PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
32078103-1	2020	BACKGROUND AND OBJECTIVES: P-glycoprotein (P-gp) has been shown previously to contribute to the intestinal absorption of verapamil, diltiazem, tacrolimus, colchicine and indinavir in situ; however, its contribution in vivo is unknown.	Diltiazem	132-141	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	27-41
32080863-10	2020	The PBPK model predicted 3.78- and 7.15-fold increases in the AUC of the potency-adjusted unbound active species with strong CYP3A4 inhibitors itraconazole and ketoconazole, respectively; and 1.62- and 2.37-fold increases with the concomitant use of moderate CYP3A4 inhibitors verapamil and diltiazem, respectively.	Diltiazem	291-300	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	125-131
32080863-10	2020	The PBPK model predicted 3.78- and 7.15-fold increases in the AUC of the potency-adjusted unbound active species with strong CYP3A4 inhibitors itraconazole and ketoconazole, respectively; and 1.62- and 2.37-fold increases with the concomitant use of moderate CYP3A4 inhibitors verapamil and diltiazem, respectively.	Diltiazem	291-300	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	259-265
32348806-11	2020	Postoperatively, the patient developed atrial fibrillation with RVR requiring diltiazem infusion (Clavien Grade II).	Diltiazem	78-87	nuclear receptor subfamily 1 group D member 2	Homo sapiens	64-67
32078103-1	2020	BACKGROUND AND OBJECTIVES: P-glycoprotein (P-gp) has been shown previously to contribute to the intestinal absorption of verapamil, diltiazem, tacrolimus, colchicine and indinavir in situ; however, its contribution in vivo is unknown.	Diltiazem	132-141	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	43-47
30471066-10	2019	In contrast, among CYP3A5 expressors receiving diltiazem, AUCss, 0-24 did not change significantly upon conversion [229 (170-296) vs. 221 (123-342) ng h/mL, p = 0.575, n = 10].	Diltiazem	47-56	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	19-25
32471244-4	2020	Diltiazem (DTZ) and cyclosporin A (CsA) were first confirmed to be potent MRP2 inhibitors in vitro.	Diltiazem	0-9	ATP binding cassette subfamily C member 2	Rattus norvegicus	74-78
32471244-4	2020	Diltiazem (DTZ) and cyclosporin A (CsA) were first confirmed to be potent MRP2 inhibitors in vitro.	Diltiazem	11-14	ATP binding cassette subfamily C member 2	Rattus norvegicus	74-78
32296344-11	2020	Moreover, in the presence of the calcium channel blocker diltiazem (35 muM) SERCA2b/b aortic rings showed higher contractions compared to SERCA2a/b, suggesting that SERCA2a (deficiency) modulates the activity of non-selective cation channels.	Diltiazem	57-66	ATPase, Ca++ transporting, cardiac muscle, slow twitch 2	Mus musculus	76-85
31963306-9	2020	Diltiazem, a calcium channel blocker, significantly inhibited succinate and maleate-induced CCK secretions from mucosal cells and STC-1 cells.	Diltiazem	0-9	cholecystokinin	Rattus norvegicus	92-95
31963306-9	2020	Diltiazem, a calcium channel blocker, significantly inhibited succinate and maleate-induced CCK secretions from mucosal cells and STC-1 cells.	Diltiazem	0-9	stanniocalcin 1	Rattus norvegicus	130-135
32329770-3	2020	Verapamil hydrochloride and diltiazem hydrochloride are combined P-glycoprotein (P-gp) and CYP3A4 inhibitors and may be associated with increases in the risk of bleeding with DOACs.	Diltiazem	28-51	ATP binding cassette subfamily B member 1	Homo sapiens	65-79
32329770-3	2020	Verapamil hydrochloride and diltiazem hydrochloride are combined P-glycoprotein (P-gp) and CYP3A4 inhibitors and may be associated with increases in the risk of bleeding with DOACs.	Diltiazem	28-51	ATP binding cassette subfamily B member 1	Homo sapiens	81-85
32329770-3	2020	Verapamil hydrochloride and diltiazem hydrochloride are combined P-glycoprotein (P-gp) and CYP3A4 inhibitors and may be associated with increases in the risk of bleeding with DOACs.	Diltiazem	28-51	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	91-97
32296344-11	2020	Moreover, in the presence of the calcium channel blocker diltiazem (35 muM) SERCA2b/b aortic rings showed higher contractions compared to SERCA2a/b, suggesting that SERCA2a (deficiency) modulates the activity of non-selective cation channels.	Diltiazem	57-66	ATPase, Ca++ transporting, cardiac muscle, slow twitch 2	Mus musculus	138-145
30458627-9	2019	Diabetes decreased protein content of both GLUT4 (the predominate insulin-sensitive glucose transporter) and AS160 (Akt Substrate at 160 kDa, the downstream protein in the signaling cascade that regulates GLUT4 trafficking) in striated muscle of diabetic rats, with a more pronounced alteration after diltiazem treatment.	Diltiazem	301-310	solute carrier family 2 member 4	Rattus norvegicus	43-48
31150622-2	2019	Here, we report the cryoelectron microscopy (cryo-EM) structures of Cav1.1 in complex with archetypal antagonistic drugs, nifedipine, diltiazem, and verapamil, at resolutions of 2.9 A, 3.0 A, and 2.7 A, respectively, and with a DHP agonist Bay K 8644 at 2.8 A.	Diltiazem	134-143	calcium voltage-gated channel subunit alpha1 S	Homo sapiens	68-74
31084979-7	2019	The most frequent interactions were amiodarone-statin for CYP3A4 and atorvastatin-verapamil-diltiazem for P-gp.	Diltiazem	92-101	ATP binding cassette subfamily B member 1	Homo sapiens	106-110
31068314-4	2019	Diltiazem hydrochloride at different concentrations also transiently up-regulated the expressions of metadherin mRNA and protein but did not inhibit the expression of P-gp protein in MHCC97H and 7402 cells.	Diltiazem	0-23	metadherin	Homo sapiens	101-111
30586744-6	2019	Two modes of intervention were tested: inhibition of the autoactivated calcium-dependent kinase (calmodulin kinase II [CaMKII]) via the AC3I peptide and diltiazem, an L-type calcium channel antagonist.	Diltiazem	153-162	calcium/calmodulin-dependent protein kinase II, beta	Mus musculus	97-117
30586744-6	2019	Two modes of intervention were tested: inhibition of the autoactivated calcium-dependent kinase (calmodulin kinase II [CaMKII]) via the AC3I peptide and diltiazem, an L-type calcium channel antagonist.	Diltiazem	153-162	calcium/calmodulin-dependent protein kinase II, beta	Mus musculus	119-125
30458627-9	2019	Diabetes decreased protein content of both GLUT4 (the predominate insulin-sensitive glucose transporter) and AS160 (Akt Substrate at 160 kDa, the downstream protein in the signaling cascade that regulates GLUT4 trafficking) in striated muscle of diabetic rats, with a more pronounced alteration after diltiazem treatment.	Diltiazem	301-310	AKT serine/threonine kinase 1	Rattus norvegicus	116-119
30458627-9	2019	Diabetes decreased protein content of both GLUT4 (the predominate insulin-sensitive glucose transporter) and AS160 (Akt Substrate at 160 kDa, the downstream protein in the signaling cascade that regulates GLUT4 trafficking) in striated muscle of diabetic rats, with a more pronounced alteration after diltiazem treatment.	Diltiazem	301-310	solute carrier family 2 member 4	Rattus norvegicus	205-210
30316389-1	2018	BACKGROUND: Inhibition of calcineurin inhibitor (CNI) metabolism with diltiazem reduces the dose of tacrolimus required to achieve its therapeutic blood concentration in kidney transplant recipients (KTRs).	Diltiazem	70-79	calcineurin binding protein 1	Homo sapiens	26-47
30284597-5	2019	RESULTS: Moderate CYP3A4 inhibition by diltiazem (240 mg/day) increased the Cmax and AUC0-  of ACT-541468 by 1.4-fold (90% confidence interval (CI): 1.2-1.6) and 2.4-fold (90% CI: 2.0-2.8), respectively, and prolonged t1/2 by 80% (90% CI: 60-90) without affecting tmax.	Diltiazem	39-48	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	18-24
30099888-1	2019	BACKGROUND: It is unknown whether diltiazem, a moderate cytochrome P450 enzyme (CYP3A4) and P-glycoprotein (P-gp) inhibitor, increases the incidence of bleeding events in combination with rivaroxaban, a CYP3A4 and P-gp substrate.	Diltiazem	34-43	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	80-86
30099888-1	2019	BACKGROUND: It is unknown whether diltiazem, a moderate cytochrome P450 enzyme (CYP3A4) and P-glycoprotein (P-gp) inhibitor, increases the incidence of bleeding events in combination with rivaroxaban, a CYP3A4 and P-gp substrate.	Diltiazem	34-43	ATP binding cassette subfamily B member 1	Homo sapiens	92-106
30099888-1	2019	BACKGROUND: It is unknown whether diltiazem, a moderate cytochrome P450 enzyme (CYP3A4) and P-glycoprotein (P-gp) inhibitor, increases the incidence of bleeding events in combination with rivaroxaban, a CYP3A4 and P-gp substrate.	Diltiazem	34-43	ATP binding cassette subfamily B member 1	Homo sapiens	108-112
29728928-0	2018	Effects of diltiazem, a moderate inhibitor of CYP3A4, on the pharmacokinetics of tamsulosin in different CYP2D6 genotypes.	Diltiazem	11-20	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	46-52
29945737-5	2018	The voltage-dependent Ca2+ channel antagonists amlodipine and diltiazem inhibited an Epo-triggered transient rise in intracellular Ca2+, similarly to a specific inhibitor (Pyr3) and a blocking antibody against the transient potential calcium channel 3 (TRPC3).	Diltiazem	62-71	erythropoietin	Homo sapiens	85-88
29945737-5	2018	The voltage-dependent Ca2+ channel antagonists amlodipine and diltiazem inhibited an Epo-triggered transient rise in intracellular Ca2+, similarly to a specific inhibitor (Pyr3) and a blocking antibody against the transient potential calcium channel 3 (TRPC3).	Diltiazem	62-71	transient receptor potential cation channel subfamily C member 3	Homo sapiens	214-251
29945737-5	2018	The voltage-dependent Ca2+ channel antagonists amlodipine and diltiazem inhibited an Epo-triggered transient rise in intracellular Ca2+, similarly to a specific inhibitor (Pyr3) and a blocking antibody against the transient potential calcium channel 3 (TRPC3).	Diltiazem	62-71	transient receptor potential cation channel subfamily C member 3	Homo sapiens	253-258
33168514-0	2018	[Diltiazem inhibits proliferation and motility of hepatocellular cells in vitro by downregulating calcium-activated chloride channel TMEM16A].	Diltiazem	1-10	anoctamin 1	Homo sapiens	133-140
33168514-5	2018	Treatment with 100 mumol/L diltiazem for 24 h significantly inhibited the proliferation of MHCC97H cells and down-regulated the mRNA and protein levels of TMEM16A.	Diltiazem	27-36	anoctamin 1	Homo sapiens	155-162
33168514-6	2018	In 7402 cells, diltiazem treatment at 50 mumol/L for 48 h resulted in the most significant inhibitory effect on the cell proliferation and TMEM16A expressions.	Diltiazem	15-24	anoctamin 1	Homo sapiens	139-146
33168514-7	2018	CONCLUSIONS: Diltiazem can transiently inhibit the invasion of hepatocellular carcinoma cells in vitro possibly by down-regulating the expression of TMEM16A at both the mRNA and protein levels.	Diltiazem	13-22	anoctamin 1	Homo sapiens	149-156
29728928-2	2018	In this study, we investigated the effects of diltiazem, a moderate inhibitor of CYP3A4, on the pharmacokinetics of tamsulosin in subjects with different CYP2D6 genotypes.	Diltiazem	46-55	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	81-87
29728928-8	2018	After diltiazem treatment, the Cmax and AUCinf of tamsulosin in each CYP2D6 genotype group were significantly increased (p < 0.0001 for all).	Diltiazem	6-15	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	69-75
29874752-7	2018	In this study, there was significant induction of CYP19A2 in individual exposures of diltiazem, fluoxetine, gemfibrozil and metformin at concentrations measured in Lake Michigan.	Diltiazem	85-94	cytochrome P450, family 19, subfamily A, polypeptide 1b	Danio rerio	50-57
30025125-1	2018	Purpose: New perspectives are needed to understand decades of contradictory reports on the neuroprotective effects of the Cav1.2 L-type calcium channel blocker d-cis-diltiazem in retinitis pigmentosa (RP) models.	Diltiazem	160-175	calcium channel, voltage-dependent, L type, alpha 1C subunit	Mus musculus	122-128
30025125-11	2018	Conclusions: D-cis-diltiazem"s unexpectedly complex spatiotemporal outer retinal oxidative stress pattern in vivo was dependent on genetic background and rod membrane depolarization, but not apparently dependent on Cav1.2 L-type calcium channels, providing a potential rationale for contradictory results in different RP models.	Diltiazem	13-28	calcium channel, voltage-dependent, L type, alpha 1C subunit	Mus musculus	215-221
29417758-10	2018	Carvedilol alone and coadministered with diltiazem and prednisolone significantly (P < .05) increased the level of hepatic superoxide dismutase and catalase, and decreased malondialdehyde compared with DOX administration alone.	Diltiazem	41-50	catalase	Rattus norvegicus	151-159
28824389-7	2017	Systemic injection of the L-VGCC blockers nifedipine and diltiazem into wild-type mice mimicked the impairment of fear extinction observed in TNC-/- mice.	Diltiazem	57-66	tenascin C	Mus musculus	142-145
28705745-3	2017	We present a case of massive diltiazem and metoprolol overdose refractory to maximal medical therapy, including intravenous calcium, glucagon, vasopressors, high dose insulin, and lipid emulsion.	Diltiazem	29-38	insulin	Homo sapiens	167-174
28766866-0	2017	Enhanced Oral Bioavailability of Diltiazem by the Influence of Gallic Acid and Ellagic Acid in Male Wistar Rats: Involvement of CYP3A and P-gp Inhibition.	Diltiazem	33-42	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	128-133
28766866-0	2017	Enhanced Oral Bioavailability of Diltiazem by the Influence of Gallic Acid and Ellagic Acid in Male Wistar Rats: Involvement of CYP3A and P-gp Inhibition.	Diltiazem	33-42	phosphoglycolate phosphatase	Rattus norvegicus	138-142
28766866-8	2017	Gallic acid and ellagic acid significantly increased the bioavailability of diltiazem due to the inhibition of both CYP3A-mediated metabolism and P-glycoprotein-mediated efflux in the intestine and/or liver.	Diltiazem	76-85	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	116-121
29115512-1	2018	The aim of the present study was to analyze the effect of diltiazem on myocardial fibrosis and remodeling of connexin43 (Cx43) in myocardial ischemic rats and mechanisms underlying these processes.	Diltiazem	58-67	gap junction protein, alpha 1	Rattus norvegicus	109-119
29115512-1	2018	The aim of the present study was to analyze the effect of diltiazem on myocardial fibrosis and remodeling of connexin43 (Cx43) in myocardial ischemic rats and mechanisms underlying these processes.	Diltiazem	58-67	gap junction protein, alpha 1	Rattus norvegicus	121-125
29115512-11	2018	The results of the present study suggest that diltiazem may serve a protective role during remodeling of myocardial ischemia, especially in fibrosis and Cx43 remodeling.	Diltiazem	46-55	gap junction protein, alpha 1	Rattus norvegicus	153-157
28214691-1	2017	Diltiazem has been used for post-transplant hypertension, but the mechanism underlying its protective effect of endothelial cells against angiotensin II (Ang II) - induced impairment remains unclear.	Diltiazem	0-9	angiotensinogen	Homo sapiens	138-152
28477381-8	2017	In the diltiazem group left ventricular (LV), stroke volume and ejection fraction increased (48+-16 vs 55+-17 mL, P=.02, and 60%+-10% vs 62%+-12% P=.03, respectively) but did not differ from controls.	Diltiazem	7-16	tumor protein, translationally-controlled 1	Homo sapiens	114-119
28090637-3	2017	In this study, we tested if the non-dihydropyridine Ca2+ channel blocker diltiazem, which previously showed potential to stop disease progression, can improve the phenotype of a HCM mouse model (Mybpc3-targeted knock-in), which is based on a mutation commonly found in patients.	Diltiazem	73-82	myosin binding protein C, cardiac	Mus musculus	195-201
28090637-8	2017	The Ca2+ channel blocker diltiazem recently showed promising beneficial effects in pre-clinical HCM, particularly in patients carrying MYBPC3 mutations.	Diltiazem	25-34	myosin binding protein C3	Homo sapiens	135-141
28090637-12	2017	Pre-treatment of cardiomyocytes with 1 mum diltiazem reduced the drop in dSL and arrhythmia frequency in KI, and attenuated the positive inotropic effect of isoprenaline.	Diltiazem	43-52	dsl	Drosophila melanogaster	73-76
28214691-1	2017	Diltiazem has been used for post-transplant hypertension, but the mechanism underlying its protective effect of endothelial cells against angiotensin II (Ang II) - induced impairment remains unclear.	Diltiazem	0-9	angiotensinogen	Homo sapiens	154-160
28214691-5	2017	Treatment with 10-6M Ang II for 24h induced a significant decrease in the mRNA and protein levels of eNOS, which was significantly increased by the pre-incubated with diltiazem (10-6M).	Diltiazem	167-176	angiotensinogen	Homo sapiens	21-27
28214691-6	2017	Treatment with 10-6M Ang II for 24h induced a significant increase in the mRNA and protein levels of p47 phox subunit of NADHP oxidase, which was significantly decreased by the pre-incubated with diltiazem.	Diltiazem	196-205	angiotensinogen	Homo sapiens	21-27
28214691-6	2017	Treatment with 10-6M Ang II for 24h induced a significant increase in the mRNA and protein levels of p47 phox subunit of NADHP oxidase, which was significantly decreased by the pre-incubated with diltiazem.	Diltiazem	196-205	inhibitor of growth family member 1	Homo sapiens	101-104
28214691-8	2017	The results reveal that diltiazem inhibits the Ang II - induced oxidative stress in HUVECs, which may be partly mediated by GHSR1a.	Diltiazem	24-33	angiotensinogen	Homo sapiens	47-53
27208646-6	2016	Creatine kinase activity was markedly increased (ranging from 520 to 845%) at all tested diltiazem concentrations at the end of the exposure indicating muscle and/or kidney damage.	Diltiazem	89-98	creatine kinase, testis isozyme	Oncorhynchus mykiss	0-15
27751805-0	2017	Effect of Ca+2 ion on the release of diltiazem hydrochloride from matrix tablets of carboxymethyl xanthan gum graft polyacrylamide.	Diltiazem	37-60	carbonic anhydrase 2	Homo sapiens	10-14
28193357-7	2017	Under the optimum experimental conditions, the good linear ranges of 4.0-4000, 8.0-10000, and 7.0-8000 ng mL-1 were obtainable for diltiazem, amlodipine, and verapamil, respectively, with the correlation of determinations (R2s) higher than 0.99 and the low limits of detection (LODs) of 1.5-3.0 ng mL-1.	Diltiazem	131-140	L1 cell adhesion molecule	Mus musculus	106-110
28193357-7	2017	Under the optimum experimental conditions, the good linear ranges of 4.0-4000, 8.0-10000, and 7.0-8000 ng mL-1 were obtainable for diltiazem, amlodipine, and verapamil, respectively, with the correlation of determinations (R2s) higher than 0.99 and the low limits of detection (LODs) of 1.5-3.0 ng mL-1.	Diltiazem	131-140	L1 cell adhesion molecule	Mus musculus	298-302
28925123-8	2016	Compared with the model group, the degree of myocardial infarct, MDA concentration in cardiac tissue and the levels of TnI in serum significantly decreased in the diltiazem group and flavonoids of Epimedium low and high doses groups (P<0.05 or P<0.01); flavonoids of Epimedium low and high doses groups and the diltiazem group also showed improvements in myocardium structure under ischemia/reperfusion injury.	Diltiazem	163-172	troponin I3, cardiac type	Rattus norvegicus	119-122
27382356-10	2016	The activation of caspase-3 by PFHxS was also inhibited by MK801, diltiazem and nifedipine.	Diltiazem	66-75	caspase 3	Rattus norvegicus	18-27
27191770-8	2016	DISCUSSION: Because suvorexant is metabolized by CYP3A4, next-day somnolence could have occurred as a result of increased plasma suvorexant concentration due to CYP3A4 inhibition by diltiazem.	Diltiazem	182-191	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	161-167
27382356-11	2016	PFHxS-increased ERK activation was inhibited by imperatorin, MK801, diltiazem and nifedipine.	Diltiazem	68-77	Eph receptor B1	Rattus norvegicus	16-19
27160091-4	2016	RESULTS: The results show that HBO and diltiazem preconditioning significantly improves cardiac function and myocardial infarction area, increases nitric oxide, endothelial nitric oxide synthase and ATPase (Na+-K+-ATPase and Ca2+-Mg2+-ATPase) activity and decreases levels of oxygen stress, myocardial enzymes and endothelin-1.	Diltiazem	39-48	endothelin 1	Rattus norvegicus	314-326
27149910-10	2016	WHAT IS NEW AND CONCLUSION: The CYP3A4*1G and CYP3A5*3 genetic polymorphisms are closely related to the trough concentration/dose ratios and pharmacokinetics of diltiazem and its main metabolites in Chinese adult renal transplant patients.	Diltiazem	161-170	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	32-38
