockers verapamil and (+)-cis-diltiazem significantly reduced the light-evoked Ca2+ re

211 e of a previous report suggesting that D-cis-diltiazem slows retinal degeneration in rd mice, this st

212 Diltiazem specifically increased transients by approxima

213 In adult rats, diltiazem suppressed (P < 0.05) intraretinal manganese u

214 orothiazide, atenolol, captopril, clonidine, diltiazem (sustained release), or prazosin.

215 , was proved by unequivocal synthesis from a diltiazem synthon.

216 teries exposed to 80 mM K+ and nifedipine or diltiazem the rises in tension and [Ca2+]i were blunted

217 Given the acetylation at C-3 in diltiazem, the 3-monoacetate (8) and diacetate (3) deriv

218 seline compared with 1294 +/- 679 mg/d after diltiazem therapy; P < 0.05) at 4 weeks while patients r

219 a2+) and by the organic Ca2+ channel blocker diltiazem, thus ruling out proton influx through H(+)-or

220 was no difference in risk of death comparing diltiazem to beta-blocker treatment (hazards ratios [HR]

221 Thus, binding of diltiazem to L-type Ca(2+) channels requires residues th

222 g/kg given i.p. shortly after ischemia), (c) diltiazem-treated (DILT) groups 1.0 to 30 mg/kg, given i

223 ONL width and cell counts of diltiazem-treated and saline-treated animals at 35 days

224 Of 55 diltiazem-treated patients, 21 (38%) were responders (di

225 rom control, dexamethasone-, nifedipine-, or diltiazem-treated rats.

226 from 100 +/- 0.9 to 85 +/- 1.6 mm Hg in the diltiazem-treated responders and from 100 +/- 1.0 to 84

227 to 130 +/- 2.0 mm Hg (mean +/- 1 SEM) in the diltiazem-treated responders and from 153 +/- 2.1 to 127

228 were prescribed monotherapy beta-blocker or diltiazem treatment at discharge.

229 ted with beta-adrenergic blocking agents and diltiazem treatment for unstable angina.

230 Patients receiving diltiazem treatment had increased risk for the primary o

231 Furthermore, we demonstrate that diltiazem treatment of dysferlin-deficient mice signific

232 For non-fatal cardiac events, diltiazem treatment was associated with a relative decre

233 When patients receiving high- and low-dose diltiazem treatment were directly compared, the HR for t

234 f rehospitalization or death associated with diltiazem use (HR 1.4; 95% CI 0.80 to 2.4).

235 each single mutant was assayed for block by diltiazem using whole-cell voltage-clamp recordings in e

236 study were nitroimidazole antifungal agents, diltiazem, verapamil, and troleandomycin; each doubles,

237 tion of nimodipine or isradipine, but not by diltiazem, verapamil, or cadmium.

238 splaced by (+)-verapamil, (-)-verapamil, and diltiazem; (+)-verapamil was approximately 10-fold more

239 cells by immunostaining were similar in the diltiazem- versus saline-treated mice.

240 e resonance energy transfer (BRET-2) assays, diltiazem was a partial agonist at GHSR1a receptors, wit

241 Intravenous diltiazem was administered as a slow 10-mg bolus dose (0

242 rillation receiving apixaban or rivaroxaban, diltiazem was associated with greater risk of serious bl

243 ts/min), heart rate control with intravenous diltiazem was attempted after adequate intravascular vol

244 en, the atypical L-type Ca2+ channel blocker diltiazem was discovered to be an agonist at the human g

245 Diltiazem was effective in achieving short-term control

246 gingival overgrowth induced by amlodipine or diltiazem was not statistically significant when compare

247 distinction in state-dependent inhibition by diltiazem, we constructed chimeric channels from alpha1C

248 pamil block of L-type Ca2+ channels, whereas diltiazem weakly blocked HERG current (IC50=17.3 micromo

249 lazine, ITU + EHNA, PD81,723, adenosine, and diltiazem were 17.5 +/- 3.4, 11.1 +/- 5.0, 3.5 +/- 0.9,

250 s of mutants that lost use dependence toward diltiazem were characterized by drastically elongated me

251 h sinus tachycardia treated with intravenous diltiazem were evaluated.

252 Seven of the known primary metabolites of diltiazem were synthesized, and three of them (MA, M1, a

253 seven veterans (24% on beta-blockers, 76% on diltiazem) were included in this study.

254 order of agonist activity of M2 > M1 > MA > diltiazem, whereas M4 and M6 metabolites displayed weak

255 Diltiazem, which is used empirically to prevent RA vasos

256 Application of diltiazem with 5-HT (30 microM) caused an increase in th

257 randomized clinical trial to compare topical diltiazem with botulinum toxin A (BTA) in the treatment

258 ic analysis verified that the interaction of diltiazem with the 5-HT3 receptor was well described by

259 g standard doses of atenolol, amlodipine, or diltiazem, without evident adverse, long-term survival c