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

4 (1A) background also increase sensitivity to diltiazem.

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

6 zothiazepine L-type calcium channel blocker, diltiazem.

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

8 )-free conditions and markedly attenuated by diltiazem.

9 e taking nifedipine, 181 amlodipine, and 186 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 ntly by application of nimodipine but not of diltiazem.

14 441 cells in the presence of CFTRinh-172 and diltiazem.

15 activity, substantially higher than that of diltiazem.

16 1 microM U-46619 were partially inhibited by diltiazem.

17 e to glucose that was partially inhibited by diltiazem.

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

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

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

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

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

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

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

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

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

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

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

29 0.0+/-15.5, atenolol: 75.9+/-11.7, digoxin + diltiazem: 67.3+/-14.1 and digoxin + atenolol: 65.0+/-9.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

58 Topical diltiazem and BTA are promising agents in the treatment

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

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

61 Thus, diltiazem and chemical analogs of diltiazem represent a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

77 Diltiazem and verapamil pretreatment had no significant

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

79 5 transmembrane segment (HHT-5411) with both diltiazem and verapamil.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

94 (2+) channel blockers nicardipine, SKF96365, diltiazem, and verapamil had no effect at appropriate do

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

115 7A, is not required for Ca2+ potentiation of diltiazem block.

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

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

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

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

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

121 Diphenhydramine, diltiazem, carbamazepine, and norfluoxetine were detecte

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

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

124 50 mg atenolol, 4) 0.25 mg digoxin + 240 mg diltiazem-CD, and 5) 0.25 mg digoxin + 50 mg atenolol; w

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

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

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

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

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

130 Diltiazem did not reduce the cumulative occurrence of ca

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

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

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

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

135 Diltiazem exposure increased the number of glutamatergic

136 Diltiazem failed to inhibit the activation of HSF.

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

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

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

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

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

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

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

144 Clonidine and diltiazem had consistent response rates regardless of re

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

180 44 placebo patients and 97 events in the 430 diltiazem patients (hazard ratio 0.79; 95% CI, 0.61-1.02

181 (2+) channels (LTCCs: nifedipine, verapamil, diltiazem) prevented the decrease in Ca(2+) transients i

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

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

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

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

186 Diltiazem reduces non-fatal reinfarction and refractory

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

188 The diltiazem-resistant components of both of these response

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

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

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

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

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

194 Diltiazem specifically increased transients by approxima

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

224 Diltiazem was effective in achieving short-term control

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

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

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

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

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

230 h sinus tachycardia treated with intravenous diltiazem were evaluated.

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

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

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

234 Diltiazem, which is used empirically to prevent RA vasos

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

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

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

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