27149910-10	2016	WHAT IS NEW AND CONCLUSION: The CYP3A4*1G and CYP3A5*3 genetic polymorphisms are closely related to the trough concentration/dose ratios and pharmacokinetics of diltiazem and its main metabolites in Chinese adult renal transplant patients.	Diltiazem	161-170	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	46-52
26826296-10	2016	The activation of AMPK was attenuated by MK801, nifedipine and diltiazem.	Diltiazem	63-72	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	18-22
26826296-12	2016	Likewise, ERK activation was not affected by compound C but was substantially reduced by MK801, nifedipine or diltiazem.	Diltiazem	110-119	Eph receptor B1	Rattus norvegicus	10-13
27149910-0	2016	Significant impacts of CYP3A4*1G and CYP3A5*3 genetic polymorphisms on the pharmacokinetics of diltiazem and its main metabolites in Chinese adult kidney transplant patients.	Diltiazem	95-104	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	23-29
27149910-0	2016	Significant impacts of CYP3A4*1G and CYP3A5*3 genetic polymorphisms on the pharmacokinetics of diltiazem and its main metabolites in Chinese adult kidney transplant patients.	Diltiazem	95-104	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	37-43
27149910-3	2016	This study was carried out to investigate the impacts of the CYP3A4*1G and CYP3A5*3 genetic polymorphisms on the trough concentration/dose ratios and pharmacokinetics of diltiazem and its main metabolites in Chinese adult renal transplant patients.	Diltiazem	170-179	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	61-67
27149910-3	2016	This study was carried out to investigate the impacts of the CYP3A4*1G and CYP3A5*3 genetic polymorphisms on the trough concentration/dose ratios and pharmacokinetics of diltiazem and its main metabolites in Chinese adult renal transplant patients.	Diltiazem	170-179	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	75-81
27149910-7	2016	RESULTS AND DISCUSSION: The dose-adjusted concentrations and pharmacokinetics of diltiazem and its main metabolites were significantly affected by CYP3A4 *1G and CYP3A5*3 alleles.	Diltiazem	81-90	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	147-153
27149910-7	2016	RESULTS AND DISCUSSION: The dose-adjusted concentrations and pharmacokinetics of diltiazem and its main metabolites were significantly affected by CYP3A4 *1G and CYP3A5*3 alleles.	Diltiazem	81-90	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	162-168
27149910-8	2016	Patients with a CYP3A4*1/*1 genotype were found to have a higher dose-adjusted trough concentration and AUC of diltiazem and its main metabolites compared with those with CYP3A4*1G*1G(P<0 05).	Diltiazem	111-120	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	16-22
27149910-9	2016	The dose-adjusted trough levels and AUC of diltiazem and its main metabolites were significantly lower in CYP3A5*1*1 carriers than in CYP3A5*3 carriers (P < 0 05).	Diltiazem	43-52	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	106-112
27149910-9	2016	The dose-adjusted trough levels and AUC of diltiazem and its main metabolites were significantly lower in CYP3A5*1*1 carriers than in CYP3A5*3 carriers (P < 0 05).	Diltiazem	43-52	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	134-140
26259627-3	2016	In this study, we report the results of a first-of-a-kind clinical trial studying late sodium (mexiletine and lidocaine) and calcium (diltiazem) current blocking drugs to counteract the effects of hERG potassium channel blocking drugs (dofetilide and moxifloxacin).	Diltiazem	134-143	ETS transcription factor ERG	Homo sapiens	197-201
26432297-10	2016	Consistent with these observations, AngII-treatment also sensitized the vaso-relaxing effects of the L-type Ca(2+) channel blocker diltiazem during K(+)-induced contractions.	Diltiazem	131-140	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	36-41
27160091-5	2016	Notably, HBO and diltiazem preconditioning significantly increased Bcl-2 protein expression and decreased Bax protein and caspase-3 mRNA expression.	Diltiazem	17-26	BCL2, apoptosis regulator	Rattus norvegicus	67-72
27160091-5	2016	Notably, HBO and diltiazem preconditioning significantly increased Bcl-2 protein expression and decreased Bax protein and caspase-3 mRNA expression.	Diltiazem	17-26	BCL2 associated X, apoptosis regulator	Rattus norvegicus	106-109
27160091-5	2016	Notably, HBO and diltiazem preconditioning significantly increased Bcl-2 protein expression and decreased Bax protein and caspase-3 mRNA expression.	Diltiazem	17-26	caspase 3	Rattus norvegicus	122-131
26024096-4	2015	Subgroups were pretreated with D-cis-diltiazem (DIL) at a dose that specifically antagonizes Ca(v)1.2 channels in vivo.	Diltiazem	31-46	calcium channel, voltage-dependent, L type, alpha 1C subunit	Mus musculus	93-101
25989107-9	2015	CA4P injection also significantly increased the cardiac troponin I level in hypertensive rats though pretreatment with diltiazem effectively blocked troponin I increase after CA4P administration.	Diltiazem	119-128	troponin I3, cardiac type	Rattus norvegicus	48-66
26398391-2	2015	Since diltiazem and verapamil, which are highly lipophilic Ca(2+) channel blockers (CCBs), exert relatively stronger immunomodulatory effects than the other types of CCBs, they would affect the Kv1.3-channel currents in lymphocytes.	Diltiazem	6-15	potassium voltage-gated channel, shaker-related subfamily, member 3	Mus musculus	194-199
26398391-6	2015	CONCLUSIONS: This study demonstrated for the first time that CCBs, such as diltiazem and verapamil, exert inhibitory effects on Kv1.3-channels expressed in lymphocytes.	Diltiazem	75-84	potassium voltage-gated channel, shaker-related subfamily, member 3	Mus musculus	128-133
25712868-5	2015	In Cav1.2-expressing cells, treatment with thapsigargin (TG), to induce passive discharge of the intracellular Ca2+ stores, resulted in Ca2+ influx that was significantly greater than in cells not expressing Cav1.2 channels, a difference that was abolished by nifedipine and diltiazem.	Diltiazem	275-284	calcium voltage-gated channel subunit alpha1 C	Homo sapiens	3-9
26498522-9	2015	In parallel experiments, ox-LDL increased the influx of extracellular calcium, activation of protein kinase C (PKC) and permeability to LDL, which was inhibited by the LOX-1blocking antibody (10 mug/ml), Ca(2+) channel blocker (Diltiazem, 50 mumol/L) and PKC-beta inhibitor (hispidin, 4 mumol/L).	Diltiazem	228-237	oxidized low density lipoprotein receptor 1	Homo sapiens	168-173
25979260-0	2015	Characterization of Species Differences in Tissue Diltiazem Deacetylation Identifies Ces2a as a Rat-Specific Diltiazem Deacetylase.	Diltiazem	50-59	carboxylesterase 2A	Rattus norvegicus	85-90
25979260-7	2015	On the basis of their tissue distribution, the Ces2a enzyme was considered to be the enzyme that was responsible for diltiazem deacetylation.	Diltiazem	117-126	carboxylesterase 2A	Rattus norvegicus	47-52
25891084-0	2015	Diltiazem augments the influence of MDR1 genotype status on cyclosporine concentration in Chinese patients with renal transplantation.	Diltiazem	0-9	ATP binding cassette subfamily B member 1	Homo sapiens	36-40
25891084-2	2015	In this study, we investigated how diltiazem altered the relationship between MDR1 genetic polymorphisms and CsA concentration in Chinese patients with renal transplantation.	Diltiazem	35-44	ATP binding cassette subfamily B member 1	Homo sapiens	78-82
25891084-12	2015	CONCLUSION: MDR1 variants influence the adjusted CsA trough concentration in Chinese patients with renal transplant, and the influence more prominent when diltiazem is co-administered.	Diltiazem	155-164	ATP binding cassette subfamily B member 1	Homo sapiens	12-16
26024096-4	2015	Subgroups were pretreated with D-cis-diltiazem (DIL) at a dose that specifically antagonizes Ca(v)1.2 channels in vivo.	Diltiazem	48-51	calcium channel, voltage-dependent, L type, alpha 1C subunit	Mus musculus	93-101
26024096-8	2015	Manganese-enhanced MRI of DIL-treated Arr1(-/-) mice suggested a greater number of operant LTCC subtypes (i.e., Ca(v)1.2, 1.3, and 1.4) in rods and inner retina than that in DIL-treated Ca(v)1.4(-/-) mice (i.e., Ca(v)1.3).	Diltiazem	26-29	S-antigen, retina and pineal gland (arrestin)	Mus musculus	38-42
26024096-8	2015	Manganese-enhanced MRI of DIL-treated Arr1(-/-) mice suggested a greater number of operant LTCC subtypes (i.e., Ca(v)1.2, 1.3, and 1.4) in rods and inner retina than that in DIL-treated Ca(v)1.4(-/-) mice (i.e., Ca(v)1.3).	Diltiazem	26-29	calcium channel, voltage-dependent, L type, alpha 1C subunit	Mus musculus	112-120
26024096-8	2015	Manganese-enhanced MRI of DIL-treated Arr1(-/-) mice suggested a greater number of operant LTCC subtypes (i.e., Ca(v)1.2, 1.3, and 1.4) in rods and inner retina than that in DIL-treated Ca(v)1.4(-/-) mice (i.e., Ca(v)1.3).	Diltiazem	26-29	calcium channel, voltage-dependent, alpha 1F subunit	Mus musculus	186-194
26024096-8	2015	Manganese-enhanced MRI of DIL-treated Arr1(-/-) mice suggested a greater number of operant LTCC subtypes (i.e., Ca(v)1.2, 1.3, and 1.4) in rods and inner retina than that in DIL-treated Ca(v)1.4(-/-) mice (i.e., Ca(v)1.3).	Diltiazem	26-29	calcium channel, voltage-dependent, L type, alpha 1D subunit	Mus musculus	212-220
25729581-3	2015	Selected Pgp transport ligands include: Amiodarone, Bepridil, Diltiazem, Dipyridamole, Nicardipine, Nifedipine, Propranolol, and Quinidine.	Diltiazem	62-71	phosphoglycolate phosphatase	Mus musculus	9-12
25731063-7	2014	Then, diltiazem (0.5 mug x kg(-1) x min(-1)) was continuously administered, and the infusion rate of remifentanil was increased to 0.3 mug x kg(-1) x min(-1).	Diltiazem	6-15	CD59 molecule (CD59 blood group)	Homo sapiens	36-42
25543971-13	2015	Among MYBPC3 mutation carriers, LV wall thickness and mass, diastolic filling, and cardiac troponin I levels improved in those taking diltiazem compared with controls.	Diltiazem	134-143	myosin binding protein C3	Homo sapiens	6-12
25233454-9	2014	A further experiment demonstrated that atenolol and diltiazem, two current drugs for treating hypertension, reduce the vanin-1 protein level.	Diltiazem	52-61	vanin 1	Homo sapiens	119-126
25126989-5	2014	Inhibiting ERdj3-mediated mutant GCase degradation while simultaneously enhancing calnexin-associated folding, by way of a diltiazem-mediated increase in ER Ca(2+) levels, yields a synergistic rescue of L444P GCase lysosomal function.	Diltiazem	123-132	DnaJ heat shock protein family (Hsp40) member B11	Homo sapiens	11-16
25126989-5	2014	Inhibiting ERdj3-mediated mutant GCase degradation while simultaneously enhancing calnexin-associated folding, by way of a diltiazem-mediated increase in ER Ca(2+) levels, yields a synergistic rescue of L444P GCase lysosomal function.	Diltiazem	123-132	glucosylceramidase beta	Homo sapiens	209-214
24604243-0	2014	Pharmacokinetic interactions between the orexin receptor antagonist almorexant and the CYP3A4 inhibitors ketoconazole and diltiazem.	Diltiazem	122-131	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	87-93
24012931-11	2013	However, the release of Muc5ac in BALF was further reduced when challenged with simultaneous instillation with MARCKS-related peptide and diltiazem, compared with MARCKS-related peptide alone (p<0.05).	Diltiazem	138-147	mucin 5AC, oligomeric mucus/gel-forming	Rattus norvegicus	24-30
24144954-1	2013	An innovative matrix, produced by thermal treatment on direct compression (DC) tablets containing polycarbophil (POL) and ethylcellulose (EC), identified as matrix forming polymers, and able to control the release of diltiazem hydrochloride, was developed.	Diltiazem	217-240	endogenous retrovirus group W member 4	Homo sapiens	113-116
24144954-7	2013	The maximum amount of diltiazem hydrochloride released by zero-order kinetics, at the lowest release rate, occurs for POL:EC ratio in the range of 1:1-2:3 with 20-30% of diluent.	Diltiazem	22-45	endogenous retrovirus group W member 4	Homo sapiens	118-124
24082061-8	2013	Indeed, diltiazem prevented the interleukin-6-induced mRNA expression of interleukin-1beta and the monocyte chemoattractant protein CCL12 in peritoneal macrophages and RAW264.7 cells independent of the intracellular calcium concentration.	Diltiazem	8-17	interleukin 6	Mus musculus	32-45
24082061-8	2013	Indeed, diltiazem prevented the interleukin-6-induced mRNA expression of interleukin-1beta and the monocyte chemoattractant protein CCL12 in peritoneal macrophages and RAW264.7 cells independent of the intracellular calcium concentration.	Diltiazem	8-17	interleukin 1 beta	Mus musculus	73-90
24082061-8	2013	Indeed, diltiazem prevented the interleukin-6-induced mRNA expression of interleukin-1beta and the monocyte chemoattractant protein CCL12 in peritoneal macrophages and RAW264.7 cells independent of the intracellular calcium concentration.	Diltiazem	8-17	chemokine (C-C motif) ligand 12	Mus musculus	132-137
25228033-6	2014	RESULTS: Compared with the MI/RI group, pretreatment with YLSF or diltiazem hydrochloride decreased the infarct area, levels of inducible nitric oxide synthase (iNOS), caspase-3 as well as the leakage of myocardial enzyme and increased activities of total nitric oxide synthase (tNOS) as well as constitutive nitric oxide synthase (cNOS).	Diltiazem	66-89	nitric oxide synthase 2	Rattus norvegicus	128-159
25228033-6	2014	RESULTS: Compared with the MI/RI group, pretreatment with YLSF or diltiazem hydrochloride decreased the infarct area, levels of inducible nitric oxide synthase (iNOS), caspase-3 as well as the leakage of myocardial enzyme and increased activities of total nitric oxide synthase (tNOS) as well as constitutive nitric oxide synthase (cNOS).	Diltiazem	66-89	nitric oxide synthase 2	Rattus norvegicus	161-165
25228033-6	2014	RESULTS: Compared with the MI/RI group, pretreatment with YLSF or diltiazem hydrochloride decreased the infarct area, levels of inducible nitric oxide synthase (iNOS), caspase-3 as well as the leakage of myocardial enzyme and increased activities of total nitric oxide synthase (tNOS) as well as constitutive nitric oxide synthase (cNOS).	Diltiazem	66-89	caspase 3	Rattus norvegicus	168-177
25228033-6	2014	RESULTS: Compared with the MI/RI group, pretreatment with YLSF or diltiazem hydrochloride decreased the infarct area, levels of inducible nitric oxide synthase (iNOS), caspase-3 as well as the leakage of myocardial enzyme and increased activities of total nitric oxide synthase (tNOS) as well as constitutive nitric oxide synthase (cNOS).	Diltiazem	66-89	nitric oxide synthase 3	Rattus norvegicus	332-336
24012931-12	2013	The intracellular level of Muc5ac in lung was increased when treated with MARCKS-related peptide alone or MARCKS-related peptide plus diltiazem (p<0.05).	Diltiazem	134-143	mucin 5AC, oligomeric mucus/gel-forming	Rattus norvegicus	27-33
24012931-14	2013	CONCLUSIONS: In the model of airway mucus hypersecretion induced by acrolein, MARCKS-related peptide attenuated mucus secretion and the inhibitory effect was enhanced by diltiazem, which may be due to a further diminution of the intracellular free calcium concentration and retention of mucin within epithelial goblet cells.	Diltiazem	170-179	myristoylated alanine rich protein kinase C substrate	Rattus norvegicus	78-84
24012931-14	2013	CONCLUSIONS: In the model of airway mucus hypersecretion induced by acrolein, MARCKS-related peptide attenuated mucus secretion and the inhibitory effect was enhanced by diltiazem, which may be due to a further diminution of the intracellular free calcium concentration and retention of mucin within epithelial goblet cells.	Diltiazem	170-179	solute carrier family 13 member 2	Rattus norvegicus	287-292
23753411-5	2013	The rs2273359 polymorphism in the GNAS-EDN3 region also replicated for same-direction association with systolic blood pressure response in the Nordic Diltiazem study, and the combined 3-study meta-analysis P value approached genome-wide significance (P=5.5 x 10(-8)).	Diltiazem	150-159	GNAS complex locus	Homo sapiens	34-38
23432535-9	2013	Results showed that CYP3A5 expressers needed more tacrolimus to reach therapeutic concentration window and were more susceptible to diltiazem-induced concentration increase than CYP3A5 non-expressers.	Diltiazem	132-141	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	20-26
23753411-5	2013	The rs2273359 polymorphism in the GNAS-EDN3 region also replicated for same-direction association with systolic blood pressure response in the Nordic Diltiazem study, and the combined 3-study meta-analysis P value approached genome-wide significance (P=5.5 x 10(-8)).	Diltiazem	150-159	endothelin 3	Homo sapiens	39-43
23381958-2	2013	This study investigated the effect of diltiazem, a moderate inhibitor of CYP3A4, on the single-dose pharmacokinetics of ACT-178882 in healthy subjects.	Diltiazem	38-47	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	73-79
23789484-6	2013	The first goal in management of cramp is to determine if there is an underlying cause and the second to use physical measures (stretching), because, pharmacologic treatments have a moderate interest because of the potential of toxicity (quinine sulfate) or a little effectiveness (vitamin B complex, naftidrofuryl, and calcium channel blockers such as diltiazem, gabapentin).	Diltiazem	352-361	cathelicidin antimicrobial peptide	Homo sapiens	32-37
27121666-7	2013	In conclusion, diltiazem markedly affected the pharmacokinetics of ACT-077825, probably via inhibition of CYP3A4 activity, without changing its safety and tolerability profile in healthy male subjects.	Diltiazem	15-24	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	106-112
23700791-0	2013	Effects of CYP3A5 and CYP2D6 genetic polymorphism on the pharmacokinetics of diltiazem and its metabolites in Chinese subjects.	Diltiazem	77-86	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	11-17
23700791-0	2013	Effects of CYP3A5 and CYP2D6 genetic polymorphism on the pharmacokinetics of diltiazem and its metabolites in Chinese subjects.	Diltiazem	77-86	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	22-28
23700791-1	2013	PURPOSE: To assess the possibility of using CYP2D6 10 +/- CYP3A5*3 as biomarkers to predict the pharmacokinetics of diltiazem and its two metabolites among healthy Chinese subjects.	Diltiazem	116-125	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	44-50
23700791-1	2013	PURPOSE: To assess the possibility of using CYP2D6 10 +/- CYP3A5*3 as biomarkers to predict the pharmacokinetics of diltiazem and its two metabolites among healthy Chinese subjects.	Diltiazem	116-125	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	58-64
23700791-9	2013	Despite this, the effect of genotype of CYP2D6 on clinical outcome of diltiazem treatment is expected to be limited.	Diltiazem	70-79	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	40-46
22841259-9	2012	The lowest CAT mean levels were noted in the CsA and diltiazem groups with highest CAT content was in the CsA and cilostazol groups.	Diltiazem	53-62	catalase	Rattus norvegicus	11-14
23300272-7	2013	Other dihydropyridines, nicardipine and Bay K8644, had similar augmenting effects on the CaSR-mediated increase in [Ca(2+)](cyt) in IPAH-PASMC; however, the nondihydropyridine blockers, such as diltiazem and verapamil, had no effect on the CaSR-mediated rise in [Ca(2+)](cyt).	Diltiazem	194-203	calcium sensing receptor	Homo sapiens	89-93
23648675-9	2013	The enzyme hydrolase activity of recombinant CES2 was substantially inhibited by diltiazem and verapamil (K(i) = 0.25 +- 0.02 and 3.84 +- 0.99 microM, respectively).	Diltiazem	81-90	carboxylesterase 2	Homo sapiens	45-49
23648675-10	2013	Hence, diltiazem, verapamil, nitrendipine and telmisartan may attenuate the drug efficacy of catalyzed prodrugs by changing the activities of CES1A1 and CES2.	Diltiazem	7-16	carboxylesterase 2	Homo sapiens	153-157
22927137-0	2012	Repeated dosing of piperine induced gene expression of P-glycoprotein via stimulated pregnane-X-receptor activity and altered pharmacokinetics of diltiazem in rats.	Diltiazem	146-155	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	55-69
22828972-13	2012	Enzyme inhibition produced by diltiazem may have contributed to decreasing CYP3A4 activity.	Diltiazem	30-39	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	75-81
22648446-15	2012	Proliferating cell nuclear antigen expression levels were significantly reduced in the atosiban and diltiazem groups compared with the control group.	Diltiazem	100-109	proliferating cell nuclear antigen	Rattus norvegicus	0-34
22841259-9	2012	The lowest CAT mean levels were noted in the CsA and diltiazem groups with highest CAT content was in the CsA and cilostazol groups.	Diltiazem	53-62	catalase	Rattus norvegicus	83-86
22513469-7	2012	The average daily food intake and body weight were significantly increased, and the serum concentrations of GH and NPY were also remarkably increased in diltiazem-treated groups compared with those in control group.	Diltiazem	153-162	gonadotropin releasing hormone receptor	Rattus norvegicus	108-110
22652334-7	2012	After pre-incubation, CYP3A4 IC(50) shifts caused by diltiazem and mifepristone were greater than 2.5- and 3.7-fold, respectively.	Diltiazem	53-62	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	22-28
22652334-8	2012	Incubation with 2mM potassium ferricyanide for 10min reversed the MDI of CYP3A4 by diltiazem, but not mifepristone.	Diltiazem	83-92	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	73-79
22652334-10	2012	The established methods were confirmed using three CYP3A4 inhibitors including diltiazem, mifepristone and amiodarone (a reversible metabolism-dependent inhibitor).	Diltiazem	79-88	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	51-57
22525200-4	2012	CYP17A1-rs11191548 associated with less DBP reduction (beta = -1.26 mmHg per unfavorable allele; P = 0.018) in patients treated with beta-blockers or diuretics, whereas there was no treatment response association in diltiazem-treated patients.	Diltiazem	216-225	cytochrome P450 family 17 subfamily A member 1	Homo sapiens	0-7
22393247-9	2012	The combination of diltiazem and lactacystin also up-regulated the levels of Bik and released Bak from Bcl-xL, indicating the involvement of the Bcl2 family pathway in this apoptosis.	Diltiazem	19-28	BCL2 interacting killer	Homo sapiens	77-80
22393247-9	2012	The combination of diltiazem and lactacystin also up-regulated the levels of Bik and released Bak from Bcl-xL, indicating the involvement of the Bcl2 family pathway in this apoptosis.	Diltiazem	19-28	BCL2 antagonist/killer 1	Homo sapiens	94-97
22393247-9	2012	The combination of diltiazem and lactacystin also up-regulated the levels of Bik and released Bak from Bcl-xL, indicating the involvement of the Bcl2 family pathway in this apoptosis.	Diltiazem	19-28	BCL2 like 1	Homo sapiens	103-109
22393247-9	2012	The combination of diltiazem and lactacystin also up-regulated the levels of Bik and released Bak from Bcl-xL, indicating the involvement of the Bcl2 family pathway in this apoptosis.	Diltiazem	19-28	BCL2 apoptosis regulator	Homo sapiens	145-149
22513469-7	2012	The average daily food intake and body weight were significantly increased, and the serum concentrations of GH and NPY were also remarkably increased in diltiazem-treated groups compared with those in control group.	Diltiazem	153-162	neuropeptide Y	Rattus norvegicus	115-118
21835977-5	2011	Using two of the optimized methods, the time-dependent inhibition kinetic parameters (K(I) and k(inact)) for four known CYP3A4 TDI (diltiazem, erythromycin, verapamil, and troleandomycin) were determined.	Diltiazem	132-141	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	120-126
22292988-14	2012	Interestingly, co-administration with nifedipine, diltiazem or mexiletine prevented the oxaliplatin-induced cold hyperalgesia and increase in the TRPM8 mRNA levels in the DRG.	Diltiazem	50-59	transient receptor potential cation channel, subfamily M, member 8	Rattus norvegicus	146-151
21689675-0	2011	Diltiazem potentiates pentobarbital-induced hypnosis via 5-HT1A and 5-HT2A/2C receptors: role for dorsal raphe nucleus.	Diltiazem	0-9	5-hydroxytryptamine receptor 1A	Rattus norvegicus	57-69
21209240-2	2011	Diltiazem interaction studies assess a given compound"s sensitivity to moderate CYP3A inhibition.	Diltiazem	0-9	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	80-85
21209240-5	2011	The GMR (midazolam + diltiazem(XR x 2 days)/midazolam + diltiazem(CR x 2 days)) for midazolam AUC(0- ) was 0.82 (90% CI, 0.73, 0.92).	Diltiazem	21-30	colony stimulating factor 2 receptor subunit alpha	Homo sapiens	4-7
21209240-5	2011	The GMR (midazolam + diltiazem(XR x 2 days)/midazolam + diltiazem(CR x 2 days)) for midazolam AUC(0- ) was 0.82 (90% CI, 0.73, 0.92).	Diltiazem	56-65	colony stimulating factor 2 receptor subunit alpha	Homo sapiens	4-7
21689675-3	2011	This study was designed to investigate the role of DRN and the serotonergic receptors 5-HT(1A) and 5-HT(2A/2C) in the augmentative effect of diltiazem on pentobarbital-induced hypnosis in rats.	Diltiazem	141-150	5-hydroxytryptamine receptor 1A	Rattus norvegicus	86-93
21689675-3	2011	This study was designed to investigate the role of DRN and the serotonergic receptors 5-HT(1A) and 5-HT(2A/2C) in the augmentative effect of diltiazem on pentobarbital-induced hypnosis in rats.	Diltiazem	141-150	5-hydroxytryptamine receptor 2A	Rattus norvegicus	99-106
21689675-15	2011	From these results, it should be presumed that the augmentative effect of diltiazem on pentobarbital-induced sleep may be related to 5-HT(1A) and 5-HT(2A/2C) receptors, and DRN may be involved.	Diltiazem	74-83	5-hydroxytryptamine receptor 1A	Rattus norvegicus	133-140
21689675-15	2011	From these results, it should be presumed that the augmentative effect of diltiazem on pentobarbital-induced sleep may be related to 5-HT(1A) and 5-HT(2A/2C) receptors, and DRN may be involved.	Diltiazem	74-83	5-hydroxytryptamine receptor 2A	Rattus norvegicus	146-153
21480191-2	2011	Seven separate drug-drug interaction (DDI) studies were performed to elucidate the in vivo effects of concomitant treatment with colchicine and known inhibitors of cytochrome P450 3A4 (CYP3A4)/P-glycoprotein (cyclosporine, ketoconazole, ritonavir, clarithromycin, azithromycin, verapamil ER [extended release]), and diltiazem ER) on the pharmacokinetics of colchicine.	Diltiazem	316-325	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	185-191
22026129-4	2011	Furthermore, the oral and intravenous pharmacokinetics of diltiazem, a P-gp substrate as well as its active metabolite, desacetyldiltiazem, was determined in rats after pretreatment with biochanin A. Pretreatment with biochanin A in a SD formulation significantly (p < 0.05) increased the AUC of desacetyldiltiazem by 3-fold, although the oral exposure of diltiazem was not altered.	Diltiazem	58-67	phosphoglycolate phosphatase	Rattus norvegicus	71-75
21704284-7	2011	The GTN caused nearly full relaxation (93.1%+-4.8%) but GTN pretreatment had limited effect in prevention of the hU-II-induced contraction, whereas diltiazem and nifedipine reduced subsequent contraction to hU-II.	Diltiazem	148-157	urotensin 2	Homo sapiens	207-212
19876599-0	2011	Inhibition of MDR1 activity and induction of apoptosis by analogues of nifedipine and diltiazem: an in vitro analysis.	Diltiazem	86-95	ATP binding cassette subfamily B member 1	Homo sapiens	14-18
20514078-0	2011	Effects of diltiazem on pharmacokinetics of tacrolimus in relation to CYP3A5 genotype status in renal recipients: from retrospective to prospective.	Diltiazem	11-20	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	70-76
20514078-2	2011	In retrospective study, when coadministered with diltiazem, mean increments in dose-adjusted C(0D7), C(max) and AUC(0-12 h) for tacrolimus were larger in CYP3A5 expressers than in CYP3A5 nonexpressers (48.7 vs 3.7%, 31.7 vs 17.2% and 38.2 vs 18.5%, respectively).	Diltiazem	49-58	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	154-160
20514078-2	2011	In retrospective study, when coadministered with diltiazem, mean increments in dose-adjusted C(0D7), C(max) and AUC(0-12 h) for tacrolimus were larger in CYP3A5 expressers than in CYP3A5 nonexpressers (48.7 vs 3.7%, 31.7 vs 17.2% and 38.2 vs 18.5%, respectively).	Diltiazem	49-58	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	180-186
20514078-4	2011	For CYP3A5 expressers, an algorithm guided by CYP3A5 and diltiazem significantly reduced tacrolimus maintenance dosage (P=0.009) and improved the accuracy of tacrolimus initial dose, resulting in reduction in out-of-range C(0) after initial dose (P=0.002) and dose adjustments (P=0.004).	Diltiazem	57-66	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	4-10
20514078-6	2011	Our study results show that CYP3A5 genotype-guided tacrolimus-diltiazem combination is a promising therapy in renal transplant recipients in the early postoperative stage.	Diltiazem	62-71	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	28-34
21545622-4	2011	COMMENT: A 63-year-old Chinese woman with hypertension and familial hypercholesterolaemia (FH) taking diltiazem 90 mg twice daily had elevation of creatine kinase (CK) to 4016 U/L and alanine aminotransferase (ALT) to 165 IU/L 4 weeks after increasing the dose of simvastatin from 40 to 80 mg daily.	Diltiazem	102-111	glutamic--pyruvic transaminase	Homo sapiens	184-208
21356216-3	2011	MAIN METHODS: Diltiazem N-demethylase activity of recombinant CYP3A4, CYP3A5, CYP3A7, and human liver microsomes (HLMs) in the presence of cannabinoids was determined.	Diltiazem	14-23	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	62-68
21356216-3	2011	MAIN METHODS: Diltiazem N-demethylase activity of recombinant CYP3A4, CYP3A5, CYP3A7, and human liver microsomes (HLMs) in the presence of cannabinoids was determined.	Diltiazem	14-23	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	70-76
21356216-3	2011	MAIN METHODS: Diltiazem N-demethylase activity of recombinant CYP3A4, CYP3A5, CYP3A7, and human liver microsomes (HLMs) in the presence of cannabinoids was determined.	Diltiazem	14-23	cytochrome P450 family 3 subfamily A member 7	Homo sapiens	78-84
21210865-2	2011	In this study, we examined the possibility that diltiazem may affect human dendritic cell (DC) functions in response to lipopolysaccharide (LPS) stimulation and may induce the generation of DC with the capacity to generate CD4(+) regulatory T cells (Tregs).	Diltiazem	48-57	CD4 molecule	Homo sapiens	223-226
21210865-4	2011	Monocyte-derived DCs were stimulated with LPS, and DCs differentiated in the presence of diltiazem showed a decreased interleukin (IL)-12 production and an enhanced IL-10 production.	Diltiazem	89-98	interleukin 10	Homo sapiens	165-170
21112316-7	2011	Further, verapamil (10 and 20mg/kg), diltiazem (10 and 20mg/kg) treatment significantly attenuated oxidative damage, level of proinflammatory mediators (TNF-alpha IL-6 and caspase-3) in quinolinic acid treated animals.	Diltiazem	37-46	caspase 3	Rattus norvegicus	172-181
22034612-8	2011	In addition, ROCE and SOCE were abolished by SKF-96365 (50 muM) and 2-aminoethyl diphenylborinate (100 muM), and were slightly decreased in the presence of diltiazem (10 muM).	Diltiazem	156-165	latexin	Homo sapiens	59-62
22034612-8	2011	In addition, ROCE and SOCE were abolished by SKF-96365 (50 muM) and 2-aminoethyl diphenylborinate (100 muM), and were slightly decreased in the presence of diltiazem (10 muM).	Diltiazem	156-165	latexin	Homo sapiens	103-106
22034612-8	2011	In addition, ROCE and SOCE were abolished by SKF-96365 (50 muM) and 2-aminoethyl diphenylborinate (100 muM), and were slightly decreased in the presence of diltiazem (10 muM).	Diltiazem	156-165	latexin	Homo sapiens	103-106
20973779-0	2011	Interaction of diltiazem with an intracellularly accessible binding site on Ca(V)1.2.	Diltiazem	15-24	immunoglobulin lambda variable 2-8	Homo sapiens	76-84
20973779-1	2011	BACKGROUND AND PURPOSE: Diltiazem inhibits Ca(V)1.2 channels and is widely used in clinical practice to treat cardiovascular diseases.	Diltiazem	24-33	immunoglobulin lambda variable 2-8	Homo sapiens	43-51
20973779-2	2011	Binding determinants for diltiazem are located on segments IIIS6, IVS6 and the selectivity filter of the pore forming alpha1 subunit of Ca(V)1.2.	Diltiazem	25-34	immunoglobulin lambda variable 2-8	Homo sapiens	136-144
20973779-6	2011	KEY RESULTS: Quaternary derivative d-cis-diltiazem inhibited Ca(V)1.2 when applied to the intracellular side of the membrane in a use-dependent manner (59 +- 4% at 300 microM) and induced only a low level of tonic (non-use-dependent) block (16 +- 2% at 300 microM) when applied to the extracellular side of the membrane.	Diltiazem	35-50	immunoglobulin lambda variable 2-8	Homo sapiens	61-69
20973779-7	2011	Mutations in IIIS6 and IVS6 that have previously been shown to reduce the sensitivity of Ca(V)1.2 to tertiary diltiazem also had reduced sensitivity to intracellularly applied qDil.	Diltiazem	110-119	immunoglobulin lambda variable 2-8	Homo sapiens	89-97
20973779-8	2011	CONCLUSION AND IMPLICATIONS: The data show that use-dependent block of in Ca(V)1.2 by diltiazem occurs by interaction with a binding site accessible via a hydrophilic route from the intracellular side of the membrane.	Diltiazem	86-95	immunoglobulin lambda variable 2-8	Homo sapiens	74-82
21210344-0	2011	Inhibition of connexin43 dephosphorylation is involved in protective effects of diltiazem on cardiac function during hypoxic injury.	Diltiazem	80-89	gap junction protein, alpha 1	Rattus norvegicus	14-24
21210344-5	2011	In this study, we assess the effect of diltiazem pretreatment upon ischemia-induced phosphorylation change of Cx43.	Diltiazem	39-48	gap junction protein, alpha 1	Rattus norvegicus	110-114
21052022-7	2011	CONCLUSION: The functional NEDD4L rs4149601 polymorphism influences the efficacy of beta-blocker and/or diuretic-based antihypertensive treatment both in terms of blood pressure reduction and cardiovascular disease protection, whereas diltiazem-based antihypertensive treatment efficacy is not influenced by this NEDD4L polymorphism.	Diltiazem	235-244	NEDD4 like E3 ubiquitin protein ligase	Homo sapiens	27-33
21929464-3	2011	RESULTS: Plasma concentrations of DTZ were higher in the SHR than the normotensive SDR and WKY rats, although the differences did not reach statistical significance (p>0.05).	Diltiazem	34-37	caveolae associated protein 2	Homo sapiens	83-86
21210344-13	2011	CONCLUSIONS: Pretreatment of diltiazem could protect the heart against hypoxia-reoxygenation injury by attenuation of dephosphorylation of Cx43.	Diltiazem	29-38	gap junction protein, alpha 1	Rattus norvegicus	139-143
21210344-14	2011	The anti-arrhythmic mechanism of diltiazem may include the preservation of phosphorylation status of Cx43 after hypoxia-reoxygenation injury.	Diltiazem	33-42	gap junction protein, alpha 1	Rattus norvegicus	101-105
20872164-3	2011	Three genes (ADH1, RNT1, and SUI1) were found to suppress the CdCl(2) sensitivity of the msb3 strain and three others (YAP6, ZEO1, and SLM1) its diltiazem-HCl sensitivity.	Diltiazem	145-158	Rab GTPase-activating protein MSB3	Saccharomyces cerevisiae S288C	89-93
20872164-3	2011	Three genes (ADH1, RNT1, and SUI1) were found to suppress the CdCl(2) sensitivity of the msb3 strain and three others (YAP6, ZEO1, and SLM1) its diltiazem-HCl sensitivity.	Diltiazem	145-158	Yap6p	Saccharomyces cerevisiae S288C	119-123
20872164-3	2011	Three genes (ADH1, RNT1, and SUI1) were found to suppress the CdCl(2) sensitivity of the msb3 strain and three others (YAP6, ZEO1, and SLM1) its diltiazem-HCl sensitivity.	Diltiazem	145-158	phosphatidylinositol 4,5-bisphosphate-binding protein	Saccharomyces cerevisiae S288C	135-139
22287853-6	2011	Mean exposure (AUC) of the CYP3A4-generated active metabolite of saxagliptin, 5-hydroxy saxagliptin, decreased with coadministration of simvastatin, diltiazem, and ketoconazole by 2%, 34%, and 88%, respectively.	Diltiazem	149-158	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	27-33
21138812-5	2010	Both diltiazem (1 muM), an L-type Ca2+ channel blocker and ryanodine (10 nM), a sarcoplasmic reticulum (SR) Ca2+ release channel opener completely suppressed the rAmylin-induced positive inotropic effect, but staurosporine (100 nM), a potent protein kinase C (PKC) inhibitor suppressed it partially.	Diltiazem	5-14	islet amyloid polypeptide	Rattus norvegicus	162-169
20872164-3	2011	Three genes (ADH1, RNT1, and SUI1) were found to suppress the CdCl(2) sensitivity of the msb3 strain and three others (YAP6, ZEO1, and SLM1) its diltiazem-HCl sensitivity.	Diltiazem	145-158	alcohol dehydrogenase ADH1	Saccharomyces cerevisiae S288C	13-17
20872164-3	2011	Three genes (ADH1, RNT1, and SUI1) were found to suppress the CdCl(2) sensitivity of the msb3 strain and three others (YAP6, ZEO1, and SLM1) its diltiazem-HCl sensitivity.	Diltiazem	145-158	ribonuclease III	Saccharomyces cerevisiae S288C	19-23
20872164-3	2011	Three genes (ADH1, RNT1, and SUI1) were found to suppress the CdCl(2) sensitivity of the msb3 strain and three others (YAP6, ZEO1, and SLM1) its diltiazem-HCl sensitivity.	Diltiazem	145-158	translation initiation factor eIF1	Saccharomyces cerevisiae S288C	29-33
22358108-1	2011	The purpose of this study was to investigate the possible effects of hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor, simvastatin, on the pharmacokinetics of diltiazem and its main metabolite, desacetyldiltiazem, in rats.	Diltiazem	173-182	3-hydroxy-3-methylglutaryl-CoA reductase	Rattus norvegicus	69-121
22358108-12	2011	The increase in diltiazem oral bioavailability might be attributable to enhanced absorption in the small intestine via the inhibition of P-gp and to reduced first-pass metabolism of diltiazem via the inhibition of the CYP3A subfamily in the small intestine and/or in the liver rather than renal elimination of diltiazem by simvastatin.	Diltiazem	16-25	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	137-141
21084035-4	2010	The possible relative risk factors included advanced age, chronic and systemic diseases, and co-administration of cytochrome P450 3A (CYP3A) enzyme-dependent metabolic drugs or its inhibitors such as clopidogrel and diltiazem.	Diltiazem	216-225	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	114-132
21084035-4	2010	The possible relative risk factors included advanced age, chronic and systemic diseases, and co-administration of cytochrome P450 3A (CYP3A) enzyme-dependent metabolic drugs or its inhibitors such as clopidogrel and diltiazem.	Diltiazem	216-225	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	134-139
21929464-5	2011	CONCLUSIONS: Although the differences were mainly quantitative and very small, the study has shown for the first time that the metabolism profiles of DTZ in SHR and WKY rats were closer to humans than SDR, and they may be more preferable rat models to study pharmacokinetic and metabolism studies of DTZ or similar agents.	Diltiazem	150-153	caveolae associated protein 2	Homo sapiens	201-204
21112467-0	2010	Case report: delirium due to a diltiazem-fentanyl CYP3A4 drug interaction.	Diltiazem	31-40	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	50-56
21112467-2	2010	Diltiazem inhibits cytochrome P450 3A4 isoenzymes.	Diltiazem	0-9	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	19-38
20150526-1	2010	Diltiazem increases systemic exposure to simvastatin via inhibition of CYP3A.	Diltiazem	0-9	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	71-76
20660906-0	2010	Diltiazem overdose: a role for high-dose insulin.	Diltiazem	0-9	insulin	Homo sapiens	41-48
20630935-7	2010	In 10 mM Ba(2+), pericyte Ca(V) currents activated with threshold depolarizations to -30 mV, were blocked by nifedipine, exhibited voltage-dependent block by diltiazem (10 muM), and conducted Ba(2+) > Ca(2+) at a ratio of ~2:1.	Diltiazem	158-167	latexin	Homo sapiens	172-175
20649567-0	2010	Alternative splicing modulates diltiazem sensitivity of cardiac and vascular smooth muscle Ca(v)1.2 calcium channels.	Diltiazem	31-40	immunoglobulin lambda variable 2-8	Homo sapiens	91-99
20649567-1	2010	BACKGROUND AND PURPOSE: As a calcium channel blocker, diltiazem acts mainly on the voltage-gated calcium channels, Ca(v)1.2, for its beneficial effects in cardiovascular diseases such as hypertension, angina and/or supraventricular arrhythmias.	Diltiazem	54-63	immunoglobulin lambda variable 2-8	Homo sapiens	115-123
20649567-2	2010	However, the effects of diltiazem on different isoforms of Ca(v)1.2 channels expressed in heart and vascular smooth muscles remain to be investigated.	Diltiazem	24-33	immunoglobulin lambda variable 2-8	Homo sapiens	59-67
20649567-3	2010	Here, we characterized the effects of diltiazem on the splice variants of Ca(v)1.2 channels, predominant in cardiac and vascular smooth muscles.	Diltiazem	38-47	immunoglobulin lambda variable 2-8	Homo sapiens	74-82
20649567-5	2010	KEY RESULTS: Under closed-channel and use-dependent block (0.03 Hz), cardiac splice variant Ca(v)1.2CM was less sensitive to diltiazem than two major smooth muscle splice variants, Ca(v)1.2SM and Ca(v)1.2b.	Diltiazem	125-134	immunoglobulin lambda variable 2-8	Homo sapiens	92-100
20649567-9	2010	CONCLUSIONS AND IMPLICATIONS: Alternative splicing of Ca(v)1.2 channels modifies diltiazem sensitivity in the heart and blood vessels.	Diltiazem	81-90	immunoglobulin lambda variable 2-8	Homo sapiens	54-62
20394732-7	2010	Our findings showed that Ni(2+) and mibefradil at concentrations that block T-type or Ca(V)3 channels, and nimodipine and diltiazem that block L-type or Ca(V)1 channels, significantly inhibited the rhZP3-initiated AR.	Diltiazem	122-131	caveolin 1	Homo sapiens	153-159
20973294-0	2010	Calcium channel blocker (diltiazem) inhibits apoptosis of vascular smooth muscle cell exposed to high glucose concentration through lectin-like oxidized low density lipoprotein receptor-1 (LOX-1) pathway.	Diltiazem	25-34	oxidized low density lipoprotein receptor 1	Homo sapiens	189-194
20973294-1	2010	AIM: to examine the role of diltiazem in the prevention of VSMC apoptosis exposed to high glucose through inhibition of LOX-1 expression.	Diltiazem	28-37	oxidized low density lipoprotein receptor 1	Homo sapiens	120-125
20973294-17	2010	This effect appears to be inhibited by diltiazem through decreasing LOX-1 expression and activity.	Diltiazem	39-48	oxidized low density lipoprotein receptor 1	Homo sapiens	68-73
20118567-7	2010	Amlodipine and diltiazem significantly increased production of IL-1alpha stimulated with concanavalin A.	Diltiazem	15-24	interleukin 1 alpha	Homo sapiens	63-72
19809509-2	2009	Two L-type calcium channel (LTCC) blockers-verapamil and diltiazem-have been reported to modulate endoplasmic reticulum (ER) folding, trafficking, and activity of GCase in human Gaucher disease fibroblasts.	Diltiazem	57-66	glucosidase, beta, acid	Mus musculus	163-168
20238051-5	2010	A 1999 study suggested that the Ca(2+) channel antagonist D-cis diltiazem delays the kinetics of rd1 rod degeneration, conferring partial rescue of scotopic vision.	Diltiazem	58-73	phosphodiesterase 6B, cGMP, rod receptor, beta polypeptide	Mus musculus	97-100
19809509-4	2009	Correspondingly, diltiazem increased GCase protein and facilitated GCase trafficking to the lysosomes of these cells.	Diltiazem	17-26	glucosidase, beta, acid	Mus musculus	37-42
19809509-4	2009	Correspondingly, diltiazem increased GCase protein and facilitated GCase trafficking to the lysosomes of these cells.	Diltiazem	17-26	glucosidase, beta, acid	Mus musculus	67-72
19809509-6	2009	In D409H homozygotes diltiazem (10 mg/kg/d via drinking water or 50-200 mg/kg/d intraperitoneally) had minor effects on increasing GCase activity in brain and liver (1.2-fold).	Diltiazem	21-30	glucosidase, beta, acid	Mus musculus	131-136
19420129-1	2009	Prediction of the extent and time course of drug-drug interactions (DDIs) between the mechanism-based inhibitor diltiazem (DTZ) and the CYP3A4 substrate midazolam (MDZ) is confounded by time- and concentration-dependent clearance of the inhibitor.	Diltiazem	112-121	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	136-142
19420129-1	2009	Prediction of the extent and time course of drug-drug interactions (DDIs) between the mechanism-based inhibitor diltiazem (DTZ) and the CYP3A4 substrate midazolam (MDZ) is confounded by time- and concentration-dependent clearance of the inhibitor.	Diltiazem	123-126	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	136-142
19420129-3	2009	Enzyme kinetic parameters (k(inact) and K(I)) for DTZ and nd-DTZ were estimated in vitro and used to model the time course of changes in the amount of CYP3A4 in the liver and gut wall, which in turn, determined the nonlinear elimination of MDZ and DTZ, and the corresponding DDI.	Diltiazem	50-53	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	151-157
19420129-3	2009	Enzyme kinetic parameters (k(inact) and K(I)) for DTZ and nd-DTZ were estimated in vitro and used to model the time course of changes in the amount of CYP3A4 in the liver and gut wall, which in turn, determined the nonlinear elimination of MDZ and DTZ, and the corresponding DDI.	Diltiazem	61-64	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	151-157
19420129-9	2009	Moreover, model simulation suggested that both DTZ and nd-DTZ contributed to the overall inhibitory effect after DTZ administration, and the values of the in vitro estimated inhibition parameters and CYP3A4 turnover rate are critical for the prediction.	Diltiazem	47-50	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	200-206
19420129-9	2009	Moreover, model simulation suggested that both DTZ and nd-DTZ contributed to the overall inhibitory effect after DTZ administration, and the values of the in vitro estimated inhibition parameters and CYP3A4 turnover rate are critical for the prediction.	Diltiazem	58-61	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	200-206
19433126-7	2009	Diltiazem (10(-5)M) and TTX (10(-5)M) decreased by 45-75% NPY levels induced by scorpion toxin in both organs.	Diltiazem	0-9	neuropeptide Y	Rattus norvegicus	58-61
19067065-9	2009	CONCLUSION: Continuous infusion of diltiazem 2 microg/kg/min prevented the decrease in CrCl during pneumoperitoneum without hemodynamic derangement.	Diltiazem	35-44	CRCL	Homo sapiens	87-91
19067065-10	2009	Although the decrease in CrCl was transient in patients with normal kidney function in this study, diltiazem may be used to prevent further kidney injury in those with elevated CrCl during laparoscopic surgery.	Diltiazem	99-108	CRCL	Homo sapiens	177-181
19067065-6	2009	CrCl during pneumoperitoneum in the diltiazem group was significantly higher than that in the control group (90.8 +/- 49.0 ml/min/1.73 m(2) vs. 54.2 +/- 31.6 ml/min/1.73 m(2)) (P = 0.026).	Diltiazem	36-45	CRCL	Homo sapiens	0-4
19374868-2	2009	In this study, we investigated the effects of the L-type calcium channel blockers such as nifedipine, efonidipine cilnidipine, diltiazem, and verapamil, on the activity of hypoxia-inducible factor-1 (HIF-1), a key transcription factor in control of hypoxia-induced gene expression.	Diltiazem	127-136	hypoxia inducible factor 1 subunit alpha	Homo sapiens	172-198
20336221-3	2009	RESULTS AND CONCLUSION: A delayed occurrence of cataract with diltiazem (CYP inhibitor) and an early onset of cataract with pioglitazone (CYP inducer) indicate that a cytochrome P450 mediated pathway may affect the initiation of cataract but not the maturation pattern.	Diltiazem	62-71	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	73-76
20336221-3	2009	RESULTS AND CONCLUSION: A delayed occurrence of cataract with diltiazem (CYP inhibitor) and an early onset of cataract with pioglitazone (CYP inducer) indicate that a cytochrome P450 mediated pathway may affect the initiation of cataract but not the maturation pattern.	Diltiazem	62-71	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	167-182
18936931-8	2009	CONCLUSION: This study demonstrated that the G2677T/A single nucleotide polymorphisms in MDR1 and MDR1 haplotypes C-G-C, T-G-T and T-T-C are associated with the CsA concentration during the very early post-transplant period in Chinese renal transplant patients co-treated with diltiazem.	Diltiazem	277-286	ATP binding cassette subfamily B member 1	Homo sapiens	89-93
18936931-8	2009	CONCLUSION: This study demonstrated that the G2677T/A single nucleotide polymorphisms in MDR1 and MDR1 haplotypes C-G-C, T-G-T and T-T-C are associated with the CsA concentration during the very early post-transplant period in Chinese renal transplant patients co-treated with diltiazem.	Diltiazem	277-286	ATP binding cassette subfamily B member 1	Homo sapiens	98-102
19145649-0	2009	Diltiazem and verapamil protect dystrophin-deficient muscle fibers of MDX mice from degeneration: a potential role in calcium buffering and sarcolemmal stability.	Diltiazem	0-9	dystrophin, muscular dystrophy	Mus musculus	32-42
19383247-8	2009	Diltiazem infusion significantly reduced IL-6 levels 3 and 24 h after reperfusion compared with the control group.	Diltiazem	0-9	interleukin-6	Oryctolagus cuniculus	41-45
19383247-9	2009	The mean IL-10 level in the diltiazem group was significantly higher than in the control group 24 h after reperfusion.	Diltiazem	28-37	interleukin-10	Oryctolagus cuniculus	9-14
19093883-0	2009	Inhibition of MDR1 activity in vitro by a novel class of diltiazem analogues: toward new candidates.	Diltiazem	57-66	ATP binding cassette subfamily B member 1	Homo sapiens	14-18
19093883-4	2009	In conclusion, experiments lead to the identification of three diltiazem-like molecules able to increase the intracellular accumulation of doxorubicin by inhibiting the MDR1 function, thus potentiating its antiproliferative activity in multidrug resistant A2780/DX3 cells.	Diltiazem	63-72	ATP binding cassette subfamily B member 1	Homo sapiens	169-173
19126300-0	2009	Increased sensitivity to diltiazem hypotensive effect in an experimental model of high-renin hypertension.	Diltiazem	25-34	renin	Rattus norvegicus	87-92
19590189-5	2009	RESULTS: Calcium channel blockers (verapamil, diltiazem and nifedipine) significantly attenuated myocardial injury, as shown by reduced release of CK and LDH, preserved SOD activity and decreased MDA production and MPO activity.	Diltiazem	46-55	myeloperoxidase	Rattus norvegicus	215-218
19126300-1	2009	OBJECTIVES: The aim of this work was to evaluate the pharmacokinetic-pharmacodynamic properties of diltiazem in an experimental model of high-renin hypertension, such as the aortic coarctated (ACo) rat, to further characterize the responsiveness of this model to calcium channel blockers.	Diltiazem	99-108	renin	Rattus norvegicus	142-147
19126300-10	2009	In addition, our results suggested an increased sensitivity to diltiazem blood pressure lowering effect in experimental renovascular hypertension with high-renin levels.	Diltiazem	63-72	renin	Rattus norvegicus	156-161
19047745-3	2008	In contrast, a third L-type VGCC blocker, diltiazem, increased Cch1-Mid1 activity.	Diltiazem	42-51	Cch1p	Saccharomyces cerevisiae S288C	63-67
19047745-3	2008	In contrast, a third L-type VGCC blocker, diltiazem, increased Cch1-Mid1 activity.	Diltiazem	42-51	Mid1p	Saccharomyces cerevisiae S288C	68-72
19069242-10	2008	The presence of EGCG significantly enhanced the oral bioavailability of diltiazem due to inhibiting cytochrome P450 (CYP) 3A4-mediated metabolism and P-glycoprotein (P-gp) mediated efflux of diltiazem in the intestine.	Diltiazem	72-81	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	150-164
18720148-3	2008	PE-D complexes containing diltiazem HCL (DTZ) or metoprolol tartrate (MTP) and lambda carrageenan were obtained at two particle size levels (<45 microm and 75-105 microm), maintained at different values of relative humidity (RH) (11, 52, 75, and 93%), and compressed.	Diltiazem	41-44	OCA2 melanosomal transmembrane protein	Homo sapiens	0-4
18720148-3	2008	PE-D complexes containing diltiazem HCL (DTZ) or metoprolol tartrate (MTP) and lambda carrageenan were obtained at two particle size levels (<45 microm and 75-105 microm), maintained at different values of relative humidity (RH) (11, 52, 75, and 93%), and compressed.	Diltiazem	26-35	OCA2 melanosomal transmembrane protein	Homo sapiens	0-4
19069242-10	2008	The presence of EGCG significantly enhanced the oral bioavailability of diltiazem due to inhibiting cytochrome P450 (CYP) 3A4-mediated metabolism and P-glycoprotein (P-gp) mediated efflux of diltiazem in the intestine.	Diltiazem	72-81	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	166-170
19069242-10	2008	The presence of EGCG significantly enhanced the oral bioavailability of diltiazem due to inhibiting cytochrome P450 (CYP) 3A4-mediated metabolism and P-glycoprotein (P-gp) mediated efflux of diltiazem in the intestine.	Diltiazem	191-200	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	150-164
19069242-10	2008	The presence of EGCG significantly enhanced the oral bioavailability of diltiazem due to inhibiting cytochrome P450 (CYP) 3A4-mediated metabolism and P-glycoprotein (P-gp) mediated efflux of diltiazem in the intestine.	Diltiazem	191-200	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	166-170
18703021-8	2008	Various non-Pgp substrates demonstrated inhibition of digoxin secretion (verapamil, mifepristone, clotrimazole, mevastatin, diltiazem and isradipine) but did not induce Pgp-mediated digoxin secretion.	Diltiazem	124-133	ATP binding cassette subfamily B member 1	Homo sapiens	12-15
18606223-7	2008	CR-A containing 50% DTZ (by weight) extended drug release by only 6h.	Diltiazem	20-23	LUC7 like 3 pre-mRNA splicing factor	Homo sapiens	0-4
18388325-6	2008	TRPC3 (canonical transient receptor potential 3) channel knockdown with short hairpin RNA and diltiazem and nimodipine, voltage-dependent Ca(2+) channel blockers, reduced the SR Ca(2+) release-independent, IP(3)-induced [Ca(2+)](i) elevation and vasoconstriction.	Diltiazem	94-103	transient receptor potential cation channel subfamily C member 3	Homo sapiens	0-5
18589174-6	2008	Among 18 TAC-treated recipients, all receiving Diltiazem (DTZ), the median C/D ratio was lower for CYP3A5 *1/*1 versus *1/*3 versus *3/*3 (1.9, 4.6, and 13.5 ng/mL per 0.1 mg/kg/d, respectively; P = .001).	Diltiazem	47-56	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	99-105
18589174-6	2008	Among 18 TAC-treated recipients, all receiving Diltiazem (DTZ), the median C/D ratio was lower for CYP3A5 *1/*1 versus *1/*3 versus *3/*3 (1.9, 4.6, and 13.5 ng/mL per 0.1 mg/kg/d, respectively; P = .001).	Diltiazem	58-61	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	99-105
18589174-12	2008	Coadministration of DTZ may further optimize the TAC level through preferential P-gp binding and CYP3A4 inhibition.	Diltiazem	20-23	ATP binding cassette subfamily B member 1	Homo sapiens	80-84
18589174-12	2008	Coadministration of DTZ may further optimize the TAC level through preferential P-gp binding and CYP3A4 inhibition.	Diltiazem	20-23	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	97-103
18423659-7	2008	In comparison RCM cTnI mutants in the helix-4/C-terminal region demonstrated a) hyper-sensitivity to Ca(2+) under loaded conditions, b) slowed myocyte mechanical relaxation and Ca(2+) transient decay, c) frequency-dependent Ca(2+)-independent diastolic tone, d) heightened myofilament incorporation and e) irreversible cellular contractile defects with acute diltiazem administration.	Diltiazem	359-368	troponin I3, cardiac type	Rattus norvegicus	18-22
17651721-5	2007	Therefore, this study evaluates the effect of two phenylalkylamines (verapamil and gallopamil) and the benzothiazepine diltiazem on I(Ca) through Ca(v)1.3 channels in mouse IHCs.	Diltiazem	119-128	calcium channel, voltage-dependent, L type, alpha 1D subunit	Mus musculus	146-154
18254660-5	2008	Diltiazem structure-activity studies suggest that it is its Ca2+ channel blocker activity that enhances the capacity of the endoplasmic reticulum to fold misfolding-prone proteins, likely by modest up-regulation of a subset of molecular chaperones, including BiP and Hsp40.	Diltiazem	0-9	heat shock protein family A (Hsp70) member 5	Homo sapiens	259-262
18254660-5	2008	Diltiazem structure-activity studies suggest that it is its Ca2+ channel blocker activity that enhances the capacity of the endoplasmic reticulum to fold misfolding-prone proteins, likely by modest up-regulation of a subset of molecular chaperones, including BiP and Hsp40.	Diltiazem	0-9	DnaJ heat shock protein family (Hsp40) member B1 pseudogene 1	Homo sapiens	267-272
19035878-9	2008	In conclusion, resveratrol significantly increased the bioavailability of diltiazem due to the inhibition of both the cytochrome P450 (CYP) 3A4-mediated metabolism and the efflux pump P-glycoprotein (P-gp) in the intestine and/or liver.	Diltiazem	74-83	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	184-198
19035878-9	2008	In conclusion, resveratrol significantly increased the bioavailability of diltiazem due to the inhibition of both the cytochrome P450 (CYP) 3A4-mediated metabolism and the efflux pump P-glycoprotein (P-gp) in the intestine and/or liver.	Diltiazem	74-83	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	200-204
17785345-5	2007	MEMRI studies revealed signal hyperintensity in the CA3 pyramidal cell layer after KA treatment, and the MEMRI signal can be attenuated by diltiazem, an L-type calcium channel blocker.	Diltiazem	139-148	carbonic anhydrase 3	Rattus norvegicus	52-55
18558792-8	2008	Diltiazem (86 events), verapamil (72), erythromycin (48) and clarithromycin (29) were the most commonly co-prescribed CYP3A4 inhibitors.	Diltiazem	0-9	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	118-124
18088512-5	2008	In the CHF model, HSYA and diltiazem restored abnormal heart function, and completely suppressed the elevated plasma atrial natriuretic polypeptide (ANP) and endothelin-1 (ET-1), serum and left-ventricular tissue inducible nitric oxide (NO) synthase (iNOS), NO and MDA, and improved the decrease in SOD.	Diltiazem	27-36	endothelin 1	Rattus norvegicus	158-170
18088512-5	2008	In the CHF model, HSYA and diltiazem restored abnormal heart function, and completely suppressed the elevated plasma atrial natriuretic polypeptide (ANP) and endothelin-1 (ET-1), serum and left-ventricular tissue inducible nitric oxide (NO) synthase (iNOS), NO and MDA, and improved the decrease in SOD.	Diltiazem	27-36	endothelin 1	Rattus norvegicus	172-176
18088512-5	2008	In the CHF model, HSYA and diltiazem restored abnormal heart function, and completely suppressed the elevated plasma atrial natriuretic polypeptide (ANP) and endothelin-1 (ET-1), serum and left-ventricular tissue inducible nitric oxide (NO) synthase (iNOS), NO and MDA, and improved the decrease in SOD.	Diltiazem	27-36	nitric oxide synthase 2	Rattus norvegicus	251-255
17574934-6	2007	However, a PM phenotype could also be caused by drug-drug interactions with CYP2D6 inhibitors or substrates such as the co-consumed cocaine and diltiazem and/or diltiazem metabolites, respectively.	Diltiazem	144-153	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	76-82
17622512-11	2007	Three patients (who all ingested diltiazem) received an insulin-loading dose; all experienced a significant sustained rise in systolic BP (>10 mmHg) during the first hour of HIET.	Diltiazem	33-42	insulin	Homo sapiens	56-63
17235687-6	2007	L-type voltage-gated calcium channel blockers (nifedipine, D-cis-diltiazem, and verapamil) were effective in blocking the Ab-induced intracellular Ca(2+) rise and induction of Bax.	Diltiazem	59-74	BCL2 associated X, apoptosis regulator	Homo sapiens	176-179
17475811-0	2007	Identification of the atypical L-type Ca2+ channel blocker diltiazem and its metabolites as ghrelin receptor agonists.	Diltiazem	59-68	growth hormone secretagogue receptor	Homo sapiens	92-108
17392390-8	2007	In addition, we established an automated assay to distinguish quasi-irreversible and irreversible binding to CYP3A in which the quasi-irreversible inhibitors such as diltiazem, verapamil, and nicardipine were dissociated from CYP3A by the addition of potassium ferricyanide, whereas the irreversible inhibitors such as clozapine, delavirdine, and mibefradil were not.	Diltiazem	166-175	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	109-114
17477368-8	2007	Data demonstrate that Sertoli cells treated with L-type voltage-operated Ca(+2) channel antagonists, nifedipine, diltiazem, or verapamil, lead to dose-dependent blockage of L-selectin-induced Ca(+2) influx.	Diltiazem	113-122	selectin L	Homo sapiens	173-183
17531162-8	2007	A reduction in the HA stimulated increase in ERK 1 & 2 expression was observed at 20 min of exposing cells to diltiazem, the calcium channel blocker, whereas, the calcium chelator, BAPTA effect on ERK 1 & 2 expression was observed within 5 min in SHR VSMCs.	Diltiazem	114-123	mitogen activated protein kinase 3	Rattus norvegicus	45-50
17531162-8	2007	A reduction in the HA stimulated increase in ERK 1 & 2 expression was observed at 20 min of exposing cells to diltiazem, the calcium channel blocker, whereas, the calcium chelator, BAPTA effect on ERK 1 & 2 expression was observed within 5 min in SHR VSMCs.	Diltiazem	114-123	methionyl aminopeptidase 2	Rattus norvegicus	52-58
17531162-8	2007	A reduction in the HA stimulated increase in ERK 1 & 2 expression was observed at 20 min of exposing cells to diltiazem, the calcium channel blocker, whereas, the calcium chelator, BAPTA effect on ERK 1 & 2 expression was observed within 5 min in SHR VSMCs.	Diltiazem	114-123	mitogen activated protein kinase 3	Rattus norvegicus	201-206
17531162-8	2007	A reduction in the HA stimulated increase in ERK 1 & 2 expression was observed at 20 min of exposing cells to diltiazem, the calcium channel blocker, whereas, the calcium chelator, BAPTA effect on ERK 1 & 2 expression was observed within 5 min in SHR VSMCs.	Diltiazem	114-123	methionyl aminopeptidase 2	Rattus norvegicus	208-214
17293381-0	2007	Sequential metabolism is responsible for diltiazem-induced time-dependent loss of CYP3A.	Diltiazem	41-50	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	82-87
17293381-2	2007	We previously reported that microsomal inactivation kinetic parameters of diltiazem underpredicted CYP3A inactivation in hepatocytes.	Diltiazem	74-83	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	99-104
17293381-3	2007	In this study, we evaluated the contributions of inactivation and reversible inhibition of CYP3A by diltiazem and its N-desmethyl (MA) and N,N-didesmethyl (MD) metabolites.	Diltiazem	100-109	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	91-96
17293381-6	2007	Inactivation of CYP3A by diltiazem was dependent on microsomal protein concentration (25, 36, and 41% decrease in CYP3A activity at 0.2, 0.4, and 0.8 mg/ml microsomal protein, respectively, incubated with 10 microM diltiazem over 20 min), whereas inactivation by MA did not seem to be protein concentration-dependent.	Diltiazem	25-34	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	16-21
17293381-6	2007	Inactivation of CYP3A by diltiazem was dependent on microsomal protein concentration (25, 36, and 41% decrease in CYP3A activity at 0.2, 0.4, and 0.8 mg/ml microsomal protein, respectively, incubated with 10 microM diltiazem over 20 min), whereas inactivation by MA did not seem to be protein concentration-dependent.	Diltiazem	25-34	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	114-119
17293381-6	2007	Inactivation of CYP3A by diltiazem was dependent on microsomal protein concentration (25, 36, and 41% decrease in CYP3A activity at 0.2, 0.4, and 0.8 mg/ml microsomal protein, respectively, incubated with 10 microM diltiazem over 20 min), whereas inactivation by MA did not seem to be protein concentration-dependent.	Diltiazem	215-224	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	16-21
17293381-8	2007	In cryopreserved hepatocytes incubated with diltiazem, time-dependent loss of CYP3A was accompanied by increased formation of MA and MD, with the MA level similar to its K(I) at higher diltiazem concentrations.	Diltiazem	44-53	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	78-83
17293381-8	2007	In cryopreserved hepatocytes incubated with diltiazem, time-dependent loss of CYP3A was accompanied by increased formation of MA and MD, with the MA level similar to its K(I) at higher diltiazem concentrations.	Diltiazem	185-194	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	78-83
17293381-10	2007	In summary, time-dependent CYP3A inactivation by MA seems to be the major contributor responsible for the loss of CYP3A in human liver microsomes and human hepatocytes incubated with diltiazem.	Diltiazem	183-192	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	27-32
17293381-10	2007	In summary, time-dependent CYP3A inactivation by MA seems to be the major contributor responsible for the loss of CYP3A in human liver microsomes and human hepatocytes incubated with diltiazem.	Diltiazem	183-192	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	114-119
17196958-3	2007	Mouse pituitary tumor cells stably transfected with approximately 0.7 kb of the rat proopiomelanocortin 5" promoter-luciferase fusion gene were stimulated by potassium chloride, corticotropin-releasing hormone (CRH) or forskolin, in the presence or absence of calcium channel blockers (nifedipine, verapamil and diltiazem).	Diltiazem	312-321	proopiomelanocortin	Rattus norvegicus	84-103
17196958-5	2007	A dose-dependent enhancement of CRH- or forskolin-stimulated proopiomelanocortin promoter activity was observed with nifedipine and verapamil, but not diltiazem.	Diltiazem	151-160	corticotropin releasing hormone	Rattus norvegicus	32-35
17304269-2	2007	Simvastatin interactions with warfarin and the cytochrome P450-3A4 inhibitor diltiazem were suspected as possible causes of the events (fatal intracranial haemorrhage with INR > 8 and myopathy).	Diltiazem	77-86	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	47-66
17068014-7	2007	In DTZ pre-treated irradiated animals, a significant increase in pro- and normoblasts, erythrocytes, leukocytes, differential leukocyte count, haematocrit and haemoglobin values, and a significant decrease in erythropoietin values, were observed compared with control.	Diltiazem	3-6	erythropoietin	Mus musculus	209-223
17068014-9	2007	Similarly, pre-treatment of DTZ caused a significant increase in erythropoietin and glutathione levels in serum in comparison with irradiated animals.	Diltiazem	28-31	erythropoietin	Mus musculus	65-79
17328247-1	2007	The purpose of this study was to investigate the effect of atorvastatin, HMG-CoA reductase inhibitor, on the pharmacokinetics of diltiazem and its active metabolite, desacetyldiltiazem, in rats.	Diltiazem	129-138	3-hydroxy-3-methylglutaryl-CoA reductase	Rattus norvegicus	73-90
17060064-9	2006	These data suggest that diuretics, dihydropyridines, ACE inhibitors, and angiotensin receptor blockers provide significant additional antihypertensive effects in hypertensive patients uncontrolled on diltiazem monotherapy.	Diltiazem	200-209	angiotensin I converting enzyme	Homo sapiens	53-56
16892207-6	2006	Concerning the diltiazem transport, the V(max)/K(m) value of human P-gp corrected by the P-gp expression level was similar to that of monkey P-gp, but was 5.6-fold higher than that of canine P-gp.	Diltiazem	15-24	ATP binding cassette subfamily B member 1	Homo sapiens	67-71
16892207-6	2006	Concerning the diltiazem transport, the V(max)/K(m) value of human P-gp corrected by the P-gp expression level was similar to that of monkey P-gp, but was 5.6-fold higher than that of canine P-gp.	Diltiazem	15-24	ATP binding cassette subfamily B member 1	Homo sapiens	89-93
16892207-6	2006	Concerning the diltiazem transport, the V(max)/K(m) value of human P-gp corrected by the P-gp expression level was similar to that of monkey P-gp, but was 5.6-fold higher than that of canine P-gp.	Diltiazem	15-24	ATP binding cassette subfamily B member 1	Homo sapiens	89-93
16892207-6	2006	Concerning the diltiazem transport, the V(max)/K(m) value of human P-gp corrected by the P-gp expression level was similar to that of monkey P-gp, but was 5.6-fold higher than that of canine P-gp.	Diltiazem	15-24	PGP	Canis lupus familiaris	89-93
17178259-5	2006	Weak or moderately potent CYP3A4 inhibitors (eg, verapamil and diltiazem) can be used cautiously with small doses of CYP3A4-dependent statins.	Diltiazem	63-72	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	26-32
17178259-5	2006	Weak or moderately potent CYP3A4 inhibitors (eg, verapamil and diltiazem) can be used cautiously with small doses of CYP3A4-dependent statins.	Diltiazem	63-72	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	117-123
16603686-7	2006	In a Ca2+-free bath solution or in diltiazem, a voltage-dependent Ca2+ channel blocker, steady membrane depolarization between -40 and +40 mV increased transient KCa current frequency up to approximately 1.6-fold.	Diltiazem	35-44	casein kappa	Homo sapiens	162-165
16126118-0	2005	Renoprotective effect of diltiazem in hypertensive type 2 diabetic patients with persistent microalbuminuria despite ACE inhibitor treatment.	Diltiazem	25-34	angiotensin I converting enzyme	Homo sapiens	117-120
16954457-3	2006	However, the potential influence of diltiazem on the anti-inflammatory cytokine IL10 in patients with UA has not been investigated.	Diltiazem	36-45	interleukin 10	Homo sapiens	80-84
16954457-4	2006	This study was designed to find out the effects of diltiazem on IL10 in UA patients.	Diltiazem	51-60	interleukin 10	Homo sapiens	64-68
16954457-11	2006	CONCLUSIONS: These findings showed that concentrations of anti-inflammatory IL10 are considerably decreased in UA patients and diltiazem treatment leads to a significant increase in IL10 concentrations.	Diltiazem	127-136	interleukin 10	Homo sapiens	182-186
16630555-6	2006	Other channel blockers tested, nifedipine and diltiazem, similarly inhibited these fMLP-stimulated responses.	Diltiazem	46-55	formyl peptide receptor 1	Homo sapiens	83-87
16421162-16	2006	CONCLUSIONS: Diltiazem suppressed collagen synthesis of human PMCs and inhibited IL-1beta-induced TGF-beta1 production on human PMCs.	Diltiazem	13-22	interleukin 1 beta	Homo sapiens	81-89
16421162-16	2006	CONCLUSIONS: Diltiazem suppressed collagen synthesis of human PMCs and inhibited IL-1beta-induced TGF-beta1 production on human PMCs.	Diltiazem	13-22	transforming growth factor beta 1	Homo sapiens	98-107
16214409-8	2006	CONCLUSIONS: Diastolic dysfunction due to increased LV stiffness in TnT-I79N mice leads to severe primary diastolic heart failure and finally to cardiac sudden death, which can be prevented by diltiazem.	Diltiazem	193-202	troponin T2, cardiac	Mus musculus	68-71
16883636-3	2006	BPI-induced vascular relaxations were also markedly attenuated by the addition of verapamil or diltiazem, while the relaxant effect of BPI was not blocked by pretreatment with indomethacine, glibenclamide, tetraethylammonium (TEA), atropine, or propranolol.	Diltiazem	95-104	bactericidal/permeability-increasing protein	Rattus norvegicus	0-3
16640453-19	2006	Ranolazine AUC is increased by CYP3A inhibitors ranging from 1.5-fold for diltiazem 180 mg once daily to 3.9-fold for ketoconazole 200 mg twice daily.	Diltiazem	74-83	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	31-36
16024008-0	2005	Effects of the CYP3A5 genetic polymorphism on the pharmacokinetics of diltiazem.	Diltiazem	70-79	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	15-21
16024008-8	2005	CONCLUSION: The results suggest that CYP3A5*3 has only a minor effect on the pharmacokinetics and metabolism of diltiazem.	Diltiazem	112-121	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	37-43
16581067-3	2006	The maitotoxin-induced Ca2+ influx was suppressed by various voltage-dependent Ca2+ channel blockers such as Co2+, Mn2+, verapamil and diltiazem.	Diltiazem	135-144	carbonic anhydrase 2	Homo sapiens	23-26
16581067-3	2006	The maitotoxin-induced Ca2+ influx was suppressed by various voltage-dependent Ca2+ channel blockers such as Co2+, Mn2+, verapamil and diltiazem.	Diltiazem	135-144	carbonic anhydrase 2	Homo sapiens	79-82
16421162-0	2006	Diltiazem suppresses collagen synthesis and IL-1beta-induced TGF-beta1 production on human peritoneal mesothelial cells.	Diltiazem	0-9	interleukin 1 beta	Homo sapiens	44-52
16421162-0	2006	Diltiazem suppresses collagen synthesis and IL-1beta-induced TGF-beta1 production on human peritoneal mesothelial cells.	Diltiazem	0-9	transforming growth factor beta 1	Homo sapiens	61-70
16421162-4	2006	The objectives of this study were to examine the effects of diltiazem on collagen- and IL-1beta-induced TGF-beta1 production on human PMCs and the signalling pathway of diltiazem in this induction.	Diltiazem	60-69	interleukin 1 beta	Homo sapiens	87-95
16421162-4	2006	The objectives of this study were to examine the effects of diltiazem on collagen- and IL-1beta-induced TGF-beta1 production on human PMCs and the signalling pathway of diltiazem in this induction.	Diltiazem	169-178	interleukin 1 beta	Homo sapiens	87-95
16421162-12	2006	Diltiazem (0.2 mM) suppressed IL-1beta- (5 ng/ml) induced TGF-beta1 production on human PMCs at both the protein and mRNA levels.	Diltiazem	0-9	interleukin 1 beta	Homo sapiens	30-38
16421162-12	2006	Diltiazem (0.2 mM) suppressed IL-1beta- (5 ng/ml) induced TGF-beta1 production on human PMCs at both the protein and mRNA levels.	Diltiazem	0-9	transforming growth factor beta 1	Homo sapiens	58-67
16421162-13	2006	Diltiazem (0.2 mM) also inhibited IL-1beta- (5 ng/ml) induced collagen I and III mRNA expression.	Diltiazem	0-9	interleukin 1 beta	Homo sapiens	34-42
16421162-15	2006	The IL-1beta-treated human PMCs increased phospho-JNK (stress-activated c-Jun N-terminal kinase) and phospho-p38 MAPK expression, while diltiazem could suppress this phenomenon.	Diltiazem	136-145	interleukin 1 beta	Homo sapiens	4-12
16630910-3	2006	Diltiazem is a calcium channel-blocking cardiac antiarrythmic, which also blocks tumor growth and P-glycoprotein.	Diltiazem	0-9	ATP binding cassette subfamily B member 1	Homo sapiens	98-112
16776949-7	2006	Compared to T1, mPAP was significantly decreased at T3 and T5, MAP significantly increased at T4 and T5, HR significantly reduced at T2 and thereafter, SV significantly increased at T3, T4 and T5 and PVR significantly increased at T3 and T5 while SVR remained unchanged after diltiazem therapy.	Diltiazem	276-285	phospholipid phosphatase 1	Mus musculus	16-20
16263803-13	2006	The difference in responses to high KCl between resting and l-NNA-constricted EA and the ability of diltiazem to block EA constriction caused by l-NNA contrasts with the lack of efferent effects in resting and SNAP-treated l-NNA-preconstricted arterioles and during ANG II-mediated vasoconstriction, suggesting a recruitment of LCC in EA when NOS is inhibited.	Diltiazem	100-109	angiogenin	Homo sapiens	266-269
16238231-7	2005	Diltiazem and verapamil are particularly prone to interactions, as they strongly inhibit the elimination of drugs undergoing the CYP3A4 and P-glycoprotein pathways.	Diltiazem	0-9	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	129-135
15863898-6	2005	Comparison of three Ca(2+) antagonists, nicardipine, nifedipine, and diltiazem revealed that only nicardipine showed such a strong inhibitory potency on the typical CYP2D6-catalyzed drug metabolism.	Diltiazem	69-78	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	165-171
16009351-6	2005	These abnormal Ca2+ events and CK release were significantly prevented by Ca2+ handling drugs, tranilast, diltiazem, and FK506.	Diltiazem	106-115	carbonic anhydrase 2	Mus musculus	15-18
16153073-2	2005	The weight loss for MCS/CSI is mainly due to the weight loss of the matrix while for MCB/AS it is mainly due to the diltiazem hydrochloride released from the tablet.	Diltiazem	116-139	Miles-Carpenter X-linked mental retardation syndrome	Homo sapiens	20-23
15547114-7	2005	In the isolated blood-perfused juxtamedullary nephron preparation, Ca(2+) channel blockade with diltiazem had a very small inhibitory effect on ET-1-induced decreases in afferent arteriolar diameter only at the lowest concentrations of ET-1.	Diltiazem	96-105	endothelin 1	Rattus norvegicus	144-148
15547114-7	2005	In the isolated blood-perfused juxtamedullary nephron preparation, Ca(2+) channel blockade with diltiazem had a very small inhibitory effect on ET-1-induced decreases in afferent arteriolar diameter only at the lowest concentrations of ET-1.	Diltiazem	96-105	endothelin 1	Rattus norvegicus	236-240
15801939-1	2005	AIMS: To determine the effect of diltiazem on intestinal CYP3A activity and protein and mRNA expression in vivo in healthy subjects.	Diltiazem	33-42	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	57-62
15858399-3	2005	CCBs are both substrates for, and in the instance of verapamil and diltiazem inhibitors of, cytochrome P450 3A4.	Diltiazem	67-76	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	92-111
15858399-4	2005	In the case of verapamil and diltiazem, this inhibitory effect increases the likelihood of drug-drug interactions with other compounds similarly metabolized by cytochrome P450 3A4.	Diltiazem	29-38	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	160-179
15797790-4	2005	The best separation of DTZ from A, B, E and F was obtained using as stationary phase a RP-8 or a monolithic RP-18.	Diltiazem	23-26	programmed cell death 2	Homo sapiens	87-91
15537499-0	2004	Diltiazem inhibits hKv1.5 and Kv4.3 currents at therapeutic concentrations.	Diltiazem	0-9	potassium voltage-gated channel subfamily A member 5	Homo sapiens	19-25
15801939-0	2005	Diltiazem inhibits human intestinal cytochrome P450 3A (CYP3A) activity in vivo without altering the expression of intestinal mRNA or protein.	Diltiazem	0-9	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	36-54
15801939-0	2005	Diltiazem inhibits human intestinal cytochrome P450 3A (CYP3A) activity in vivo without altering the expression of intestinal mRNA or protein.	Diltiazem	0-9	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	56-61
15801939-7	2005	CONCLUSION: Diltiazem decreased small bowel CYP3A activity by 62% as a result of irreversible inhibition with no corresponding change in intestinal CYP3A4 mRNA or protein concentrations.	Diltiazem	12-21	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	44-49
15652234-0	2005	Inhibition of interleukin-12 expression in diltiazem-treated dendritic cells through the reduction of nuclear factor-kappa B transcriptional activity.	Diltiazem	43-52	nuclear factor kappa B subunit 1	Homo sapiens	102-124
15652234-4	2005	Here, we extended our analysis studying the effect of diltiazem on the transcription of IL-12 p35 and p40 subunits focusing on the activity of nuclear factor-kappa B (NF-kappa B).	Diltiazem	54-63	interleukin 12A	Homo sapiens	94-97
15652234-4	2005	Here, we extended our analysis studying the effect of diltiazem on the transcription of IL-12 p35 and p40 subunits focusing on the activity of nuclear factor-kappa B (NF-kappa B).	Diltiazem	54-63	interleukin 9	Homo sapiens	102-105
15652234-5	2005	A marked reduction of NF-kappa B binding to the kappa B sequences present within the p35 and p40 subunit promoters was observed in diltiazem-treated DCs following the stimulation with lipopolysaccharide (LPS) or CD40L.	Diltiazem	131-140	nuclear factor kappa B subunit 1	Homo sapiens	22-32
15652234-5	2005	A marked reduction of NF-kappa B binding to the kappa B sequences present within the p35 and p40 subunit promoters was observed in diltiazem-treated DCs following the stimulation with lipopolysaccharide (LPS) or CD40L.	Diltiazem	131-140	interleukin 12A	Homo sapiens	85-88
15652234-5	2005	A marked reduction of NF-kappa B binding to the kappa B sequences present within the p35 and p40 subunit promoters was observed in diltiazem-treated DCs following the stimulation with lipopolysaccharide (LPS) or CD40L.	Diltiazem	131-140	interleukin 9	Homo sapiens	93-96
15652234-5	2005	A marked reduction of NF-kappa B binding to the kappa B sequences present within the p35 and p40 subunit promoters was observed in diltiazem-treated DCs following the stimulation with lipopolysaccharide (LPS) or CD40L.	Diltiazem	131-140	CD40 ligand	Homo sapiens	212-217
15652234-6	2005	In order to examine the mechanisms by which NF-kappa B binding activity is reduced by diltiazem, we analyzed the NF-kappa B inhibitor, I kappa B alpha.	Diltiazem	86-95	nuclear factor kappa B subunit 1	Homo sapiens	44-54
15652234-6	2005	In order to examine the mechanisms by which NF-kappa B binding activity is reduced by diltiazem, we analyzed the NF-kappa B inhibitor, I kappa B alpha.	Diltiazem	86-95	nuclear factor kappa B subunit 1	Homo sapiens	113-123
15652234-6	2005	In order to examine the mechanisms by which NF-kappa B binding activity is reduced by diltiazem, we analyzed the NF-kappa B inhibitor, I kappa B alpha.	Diltiazem	86-95	NFKB inhibitor alpha	Homo sapiens	135-150
15652234-8	2005	On the other hand, the subcellular distribution of NF-kappa B subunits was clearly affected in diltiazem-treated DCs following LPS stimulation, with a reduced nuclear translocation of p65, and RelB, and a nuclear accumulation of p50 subunit.	Diltiazem	95-104	nuclear factor kappa B subunit 1	Homo sapiens	51-61
15652234-8	2005	On the other hand, the subcellular distribution of NF-kappa B subunits was clearly affected in diltiazem-treated DCs following LPS stimulation, with a reduced nuclear translocation of p65, and RelB, and a nuclear accumulation of p50 subunit.	Diltiazem	95-104	RELA proto-oncogene, NF-kB subunit	Homo sapiens	184-187
15652234-8	2005	On the other hand, the subcellular distribution of NF-kappa B subunits was clearly affected in diltiazem-treated DCs following LPS stimulation, with a reduced nuclear translocation of p65, and RelB, and a nuclear accumulation of p50 subunit.	Diltiazem	95-104	RELB proto-oncogene, NF-kB subunit	Homo sapiens	193-197
15652234-8	2005	On the other hand, the subcellular distribution of NF-kappa B subunits was clearly affected in diltiazem-treated DCs following LPS stimulation, with a reduced nuclear translocation of p65, and RelB, and a nuclear accumulation of p50 subunit.	Diltiazem	95-104	nuclear factor kappa B subunit 1	Homo sapiens	229-232
15652234-9	2005	Thus, all together, our data provided evidence that in addition to the inhibition of p65/p50 nuclear translocation, the selective induction and translocation of p50/p50 homodimers is an important mechanism by which diltiazem inhibits NF-kappa B activity, and in turn, IL-12 expression.	Diltiazem	215-224	RELA proto-oncogene, NF-kB subunit	Homo sapiens	85-88
15652234-9	2005	Thus, all together, our data provided evidence that in addition to the inhibition of p65/p50 nuclear translocation, the selective induction and translocation of p50/p50 homodimers is an important mechanism by which diltiazem inhibits NF-kappa B activity, and in turn, IL-12 expression.	Diltiazem	215-224	nuclear factor kappa B subunit 1	Homo sapiens	89-92
15652234-9	2005	Thus, all together, our data provided evidence that in addition to the inhibition of p65/p50 nuclear translocation, the selective induction and translocation of p50/p50 homodimers is an important mechanism by which diltiazem inhibits NF-kappa B activity, and in turn, IL-12 expression.	Diltiazem	215-224	nuclear factor kappa B subunit 1	Homo sapiens	161-164
15652234-9	2005	Thus, all together, our data provided evidence that in addition to the inhibition of p65/p50 nuclear translocation, the selective induction and translocation of p50/p50 homodimers is an important mechanism by which diltiazem inhibits NF-kappa B activity, and in turn, IL-12 expression.	Diltiazem	215-224	nuclear factor kappa B subunit 1	Homo sapiens	161-164
15652234-9	2005	Thus, all together, our data provided evidence that in addition to the inhibition of p65/p50 nuclear translocation, the selective induction and translocation of p50/p50 homodimers is an important mechanism by which diltiazem inhibits NF-kappa B activity, and in turn, IL-12 expression.	Diltiazem	215-224	nuclear factor kappa B subunit 1	Homo sapiens	234-244
15531380-4	2004	After the combined treatment period, Cmax of HMG-CoA reductase inhibitor was elevated from 7.8 +/- 2.6 ng/ml to 15.4 +/- 7.9 ng/ml (P < 0.01) and AUC0-6h from 21.7 +/- 4.9 ng x hr/ml to 43.3 +/- 23.4 ng x hr/ml (P < 0.01), while Cmax of diltiazem was decreased from 74.2 +/- 36.4 ng/ml to 58.6 +/- 18.9 ng/ml (P < 0.05) and its AUC0-6h from 365 +/- 153 ng x hr/ml to 287 +/- 113 ng x hr/ml (P < 0.01).	Diltiazem	243-252	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	45-62
15531380-7	2004	These apparent pharmacokinetic interactions, namely the increase of HMG-CoA reductase inhibitor concentration by diltiazem and the decrease of diltiazem concentration by simvastatin, enhance the cholesterol-lowering effects of simvastatin during combined treatment.	Diltiazem	113-122	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	68-85
15678082-5	2005	It was found that diltiazem substantially inhibited I(to1) in a concentration-dependent manner, with an IC(50) of 29.2+/-2.4 microM, and nifedipine showed a similar effect (IC(50)=26.8+/-2.1 muM).	Diltiazem	18-27	latexin	Homo sapiens	191-194
15537499-0	2004	Diltiazem inhibits hKv1.5 and Kv4.3 currents at therapeutic concentrations.	Diltiazem	0-9	potassium voltage-gated channel subfamily D member 3	Homo sapiens	30-35
15537499-4	2004	RESULTS: Diltiazem (0.01 nM-500 muM) blocked hKv1.5 channels, in a frequency-dependent manner exhibiting a biphasic dose-response curve (IC(50)=4.8+/-1.5 nM and 42.3+/-3.6 muM).	Diltiazem	9-18	latexin	Homo sapiens	32-35
15537499-4	2004	RESULTS: Diltiazem (0.01 nM-500 muM) blocked hKv1.5 channels, in a frequency-dependent manner exhibiting a biphasic dose-response curve (IC(50)=4.8+/-1.5 nM and 42.3+/-3.6 muM).	Diltiazem	9-18	potassium voltage-gated channel subfamily A member 5	Homo sapiens	45-51
15537499-4	2004	RESULTS: Diltiazem (0.01 nM-500 muM) blocked hKv1.5 channels, in a frequency-dependent manner exhibiting a biphasic dose-response curve (IC(50)=4.8+/-1.5 nM and 42.3+/-3.6 muM).	Diltiazem	9-18	latexin	Homo sapiens	172-175
15537499-7	2004	Diltiazem (0.1 nM-100 muM) also blocked Kv4.3 channels in a frequency-dependent manner exhibiting a biphasic dose-response curve (IC(50)=62.6+/-11.1 nM and 109.9+/-12.8 muM).	Diltiazem	0-9	latexin	Homo sapiens	22-25
15537499-7	2004	Diltiazem (0.1 nM-100 muM) also blocked Kv4.3 channels in a frequency-dependent manner exhibiting a biphasic dose-response curve (IC(50)=62.6+/-11.1 nM and 109.9+/-12.8 muM).	Diltiazem	0-9	potassium voltage-gated channel subfamily D member 3	Homo sapiens	40-45
15537499-7	2004	Diltiazem (0.1 nM-100 muM) also blocked Kv4.3 channels in a frequency-dependent manner exhibiting a biphasic dose-response curve (IC(50)=62.6+/-11.1 nM and 109.9+/-12.8 muM).	Diltiazem	0-9	latexin	Homo sapiens	169-172
15537499-10	2004	Diltiazem, 10 nM, shifted to more negative potentials the voltage-dependence of Kv4.3 channel inactivation (Vh=-33.1+/-2.3 mV vs -38.2+/-3.5 mV, n=6, Plt;0.05) the blockade increasing at potentials at which the amount of inactivated channels increased.	Diltiazem	0-9	potassium voltage-gated channel subfamily D member 3	Homo sapiens	80-85
15537499-11	2004	CONCLUSION: The results demonstrated for the first time that diltiazem, at therapeutic concentrations, decreased hKv1.5 and Kv4.3 currents by binding to the open and the inactivated state of the channels.	Diltiazem	61-70	potassium voltage-gated channel subfamily A member 5	Homo sapiens	113-119
15537499-11	2004	CONCLUSION: The results demonstrated for the first time that diltiazem, at therapeutic concentrations, decreased hKv1.5 and Kv4.3 currents by binding to the open and the inactivated state of the channels.	Diltiazem	61-70	potassium voltage-gated channel subfamily D member 3	Homo sapiens	124-129
15627720-8	2004	Diltiazem (10 micromol/l) significantly dilated AA (26.8 +/- 2.2%), and prevented Ang II-mediated constriction of AA.	Diltiazem	0-9	angiotensinogen	Rattus norvegicus	82-88
15681897-9	2004	However, ketoconazole and cyclosporin A, which are specific CYP3A inhibitors, inhibited the metabolic extraction of diltiazem (0.05 mM) by only about 20% at the concentration (40 microM) at which they inhibited CYP3A almost completely, suggesting that the contribution of CYP3A to intestinal diltiazem metabolism is not marked.	Diltiazem	116-125	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	60-65
15681897-9	2004	However, ketoconazole and cyclosporin A, which are specific CYP3A inhibitors, inhibited the metabolic extraction of diltiazem (0.05 mM) by only about 20% at the concentration (40 microM) at which they inhibited CYP3A almost completely, suggesting that the contribution of CYP3A to intestinal diltiazem metabolism is not marked.	Diltiazem	116-125	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	211-216
15681897-9	2004	However, ketoconazole and cyclosporin A, which are specific CYP3A inhibitors, inhibited the metabolic extraction of diltiazem (0.05 mM) by only about 20% at the concentration (40 microM) at which they inhibited CYP3A almost completely, suggesting that the contribution of CYP3A to intestinal diltiazem metabolism is not marked.	Diltiazem	116-125	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	211-216
15688675-1	2004	Both beta-adrenergic receptor antagonist drugs (beta-blockers) and non-dihydropyridine calcium-channel blockers (non-DHP CCBs), ie, diltiazem and verapamil, can cause sinus arrest or severe sinus bradycardia, and when drugs from the two classes are used together, these effects may be more than additive.	Diltiazem	132-141	dihydropyrimidinase	Homo sapiens	117-120
15304427-9	2004	Aprepitant was a moderate inhibitor of CYP3A4, with Ki values of approximately 10 microM for the 1"- and 4-hydroxylation of midazolam, and the N-demethylation of diltiazem, respectively.	Diltiazem	162-171	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	39-45
15059841-7	2004	Additional ABC transporter substrate inhibitors like quinidine, diltiazem, and ritonavir also enhanced transduction 2- to 3-fold, although ABC transporter inhibitors that are not substrates did not.	Diltiazem	64-73	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	11-26
15142846-5	2004	Interestingly, coinfusion of ghrelin with diltiazem completely restored myocardial contractile function that was decreased 30 +/- 3% (P < 0.01) by diltiazem alone.	Diltiazem	150-159	ghrelin and obestatin prepropeptide	Rattus norvegicus	29-36
15142846-10	2004	Furthermore, the data obtained from diltiazem infusion suggest that ghrelin has a role in regulation of contractility when L-type Ca(2+) channels are blocked.	Diltiazem	36-45	ghrelin and obestatin prepropeptide	Rattus norvegicus	68-75
15377640-1	2004	The objectives of this study were to characterize and compare the reversible inhibition and time-dependent inactivation of cytochromes P450 3A4 and 3A5 (CYP3A4 and CYP3A5) by erythromycin, diltiazem, and nicardipine.	Diltiazem	189-198	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	153-159
15377640-1	2004	The objectives of this study were to characterize and compare the reversible inhibition and time-dependent inactivation of cytochromes P450 3A4 and 3A5 (CYP3A4 and CYP3A5) by erythromycin, diltiazem, and nicardipine.	Diltiazem	189-198	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	164-170
15377640-11	2004	In conclusion, erythromycin, diltiazem, and nicardipine were weaker inhibitors of CYP3A5 and inactivated the enzyme at a slower rate than their respective effects on CYP3A4.	Diltiazem	29-38	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	82-88
15377640-11	2004	In conclusion, erythromycin, diltiazem, and nicardipine were weaker inhibitors of CYP3A5 and inactivated the enzyme at a slower rate than their respective effects on CYP3A4.	Diltiazem	29-38	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	166-172
15272217-1	2004	We examined the combined effects of the calcium channel blockers 1,4-dihydropyridine (benidipine) and benzothiazepine (diltiazem) on vasopressin-induced myocardial ischemia in anesthetized rats, an experimental model of angina.	Diltiazem	119-128	arginine vasopressin	Rattus norvegicus	133-144
15167950-18	2004	By comparison, long-acting dihydropyridines such as diltiazem and verapamil are less potent vasodilators and may primarily decrease the resistance of the efferent arteriole, similar to the ACE inhibitors.	Diltiazem	52-61	angiotensin I converting enzyme	Homo sapiens	189-192
15102955-10	2004	INS-1 cells expressing Ca(v)1.2/DHPi containing the II-III loop of Ca(v)1.3 demonstrated a nifedipine-resistant slow increase in [Ca(2+)](i) and nifedipine-resistant insulin secretion in response to glucose that was partially inhibited by diltiazem.	Diltiazem	239-248	insulin 1	Rattus norvegicus	0-5
15370956-5	2004	Midazolam metabolism was also inhibited in vitro by typical chemical inhibitors of CYP3A, such as ketoconazole, erythromycin and diltiazem, and the apparent K(i) values for ketoconazole, erythromycin and diltiazem were 0.127, 94.2 and 29.6 microM, respectively.	Diltiazem	129-138	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	83-88
14764344-1	2002	We study the effect of diltiazem on cultured vascular smooth muscle cells from humans and rats, paying special attention to its activity in relation to the concentrations applied, incubation times after addition and the capacity to act against the mitogenic activity of insulin and insulin-like growth factor 1 (IGF-1).	Diltiazem	23-32	insulin	Homo sapiens	270-277
15555475-13	2004	Concurrent use of inhibitors of the cytochrome P450 3A4 isozyme (eg, ketoconazole, diltiazem, cimetidine, atenolol) can significantly elevate serum concentrations of alfuzosin and enhance its pharmacodynamic effects.	Diltiazem	83-92	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	36-55
15133284-5	2004	DTZ maintained the higher erythropoietin level in blood, which acted on bone marrow and spleen colony forming unit for erythroblast (CFU-E), and stimulated such cells to produce RBCs.	Diltiazem	0-3	erythropoietin	Mus musculus	26-40
15133284-6	2004	These results confirm that DTZ has the potency to alter anaemic condition favorably through the protection of bone marrow stem cells, and subsequently it maintains the higher number of pro- and normoblasts in bone marrow, RBC counts, hemoglobin (Hb), hematocrit (Hct) percentage, and erythropoietin level in blood and the lower myeloid/erythroid ratio in bone marrow.	Diltiazem	27-30	erythropoietin	Mus musculus	284-298
15037208-5	2004	Treatment with 1 microM diltiazem enhanced the post-ischemic recovery of LVDP associated with attenuation of the ischemia-induced accumulation of tissue Na+, increase in cytochrome c in the cytosolic fraction, and decrease in myocardial OCR, and restoration of the myocardial HEPs during reperfusion.	Diltiazem	24-33	cytochrome c, somatic	Homo sapiens	170-182
12943684-5	2003	Stimulation with orexin-A produced a dose-dependent release of cholecystokinin (CCK), which was abolished by removal of extracellular Ca(2+) or the presence of the voltage-gated L-type Ca(2+)-channel blocker diltiazem (10 microM).	Diltiazem	208-217	hypocretin neuropeptide precursor	Homo sapiens	17-23
12943684-5	2003	Stimulation with orexin-A produced a dose-dependent release of cholecystokinin (CCK), which was abolished by removal of extracellular Ca(2+) or the presence of the voltage-gated L-type Ca(2+)-channel blocker diltiazem (10 microM).	Diltiazem	208-217	cholecystokinin	Homo sapiens	63-78
12943684-5	2003	Stimulation with orexin-A produced a dose-dependent release of cholecystokinin (CCK), which was abolished by removal of extracellular Ca(2+) or the presence of the voltage-gated L-type Ca(2+)-channel blocker diltiazem (10 microM).	Diltiazem	208-217	cholecystokinin	Homo sapiens	80-83
12951478-4	2003	The simultaneous addition of GBE to small intestine and liver microsomes inhibited the formation of N-demethyl DTZ (MA), an active metabolite of DTZ produced by CYP3A, in a concentration-dependent manner, with an IC(50) of about 50 and 182 microg/ml, respectively.	Diltiazem	111-114	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	161-166
12951478-9	2003	These results indicated that the concomitant use of GBE in rats increased the bioavailability of DTZ by inhibiting both intestinal and hepatic metabolism, at least in part, via a mechanism-based inhibition for CYP3A.	Diltiazem	97-100	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	210-215
14518598-0	2003	L-calcium channel blockade induced by diltiazem inhibits proliferation, migration and F-actin membrane rearrangements in human vascular smooth muscle cells stimulated with insulin and IGF-1.	Diltiazem	38-47	insulin	Homo sapiens	172-179
14518598-0	2003	L-calcium channel blockade induced by diltiazem inhibits proliferation, migration and F-actin membrane rearrangements in human vascular smooth muscle cells stimulated with insulin and IGF-1.	Diltiazem	38-47	insulin like growth factor 1	Homo sapiens	184-189
14518598-4	2003	Diltiazem (10(-7)-10(-6) M) reduced insulin-induced mitotic activity in cultured human vascular SMC more effectively than in IGF-1-induced mitotic activity, but at 10(-5) M, the inhibitory effects were similar.	Diltiazem	0-9	insulin	Homo sapiens	36-43
14518598-5	2003	Diltiazem also showed a clear inhibition of migration ability, both under basal conditions (p < 0.05) and after addition of insulin (p = 0.0001) and IGF-1 (p < 0.0001).	Diltiazem	0-9	insulin	Homo sapiens	127-134
14518598-5	2003	Diltiazem also showed a clear inhibition of migration ability, both under basal conditions (p < 0.05) and after addition of insulin (p = 0.0001) and IGF-1 (p < 0.0001).	Diltiazem	0-9	insulin like growth factor 1	Homo sapiens	152-157
14518598-6	2003	Finally, diltiazem inhibited membrane ruffling induced both by insulin and IGF-1 in a similar manner, and similar results were obtained with SMC from rat aorta.	Diltiazem	9-18	insulin	Homo sapiens	63-70
14518598-6	2003	Finally, diltiazem inhibited membrane ruffling induced both by insulin and IGF-1 in a similar manner, and similar results were obtained with SMC from rat aorta.	Diltiazem	9-18	insulin-like growth factor 1	Rattus norvegicus	75-80
13679549-7	2003	Expression of glycoprotein IIb/IIIa and P-selectin was significantly inhibited in vitro by diltiazem in the concentration of 200 ng/ml or higher, but not 50 ng/ml.	Diltiazem	91-100	selectin P	Homo sapiens	40-50
12869655-1	2003	Diltiazem block of Cav1.2 is frequency-dependent and potentiated by Ca2+.	Diltiazem	0-9	calcium voltage-gated channel subunit alpha1 C	Homo sapiens	19-25
12869655-7	2003	Potentiation of diltiazem block of closed Cav1.2 channels in Ca2+ was abolished in the E1118Q, F1117G (domain III), and E1419Q mutants.	Diltiazem	16-25	calcium voltage-gated channel subunit alpha1 C	Homo sapiens	42-48
12869655-10	2003	We conclude that, in Ba2+, E1419 slows recovery from diltiazem block of depolarized Cav1.2 channels, but in Ca2+, E1118, E1419, and F1117 form a Ca2+ binding site that mediates the potentiation of diltiazem block of both closed and inactivated Cav1.2 channels.	Diltiazem	53-62	calcium voltage-gated channel subunit alpha1 C	Homo sapiens	84-90
12709682-6	2003	At the end of CPB, the mean IL-6 level in the control group was significantly higher than in the diltiazem group (p=0.015), and at 3 hours after CPB the difference was even greater (p=0.002).	Diltiazem	97-106	interleukin 6	Homo sapiens	28-32
12709682-8	2003	CONCLUSIONS: Diltiazem inhibits the release of the pro-inflammatory cytokine IL-6, which is strong evidence for its anti-inflammatory effect.	Diltiazem	13-22	interleukin 6	Homo sapiens	77-81
12527180-6	2003	Papp of mannitol and diltiazem in the presence of CDP-Ch ranged from 0.53 x 10(-6) to 8.52 x 10(-6) cm/s and from 1.30 x 10(-5) to 2.71 x 10(-5) cm/s, respectively.	Diltiazem	21-30	cut like homeobox 1	Homo sapiens	50-53
12243603-7	2002	Rhabdomyolysis resulting from the drug interaction between diltiazem and other HMG-CoA reductase inhibitors has been described in the literature.	Diltiazem	59-68	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	79-96
15499178-6	2004	In addition, the correlation coefficients of CYP3A5 contents with the rates of diltiazem N-demethylation, midazolam 1"-hydroxylation and testosterone 6beta- hydroxylation were higher than those of CYP3A4, although the value of CYP3A5 with the midazolam 4-hydroxylation rate was similar to that of CYP3A4.	Diltiazem	79-88	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	45-51
15499178-8	2004	The apparent V(max)/K(m) values for recombinant CYP3A5 indicated the greater contributions to diltiazem N-demethylation and midazolam 1"-hydroxylation as compared with CYP3A4.	Diltiazem	94-103	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	48-54
15499178-9	2004	These results suggest that polymorphic CYP3A5 contributes markedly to the drug oxidations, particularly diltiazem N-demethylation, midazolam 1"- hydroxylation and testosterone 6beta-hydroxylation by liver microsomes from Japanese subjects.	Diltiazem	104-113	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	39-45
14981072-4	2004	The Ca2+ channel blockers verapamil and diltiazem (10(-6) mol/L) abolished the maintained ET-1-induced [Ca2+]i, but only partially inhibited ET-1-induced cell contraction to 18%.	Diltiazem	40-49	endothelin 1	Homo sapiens	90-94
14981072-4	2004	The Ca2+ channel blockers verapamil and diltiazem (10(-6) mol/L) abolished the maintained ET-1-induced [Ca2+]i, but only partially inhibited ET-1-induced cell contraction to 18%.	Diltiazem	40-49	endothelin 1	Homo sapiens	141-145
15001203-2	2004	This study was designed to investigate whether treatment with felodipine or diltiazem has any effect on plasma levels of MMP-2 and MMP-9 in essential hypertensive patients.	Diltiazem	76-85	matrix metallopeptidase 2	Homo sapiens	121-126
14600078-5	2003	Ca2+ channel blockers verapamil and diltiazem (10-6 M) abolished maintained PGF2alpha-induced [Ca2+]i increase but only partially inhibited PGF2alpha-induced cell contraction to 17%.	Diltiazem	36-45	carbonic anhydrase 2	Homo sapiens	0-3
14600078-5	2003	Ca2+ channel blockers verapamil and diltiazem (10-6 M) abolished maintained PGF2alpha-induced [Ca2+]i increase but only partially inhibited PGF2alpha-induced cell contraction to 17%.	Diltiazem	36-45	carbonic anhydrase 2	Homo sapiens	95-98
12574144-11	2003	In contrast, L-type Ca2+ channel blockade with diltiazem partially prevented ( approximately 50%) the inotropic response to IGF-1.	Diltiazem	47-56	insulin like growth factor 1	Homo sapiens	124-129
12610742-5	2003	Fractions demonstrating significant CYP3A4 inhibitory activity, as measured by the relative reduction in N-demethylation of diltiazem in transfected human liver epithelial cells, were subsequently separated by preparative thin-layer chromatography.	Diltiazem	124-133	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	36-42
12610742-8	2003	RESULTS: Of the identified components in grapefruit peel, only epoxybergamottin demonstrated a concentration-dependent inhibition of the CYP3A4-mediated N-demethylation of diltiazem.	Diltiazem	172-181	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	137-143
12623755-5	2003	Other calcium channel antagonists, nifedipine, diltiazem and verapamil, also enhanced the gene expression of CYP2B1, CYP2B2, CYP3A1 and CYP3A2, although these showed no capacity for activating CYP1A1 and CYP1A2 genes.	Diltiazem	47-56	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	109-115
12623755-5	2003	Other calcium channel antagonists, nifedipine, diltiazem and verapamil, also enhanced the gene expression of CYP2B1, CYP2B2, CYP3A1 and CYP3A2, although these showed no capacity for activating CYP1A1 and CYP1A2 genes.	Diltiazem	47-56	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	117-123
12623755-5	2003	Other calcium channel antagonists, nifedipine, diltiazem and verapamil, also enhanced the gene expression of CYP2B1, CYP2B2, CYP3A1 and CYP3A2, although these showed no capacity for activating CYP1A1 and CYP1A2 genes.	Diltiazem	47-56	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	125-131
12623755-5	2003	Other calcium channel antagonists, nifedipine, diltiazem and verapamil, also enhanced the gene expression of CYP2B1, CYP2B2, CYP3A1 and CYP3A2, although these showed no capacity for activating CYP1A1 and CYP1A2 genes.	Diltiazem	47-56	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	136-142
12623755-5	2003	Other calcium channel antagonists, nifedipine, diltiazem and verapamil, also enhanced the gene expression of CYP2B1, CYP2B2, CYP3A1 and CYP3A2, although these showed no capacity for activating CYP1A1 and CYP1A2 genes.	Diltiazem	47-56	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	193-199
12623755-5	2003	Other calcium channel antagonists, nifedipine, diltiazem and verapamil, also enhanced the gene expression of CYP2B1, CYP2B2, CYP3A1 and CYP3A2, although these showed no capacity for activating CYP1A1 and CYP1A2 genes.	Diltiazem	47-56	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	204-210
12235455-0	2002	Pharmacokinetics of diltiazem and its metabolites in relation to CYP2D6 genotype.	Diltiazem	20-29	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	65-71
12235455-1	2002	OBJECTIVES: Recently, it was shown in vitro that the polymorphic enzyme cytochrome P450 (CYP) 2D6 mediates O-demethylation of diltiazem.	Diltiazem	126-135	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	72-97
12235455-12	2002	Because these metabolites exhibit pharmacologic properties of possible importance, individual CYP2D6 activity might be an aspect to consider in the clinical use of diltiazem.	Diltiazem	164-173	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	94-100
14764344-1	2002	We study the effect of diltiazem on cultured vascular smooth muscle cells from humans and rats, paying special attention to its activity in relation to the concentrations applied, incubation times after addition and the capacity to act against the mitogenic activity of insulin and insulin-like growth factor 1 (IGF-1).	Diltiazem	23-32	insulin-like growth factor 1	Rattus norvegicus	282-310
14764344-1	2002	We study the effect of diltiazem on cultured vascular smooth muscle cells from humans and rats, paying special attention to its activity in relation to the concentrations applied, incubation times after addition and the capacity to act against the mitogenic activity of insulin and insulin-like growth factor 1 (IGF-1).	Diltiazem	23-32	insulin-like growth factor 1	Rattus norvegicus	312-317
12072188-2	2002	Herein, we demonstrate that diltiazem, in association with granulocyte macrophage-colony-stimulating factor (GM-CSF) and interleukin-4 (IL-4), induces monocytes to differentiate into cells with many of the characteristic of DC.	Diltiazem	28-37	colony stimulating factor 2	Homo sapiens	59-107
12072188-2	2002	Herein, we demonstrate that diltiazem, in association with granulocyte macrophage-colony-stimulating factor (GM-CSF) and interleukin-4 (IL-4), induces monocytes to differentiate into cells with many of the characteristic of DC.	Diltiazem	28-37	colony stimulating factor 2	Homo sapiens	109-115
12072188-2	2002	Herein, we demonstrate that diltiazem, in association with granulocyte macrophage-colony-stimulating factor (GM-CSF) and interleukin-4 (IL-4), induces monocytes to differentiate into cells with many of the characteristic of DC.	Diltiazem	28-37	interleukin 4	Homo sapiens	121-134
12072188-2	2002	Herein, we demonstrate that diltiazem, in association with granulocyte macrophage-colony-stimulating factor (GM-CSF) and interleukin-4 (IL-4), induces monocytes to differentiate into cells with many of the characteristic of DC.	Diltiazem	28-37	interleukin 4	Homo sapiens	136-140
12072188-4	2002	Importantly, diltiazem-induced DCs have an impaired responsiveness to lipopolysaccharide and CD40 ligand because they produce decreased levels of IL-12 and reveal a reduced ability to stimulate alloreactive T-cell responses as well as in inducing interferon-gamma producing Th1 cells.	Diltiazem	13-22	CD40 molecule	Homo sapiens	93-97
12072188-4	2002	Importantly, diltiazem-induced DCs have an impaired responsiveness to lipopolysaccharide and CD40 ligand because they produce decreased levels of IL-12 and reveal a reduced ability to stimulate alloreactive T-cell responses as well as in inducing interferon-gamma producing Th1 cells.	Diltiazem	13-22	interferon gamma	Homo sapiens	247-263
11901316-9	2002	A dose-dependent reduction in TNF-alpha production was demonstrated with diltiazem and verapamil (p < 0.05), with no effect induced by EGTA.	Diltiazem	73-82	tumor necrosis factor	Oryctolagus cuniculus	30-39
12011785-8	2002	In the control group, dopamine-only, and diltiazem-only groups beta(2)-microglobulin was statistically higher 72 hours postoperative than preoperatively (p<0.05).	Diltiazem	41-50	beta-2-microglobulin	Homo sapiens	63-84
12037132-13	2002	We confirmed that Ca(2+) enters the cells through the dihydropyridine receptor (DHPR, also known as the L-channel) by demonstrating inhibition by diltiazem.	Diltiazem	146-155	calcium voltage-gated channel subunit alpha1 S	Homo sapiens	54-78
12037132-13	2002	We confirmed that Ca(2+) enters the cells through the dihydropyridine receptor (DHPR, also known as the L-channel) by demonstrating inhibition by diltiazem.	Diltiazem	146-155	quinoid dihydropteridine reductase	Homo sapiens	80-84
11959131-5	2002	We found that treatment of CsA (20 microM) alone caused 20-30% cell death, which was apparently (30-40%) enhanced by diltiazem at 100 microg/ml, accompanied by more severe DNA fragmentation, activation of caspases, and a decreased level of Bcl-2.	Diltiazem	117-126	BCL2 apoptosis regulator	Canis lupus familiaris	240-245
11959131-6	2002	The caspase inhibitor ZVAD-fmk or Bcl-2 overexpression was capable of suppressing apoptosis induced by the synergistic effect of diltiazem and CsA.	Diltiazem	129-138	BCL2 apoptosis regulator	Canis lupus familiaris	34-39
11855685-8	2002	The blockade of Ca2+ channels by diltiazem inhibits the in vitro stimulation by IGF1 and insulin on SMC proliferation and migration.	Diltiazem	33-42	insulin	Homo sapiens	89-96
11744603-1	2002	It has earlier been shown that the isoenzymes CYP2D6 and CYP3A4 are involved in O- and N-demethylation of diltiazem (DTZ), respectively.	Diltiazem	106-115	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	46-52
11744603-1	2002	It has earlier been shown that the isoenzymes CYP2D6 and CYP3A4 are involved in O- and N-demethylation of diltiazem (DTZ), respectively.	Diltiazem	106-115	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	57-63
11744603-1	2002	It has earlier been shown that the isoenzymes CYP2D6 and CYP3A4 are involved in O- and N-demethylation of diltiazem (DTZ), respectively.	Diltiazem	117-120	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	46-52
11744603-1	2002	It has earlier been shown that the isoenzymes CYP2D6 and CYP3A4 are involved in O- and N-demethylation of diltiazem (DTZ), respectively.	Diltiazem	117-120	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	57-63
11744603-2	2002	Apparently, CYP3A4 plays a more prominent role than CYP2D6 in the overall metabolism of DTZ.	Diltiazem	88-91	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	12-18
11744603-2	2002	Apparently, CYP3A4 plays a more prominent role than CYP2D6 in the overall metabolism of DTZ.	Diltiazem	88-91	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	52-58
11744603-9	2002	Metabolism mediated through CYP2D6 is associated with a substantial interindividual variability, and since M1 expresses pharmacological activity, individual CYP2D6 metabolic capacity might be an aspect to consider when using DTZ.	Diltiazem	225-228	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	28-34
11744603-9	2002	Metabolism mediated through CYP2D6 is associated with a substantial interindividual variability, and since M1 expresses pharmacological activity, individual CYP2D6 metabolic capacity might be an aspect to consider when using DTZ.	Diltiazem	225-228	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	157-163
11855685-8	2002	The blockade of Ca2+ channels by diltiazem inhibits the in vitro stimulation by IGF1 and insulin on SMC proliferation and migration.	Diltiazem	33-42	insulin like growth factor 1	Homo sapiens	80-84
11795484-6	2001	The synergism of 5-HT and PAF in platelet aggregation was inhibited by calcium (Ca2+) channel blockers, verapamil and diltiazem, phospholipase C (PLC) inhibitor, U73122, cyclooxygenase (COX) inhibitor, indomethacin, and MEK inhibitor, PD98059.	Diltiazem	118-127	PCNA clamp associated factor	Homo sapiens	26-29
11240977-8	2001	The venodilation caused by diltiazem was also attenuated by angiotensin II, but this attenuating effect was smaller compared with that caused by nitroglycerin.	Diltiazem	27-36	angiotensinogen	Homo sapiens	60-74
11605028-7	2001	In Western blotting, matrix metalloproteinase (MMP)-1 (tissue collagenase) but not MMP-2 (72-kDa gelatinase) expression was upregulated by PDGF and phorbol ester (TPA), which were reduced by diltiazem in a dose-dependent manner.	Diltiazem	191-200	matrix metallopeptidase 1	Homo sapiens	21-53
11605028-11	2001	Our data suggest that diltiazem inhibits not only proliferation but also MMP-1 expression and collagenolytic activity in PDGF-stimulated SMC.	Diltiazem	22-31	matrix metallopeptidase 1	Homo sapiens	73-78
11458989-5	2001	The potentiated component of stretch-induced tone in the presence of 30 pM ET-1 was largely attenuated by Ca2+ channel blockers, nimodipine (1 microM) or diltiazem (1 microM).	Diltiazem	154-163	endothelin 1	Canis lupus familiaris	75-79
11396927-3	2001	A Ca(2+) channel blocker diltiazem and a calmodulin inhibitor W-7 reduced the scavenger receptor activity of the macrophages plated on FN-coated substrate to the level of the cells plated on uncoated substrate, as assessed by oxLDL binding, while the scavenger receptor activity of the macrophages on uncoated substrate was little affected.	Diltiazem	25-34	fibronectin 1	Mus musculus	135-137
11396927-4	2001	Similarly, FN-induced enhancement of the scavenger receptor activity assessed by oxLDL uptake was selectively inhibited by Ca(2+) channel blockers (diltiazem, nifedipine, verapamil) and calmodulin inhibitors (W-7, trifluoperazine).	Diltiazem	148-157	fibronectin 1	Mus musculus	11-13
11396927-6	2001	This increase in the Ca(2+) level was inhibited by diltiazem and RGD-containing peptides present in cell adhesive region of FN.	Diltiazem	51-60	fibronectin 1	Mus musculus	124-126
11422004-3	2001	Kinetics of CYP3A4 inactivation by verapamil and diltiazem were determined using testosterone as the substrate.	Diltiazem	49-58	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	12-18
11422004-12	2001	However, verapamil and diltiazem are moderate mechanism-based inhibitors of CYP3A4 and therefore may still cause significant inhibition of simvastatin metabolism in vivo during chronic therapy.	Diltiazem	23-32	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	76-82
11916358-6	2001	After 4 weeks the level of plasma BNP in the diltiazem treatment group was lower than in the no treatment group [55+/-3 pg/mL vs 85+/-5 pg/mL (P < 0.05)].	Diltiazem	45-54	natriuretic peptide B	Homo sapiens	34-37
11916358-10	2001	In this study, diltiazem significantly improved systolic function and reduced the level of plasma BNP after myocardial infarction, which suggest that diltiazem may have a beneficial effect on myocardial infarction without congestive heart failure.	Diltiazem	15-24	natriuretic peptide B	Homo sapiens	98-101
11916358-10	2001	In this study, diltiazem significantly improved systolic function and reduced the level of plasma BNP after myocardial infarction, which suggest that diltiazem may have a beneficial effect on myocardial infarction without congestive heart failure.	Diltiazem	150-159	natriuretic peptide B	Homo sapiens	98-101
11605028-0	2001	Diltiazem, a calcium antagonist, inhibits matrix metalloproteinase-1 (tissue collagenase) production and collagenolytic activity in human vascular smooth muscle cells.	Diltiazem	0-9	matrix metallopeptidase 1	Homo sapiens	42-88
11560871-0	2001	Effects of CYP3A4 inhibition by diltiazem on pharmacokinetics and dynamics of diazepam in relation to CYP2C19 genotype status.	Diltiazem	32-41	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	11-17
11560871-3	2001	The aim of this study was to assess the effect of diltiazem, a CYP3A4 inhibitor, on pharmacokinetics and dynamics of diazepam in relation to CYP2C19 genotype status.	Diltiazem	50-59	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	63-69
11560871-3	2001	The aim of this study was to assess the effect of diltiazem, a CYP3A4 inhibitor, on pharmacokinetics and dynamics of diazepam in relation to CYP2C19 genotype status.	Diltiazem	50-59	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	141-148
11560871-9	2001	Diltiazem affects the pharmacokinetics of diazepam in the PM and EM groups of CYP2C19.	Diltiazem	0-9	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	78-85
11560871-10	2001	Inhibition of CYP3A4 by a concomitant substrate drug like diltiazem may cause a pharmacokinetic interaction with diazepam irrespective of CYP2C19 genotype status, but whether this interaction would reflect a pharmacodynamic change of diazepam remains unconfirmed by our study.	Diltiazem	58-67	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	14-20
11560871-10	2001	Inhibition of CYP3A4 by a concomitant substrate drug like diltiazem may cause a pharmacokinetic interaction with diazepam irrespective of CYP2C19 genotype status, but whether this interaction would reflect a pharmacodynamic change of diazepam remains unconfirmed by our study.	Diltiazem	58-67	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	138-145
11457719-6	2001	The Ca(2+) channel blocker diltiazem and the Ca(2+)-specific chelator EGTA-AM abolished high [K(+)](e)-induced HSP-72 expression by 69.7 and 75.2%, respectively, indicating that the transcriptional induction of HSP-72 involves Ca(2+) influx.	Diltiazem	27-36	heat shock protein family A (Hsp70) member 1A	Homo sapiens	111-117
11457719-6	2001	The Ca(2+) channel blocker diltiazem and the Ca(2+)-specific chelator EGTA-AM abolished high [K(+)](e)-induced HSP-72 expression by 69.7 and 75.2%, respectively, indicating that the transcriptional induction of HSP-72 involves Ca(2+) influx.	Diltiazem	27-36	heat shock protein family A (Hsp70) member 1A	Homo sapiens	211-217
11483409-4	2001	Application of Ca(2+) channel blockers, diltiazem and Ni(2+), inhibited the bradykinin-induced Ca(2+) mobilization, indicating that Ca(2+) influx was required for the bradykinin-induced responses.	Diltiazem	40-49	kininogen 1	Canis lupus familiaris	76-86
11483409-4	2001	Application of Ca(2+) channel blockers, diltiazem and Ni(2+), inhibited the bradykinin-induced Ca(2+) mobilization, indicating that Ca(2+) influx was required for the bradykinin-induced responses.	Diltiazem	40-49	kininogen 1	Canis lupus familiaris	167-177
11472982-7	2001	In addition, treatment of HPASM cells with two drug types used in the management of PH-cicaprost, a stable prostacyclin-mimetic; or diltiazem, a calcium-channel blocker-reduced ET-1 release from these cells.	Diltiazem	132-141	endothelin 1	Homo sapiens	177-181
11240977-9	2001	CONCLUSIONS: These findings suggest that an enhanced angiotensin II level might attenuate the venodilation caused by nitroglycerin and diltiazem, and pretreatment with losartan might decrease the attenuating effect of angiotensin II.	Diltiazem	135-144	angiotensinogen	Homo sapiens	53-67
11239245-3	2001	METHODS: D-cis-diltiazem was delivered orally twice daily to rcd1 affected dogs beginning at 4 weeks of age; untreated age-matched rcd1 dogs served as controls.	Diltiazem	9-24	phosphodiesterase 6B	Canis lupus familiaris	61-65
11239245-1	2001	PURPOSE: D-cis-diltiazem, a calcium channel blocker, has been reported to enhance photoreceptor survival in the rd mouse, a model of retinitis pigmentosa (RP) resulting from mutation of the PDE6B gene.	Diltiazem	9-24	phosphodiesterase 6B, cGMP, rod receptor, beta polypeptide	Mus musculus	190-195
11239245-2	2001	We tested the hypothesis that diltiazem treatment would similarly rescue the canine rcd1 model of RP, which is also caused by a null mutation in the PDE6B gene.	Diltiazem	30-39	phosphodiesterase 6B	Canis lupus familiaris	84-88
11239245-2	2001	We tested the hypothesis that diltiazem treatment would similarly rescue the canine rcd1 model of RP, which is also caused by a null mutation in the PDE6B gene.	Diltiazem	30-39	phosphodiesterase 6B	Canis lupus familiaris	149-154
11239245-9	2001	CONCLUSIONS: Treatment of rcd1 affected dogs with D-cis-diltiazem did not modify the photoreceptor disease when results were assessed using either ERG or histopathologic criteria.	Diltiazem	50-65	phosphodiesterase 6B	Canis lupus familiaris	26-30
11139439-8	2000	Both diltiazem (10 microM) and SK-F 96365 (10 microM) significantly inhibited the thrombin-induced elevations of [Ca(2+)](i) and tension, and their effects were additive.	Diltiazem	5-14	coagulation factor II	Rattus norvegicus	82-90
11087244-8	2000	In the continuous presence of BAY K, diltiazem reversed the effects of BAY K. Diltiazem alone increased ANP secretion and ANP concentration along with a decrease in atrial dynamics.	Diltiazem	37-46	natriuretic peptides A	Oryctolagus cuniculus	104-107
11087244-8	2000	In the continuous presence of BAY K, diltiazem reversed the effects of BAY K. Diltiazem alone increased ANP secretion and ANP concentration along with a decrease in atrial dynamics.	Diltiazem	37-46	natriuretic peptides A	Oryctolagus cuniculus	122-125
11087244-8	2000	In the continuous presence of BAY K, diltiazem reversed the effects of BAY K. Diltiazem alone increased ANP secretion and ANP concentration along with a decrease in atrial dynamics.	Diltiazem	78-87	natriuretic peptides A	Oryctolagus cuniculus	104-107
11087244-8	2000	In the continuous presence of BAY K, diltiazem reversed the effects of BAY K. Diltiazem alone increased ANP secretion and ANP concentration along with a decrease in atrial dynamics.	Diltiazem	78-87	natriuretic peptides A	Oryctolagus cuniculus	122-125
11087244-9	2000	Diltiazem shifted relationships between ANP secretion and atrial stroke volume or ECF translocation leftward.	Diltiazem	0-9	natriuretic peptides A	Oryctolagus cuniculus	40-43
11220491-5	2000	Gal-evoked contractions were attenuated by diminished extracellular Ca2+ concentration and by diltiazem.	Diltiazem	94-103	galanin and GMAP prepropeptide	Rattus norvegicus	0-3
11093762-5	2000	Thus, amino acids specific to the L-type channel that confer DHP sensitivity in an alpha(1A) background also increase sensitivity to diltiazem.	Diltiazem	133-142	dihydropyrimidinase	Homo sapiens	61-64
11093762-5	2000	Thus, amino acids specific to the L-type channel that confer DHP sensitivity in an alpha(1A) background also increase sensitivity to diltiazem.	Diltiazem	133-142	calcium voltage-gated channel subunit alpha1 A	Homo sapiens	83-91
11093762-9	2000	Thus, binding of diltiazem to L-type Ca(2+) channels requires residues that overlap those that are critical for DHP and PA block as well as residues unique to diltiazem.	Diltiazem	17-26	dihydropyrimidinase	Homo sapiens	112-115
11038161-9	2000	Diltiazem, testosterone, and verapamil were metabolized predominantly by CYP3A4.	Diltiazem	0-9	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	73-79
11151747-0	2000	CYP2D6 is involved in O-demethylation of diltiazem.	Diltiazem	41-50	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	0-6
11151747-3	2000	The aim of this in vitro study was to investigate whether O-demethylation of DTZ is mediated by cytochrome P450-2D6 (CYP2D6).	Diltiazem	77-80	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	96-115
11151747-3	2000	The aim of this in vitro study was to investigate whether O-demethylation of DTZ is mediated by cytochrome P450-2D6 (CYP2D6).	Diltiazem	77-80	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	117-123
11151747-4	2000	METHODS: DTZ was incubated with transfected human liver epithelial (THLE) cells expressing CYP2D6 (T5-2D6 clone).	Diltiazem	9-12	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	91-97
11151747-5	2000	Metabolism of DTZ was studied over a concentration range of 12.5-400 microM and in the presence of quinidine (a CYP2D6 inhibitor) or erythromycin (a CYP3A4 inhibitor).	Diltiazem	14-17	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	112-118
11151747-5	2000	Metabolism of DTZ was studied over a concentration range of 12.5-400 microM and in the presence of quinidine (a CYP2D6 inhibitor) or erythromycin (a CYP3A4 inhibitor).	Diltiazem	14-17	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	149-155
11151747-9	2000	RESULTS: Desacetyl-O-demethyl-DTZ (M4) was exclusively produced during incubations of DTZ with THLE cells expressing CYP2D6.	Diltiazem	30-33	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	117-123
11151747-14	2000	CONCLUSION: Evidence was provided in vitro that O-demethylation of DTZ is mediated by the polymorphic isoenzyme CYP2D6.	Diltiazem	67-70	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	112-118
11151747-15	2000	Involvement of CYP2D6 in the metabolism of DTZ may have clinical implications regarding pharmacokinetic variability and interactions.	Diltiazem	43-46	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	15-21
10821339-4	2000	The effects of insulin on the membrane fluidity were potentiated in the presence of extracellular Ca2+, and in contrast, were antagonized by the Ca2+ channel blocker diltiazem.	Diltiazem	166-175	insulin	Homo sapiens	15-22
10950845-2	2000	Rates for loss of CYP3A4 enzymatic activity resulting from metabolic intermediate complex formation and the concentration dependencies thereof were determined in vitro for clarithromycin, fluoxetine, and N-desmethyl diltiazem, which is the primary metabolite of diltiazem.	Diltiazem	216-225	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	18-24
10950845-4	2000	Based on the predicted rates combined with published rates for in vivo CYP3A degradation, our model predicts that fluoxetine, clarithromycin, and the primary metabolite of diltiazem reduce the steady-state concentration of liver CYP3A4 to approximately 72, 39, or 21% of initial levels, respectively.	Diltiazem	172-181	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	71-76
10950845-4	2000	Based on the predicted rates combined with published rates for in vivo CYP3A degradation, our model predicts that fluoxetine, clarithromycin, and the primary metabolite of diltiazem reduce the steady-state concentration of liver CYP3A4 to approximately 72, 39, or 21% of initial levels, respectively.	Diltiazem	172-181	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	229-235
10950845-7	2000	The major implication of this work is that fluoxetine, clarithromycin, and the primary metabolite of diltiazem, at clinically relevant concentrations, inactivate CYP3A4 enzymatic activity at rates sufficient to affect in vivo concentrations of CYP3A4 and thereby affect the clearance of compounds eliminated by this pathway.	Diltiazem	101-110	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	162-168
10950845-7	2000	The major implication of this work is that fluoxetine, clarithromycin, and the primary metabolite of diltiazem, at clinically relevant concentrations, inactivate CYP3A4 enzymatic activity at rates sufficient to affect in vivo concentrations of CYP3A4 and thereby affect the clearance of compounds eliminated by this pathway.	Diltiazem	101-110	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	244-250
11256234-6	2000	The NADPH cytochrome P-450 reductase activity was significantly decreased by nifedipine and diltiazem.	Diltiazem	92-101	cytochrome p450 oxidoreductase	Rattus norvegicus	4-36
10971313-1	2000	AIMS: To study whether intravenous diltiazem, a calcium channel blocker commonly prescribed for hypertension and stable angina, is an inhibitor of the CYP3A enzymes by using oral lovastatin, an HMG Co-A reductase inhibitor, as a substrate.	Diltiazem	35-44	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	151-156
10802029-9	2000	The increase in GFAP-IR produced by exposure to acidic medium was blocked by pretreatment with nickel ions, by such blockers of L-type calcium channels as nifedipine, verapamil and diltiazem, by calpain inhibitor I, or by the intracellular calcium chelator, BAPTA-AM.	Diltiazem	181-190	glial fibrillary acidic protein	Homo sapiens	16-20
10781015-14	2000	Similar selective inhibition of the L-NOARG-resistant relaxation to thrombin, but not SFLLRN, occurred with verapamil (1 microM) and diltiazem (3 microM).	Diltiazem	133-142	coagulation factor II, thrombin	Homo sapiens	68-76
10760083-10	2000	VLDL-induced MCP-1 expression and monocyte adhesion were blocked by a protein kinase C inhibitor (staurosporine), as well as a calcium channel blocker (diltiazem).	Diltiazem	152-161	CD320 antigen	Mus musculus	0-4
10760083-10	2000	VLDL-induced MCP-1 expression and monocyte adhesion were blocked by a protein kinase C inhibitor (staurosporine), as well as a calcium channel blocker (diltiazem).	Diltiazem	152-161	chemokine (C-C motif) ligand 2	Mus musculus	13-18
10860024-3	2000	HERG is blocked by bepridil (EC50 = 0.55 microM), verapamil (EC50 = 0.83 microM) and mibefradil (EC50 = 1.43 microM), whereas nitrendipine and diltiazem have negligible effects.	Diltiazem	143-152	potassium voltage-gated channel subfamily H member 2	Homo sapiens	0-4
10741630-2	2000	Diltiazem is a substrate and an inhibitor of CYP3A enzymes and is commonly coadministered with cholesterol-lowering agents such as simvastatin.	Diltiazem	0-9	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	45-50
10741630-9	2000	CONCLUSION: Diltiazem coadministration resulted in a significant interaction with simvastatin, probably by inhibiting CYP3A-mediated metabolism.	Diltiazem	12-21	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	118-123
10741630-10	2000	Concomitant use of diltiazem or other potent inhibitors of CYP3A with simvastatin should be avoided, or close clinical monitoring should be used.	Diltiazem	19-28	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	59-64
10776932-2	2000	Recently, nifedipine and diltiazem have often been used to control CsA-related hypertension in organ transplant patients.	Diltiazem	25-34	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	67-70
10776932-10	2000	Neither nifedipine nor diltiazem suppressed rat growth when used independently; however, rat growth reduced by CsA was further suppressed by a combined use of diltiazem, but not nifedipine.	Diltiazem	159-168	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	111-114
10776932-11	2000	CsA blood levels were reduced by concurrent oral treatment with nifedipine or diltiazem along with the blood levels of those calcium channel blockers when treatment was in combination with CsA.	Diltiazem	78-87	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	0-3
10640508-7	2000	Unlike the observations with mibefradil, a potent irreversible inhibitor of CYP3A, the NADPH-dependent inhibition of CYP3A activity by nicardipine and verapamil was completely reversible on dialysis, whereas that by diltiazem was partially restored (80%).	Diltiazem	216-225	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	117-122
10640508-8	2000	Additional experiments revealed that nicardipine, verapamil, and diltiazem formed cytochrome P-450-iron (II)-metabolite complex in both human liver microsomes and recombinant CYP3A4.	Diltiazem	65-74	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	175-181
10640508-10	2000	These present findings that the CYP3A inhibition caused by nicardipine, verapamil, and diltiazem is, at least in part, quasi-irreversible provide a rational basis for pharmacokinetically significant interactions reported when they were coadministered with agents that are cleared primarily by CYP3A-mediated pathways.	Diltiazem	87-96	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	32-37
10640508-10	2000	These present findings that the CYP3A inhibition caused by nicardipine, verapamil, and diltiazem is, at least in part, quasi-irreversible provide a rational basis for pharmacokinetically significant interactions reported when they were coadministered with agents that are cleared primarily by CYP3A-mediated pathways.	Diltiazem	87-96	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	293-298
10640297-0	2000	Nifedipine and diltiazem but not verapamil up-regulate endothelial nitric-oxide synthase expression.	Diltiazem	15-24	nitric oxide synthase 3	Homo sapiens	55-88
10640297-7	2000	Similarly, eNOS protein abundance was increased significantly by nifedipine (P <.05) and diltiazem (P <.05).	Diltiazem	92-101	nitric oxide synthase 3	Homo sapiens	11-15
10718121-0	2000	Metabolite-intermediate complexation and inhibition of microsomal CYP3A in rat liver by diltiazem.	Diltiazem	88-97	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	66-71
10718121-2	2000	The formation of metabolite intermediate (MI)-complexes between cytochrome P450 (CYP) and the alkylamine-substituted drugs diltiazem (DTZ) and desipramine (DES) and their effect on CYP activities was investigated in rat liver.	Diltiazem	123-132	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	64-79
10718121-2	2000	The formation of metabolite intermediate (MI)-complexes between cytochrome P450 (CYP) and the alkylamine-substituted drugs diltiazem (DTZ) and desipramine (DES) and their effect on CYP activities was investigated in rat liver.	Diltiazem	123-132	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	81-84
10718121-2	2000	The formation of metabolite intermediate (MI)-complexes between cytochrome P450 (CYP) and the alkylamine-substituted drugs diltiazem (DTZ) and desipramine (DES) and their effect on CYP activities was investigated in rat liver.	Diltiazem	123-132	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	181-184
10718121-2	2000	The formation of metabolite intermediate (MI)-complexes between cytochrome P450 (CYP) and the alkylamine-substituted drugs diltiazem (DTZ) and desipramine (DES) and their effect on CYP activities was investigated in rat liver.	Diltiazem	134-137	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	64-79
10718121-2	2000	The formation of metabolite intermediate (MI)-complexes between cytochrome P450 (CYP) and the alkylamine-substituted drugs diltiazem (DTZ) and desipramine (DES) and their effect on CYP activities was investigated in rat liver.	Diltiazem	134-137	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	81-84
10718121-2	2000	The formation of metabolite intermediate (MI)-complexes between cytochrome P450 (CYP) and the alkylamine-substituted drugs diltiazem (DTZ) and desipramine (DES) and their effect on CYP activities was investigated in rat liver.	Diltiazem	134-137	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	181-184
10718121-4	2000	Dexamethasone and phenobarbitone pretreatment enhanced MI-complexation by DTZ (36% and 11% of total CYP complexed, respectively), whereas beta-naphthoflavone induction was without effect.	Diltiazem	74-77	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	100-103
10644660-6	2000	The sustained response to 1 microM ANG II was attenuated by diltiazem and was reduced to a value less than baseline in the absence of external Ca(2+).	Diltiazem	60-69	angiogenin	Homo sapiens	35-38
10860024-5	2000	Similarly, KvLQT1-IsK is inhibited by bepridil (EC50 = 10.0 microM) and mibefradil (EC50 = 11.8 microM), whilst being insensitive to nitrendipine, diltiazem or verapamil.	Diltiazem	147-156	potassium voltage-gated channel subfamily E regulatory subunit 1	Homo sapiens	18-21
10070046-12	1999	L-type Ca2+ channel blockers nifedipine and diltiazem (3-10 microM) markedly attenuated DBI-stimulated Ca2+ oscillations.	Diltiazem	44-53	diazepam binding inhibitor	Rattus norvegicus	88-91
10583033-1	1999	AIMS: To investigate whether an interaction between diltiazem and the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor simvastatin may enhance the cholesterol-lowering response to simvastatin in diltiazem-treated patients.	Diltiazem	214-223	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	70-127
10563472-8	1999	Superoxide stimulated TNF-alpha secretion was inhibited by intracellular Ca2+-buffers (MAPT-AM and BAPT-AM) or VOC operating antagonists (diltiazem and verapamil) and only to a small extent by pharmacological inhibitors of ligand-gated pathways (TMB-8 and SKF 96368).	Diltiazem	138-147	tumor necrosis factor	Homo sapiens	22-31
10454485-1	1999	Diltiazem (DTZ) N-demethylation occurs by cytochrome P-450 (CYP) 3A based on the following observations: 1) a single enzyme Michaelis-Menten model of metabolite formation, 2) high correlations of DTZ N-demethylation activity to other CYP3A activities, 3) inhibition of DTZ N-demethylation activity by triacetyloleandomycin, and 4) DTZ N-demethylation activity by expressed CYP3A enzymes only.	Diltiazem	0-9	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	42-67
10454485-1	1999	Diltiazem (DTZ) N-demethylation occurs by cytochrome P-450 (CYP) 3A based on the following observations: 1) a single enzyme Michaelis-Menten model of metabolite formation, 2) high correlations of DTZ N-demethylation activity to other CYP3A activities, 3) inhibition of DTZ N-demethylation activity by triacetyloleandomycin, and 4) DTZ N-demethylation activity by expressed CYP3A enzymes only.	Diltiazem	0-9	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	234-239
10454485-1	1999	Diltiazem (DTZ) N-demethylation occurs by cytochrome P-450 (CYP) 3A based on the following observations: 1) a single enzyme Michaelis-Menten model of metabolite formation, 2) high correlations of DTZ N-demethylation activity to other CYP3A activities, 3) inhibition of DTZ N-demethylation activity by triacetyloleandomycin, and 4) DTZ N-demethylation activity by expressed CYP3A enzymes only.	Diltiazem	0-9	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	373-378
10454485-1	1999	Diltiazem (DTZ) N-demethylation occurs by cytochrome P-450 (CYP) 3A based on the following observations: 1) a single enzyme Michaelis-Menten model of metabolite formation, 2) high correlations of DTZ N-demethylation activity to other CYP3A activities, 3) inhibition of DTZ N-demethylation activity by triacetyloleandomycin, and 4) DTZ N-demethylation activity by expressed CYP3A enzymes only.	Diltiazem	11-14	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	42-67
10454485-1	1999	Diltiazem (DTZ) N-demethylation occurs by cytochrome P-450 (CYP) 3A based on the following observations: 1) a single enzyme Michaelis-Menten model of metabolite formation, 2) high correlations of DTZ N-demethylation activity to other CYP3A activities, 3) inhibition of DTZ N-demethylation activity by triacetyloleandomycin, and 4) DTZ N-demethylation activity by expressed CYP3A enzymes only.	Diltiazem	11-14	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	234-239
10454485-1	1999	Diltiazem (DTZ) N-demethylation occurs by cytochrome P-450 (CYP) 3A based on the following observations: 1) a single enzyme Michaelis-Menten model of metabolite formation, 2) high correlations of DTZ N-demethylation activity to other CYP3A activities, 3) inhibition of DTZ N-demethylation activity by triacetyloleandomycin, and 4) DTZ N-demethylation activity by expressed CYP3A enzymes only.	Diltiazem	11-14	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	373-378
10454485-3	1999	A 30-min preincubation of DTZ in expressed CYPs inhibited CYP3A4(+b(5)) by 100%, of which 55% was due to formation of a metabolite intermediate complex (MIC), which is an inactive form of CYP.	Diltiazem	26-29	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	58-64
10454485-5	1999	In experiments to assess simultaneous MIC formation and loss of CYP3A activity, DTZ caused greater than 80% inhibition of midazolam hydroxylation after a 60-min preincubation in human liver microsomes.	Diltiazem	80-83	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	64-69
10454485-7	1999	The mechanistic inhibition was characterized in expressed CYP3A4(+b(5)), which exhibited a concentration-dependent formation of MIC by DTZ (1-100 microM) with an estimated k(inact) of 0.17 min(-1) and K(I) of 2.2 microM.	Diltiazem	135-138	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	58-64
10454485-9	1999	This study showed that DTZ inhibition of CYP3A substrate metabolism occurs primarily by MIC formation.	Diltiazem	23-26	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	41-46
10454523-2	1999	In this study, we examined whether treatment with the calcium channel antagonists, nicardipine, nifedipine or diltiazem, alters cytochrome P-450 2B or 3A (CYP2B or CYP3A, respectively) expression in rat liver.	Diltiazem	110-119	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	164-169
10444449-7	1999	Pretreatment of rats with calcium channel antagonists (i.e., diltiazem, nifedipine, or verapamil) before LPS exposure attenuated the serum ALT level and iNOS mRNA expression in the liver.	Diltiazem	61-70	nitric oxide synthase 2	Rattus norvegicus	153-157
10475144-8	1999	RESULTS: DTZ decreased resting DBP from 84 +/- 13 to 79 +/- 10 mmHg (p > 0.05), and HR from 89 +/- 11 to 82 +/- 13 bpm (p < 0.05).	Diltiazem	9-12	D-box binding PAR bZIP transcription factor	Homo sapiens	31-34
10475144-10	1999	DTZ limited these increases to 21% for SBP, 5% for DBP, and 44% for HR (p < 0.05 for drug effect).	Diltiazem	0-3	selenium binding protein 1	Homo sapiens	39-42
10475144-10	1999	DTZ limited these increases to 21% for SBP, 5% for DBP, and 44% for HR (p < 0.05 for drug effect).	Diltiazem	0-3	D-box binding PAR bZIP transcription factor	Homo sapiens	51-54
10739111-5	2000	In other experiments carried out on endothelium-removed preparations and in medium containing the calcium antagonist, diltiazem (10(-5) and 10(-6) M), the contraction dose-response curves were significantly reduced and the same happened in the presence of the inhibitor of sarcoplasmic reticulum Ca-2+-ATPase, cyclopiazonic acid (CPA) (3 x 10(-6) M).	Diltiazem	118-127	carboxypeptidase A3	Rattus norvegicus	310-337
10410178-10	1999	Diltiazem inhibits CYP3A, P-glycoprotein, and tacrolimus metabolism in vitro.	Diltiazem	0-9	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	19-24
10410178-10	1999	Diltiazem inhibits CYP3A, P-glycoprotein, and tacrolimus metabolism in vitro.	Diltiazem	0-9	ATP binding cassette subfamily B member 1	Homo sapiens	26-40
10377955-1	1999	Ca antagonists of different classes (verapamil, nifedipine, nicardipinc, diltiazem) in a concentration of 10(-5) M and higher are known to suppress Ca2+ transport into the lymphocyte cytosol, changing a normal response of lymphocytes to mitogens and antigens and so inhibiting their proliferation, as well as IL-2-induced cell proliferation, and their receptor expression on the surface of lymphocytes without cell cytotoxicity.	Diltiazem	73-82	interleukin 2	Rattus norvegicus	309-313
10226093-2	1999	We investigated the underlying molecular mechanism responsible for IL-6 induction in response to the CCB amlodipine, diltiazem, and verapamil in primary human vascular smooth muscle cells (VSMC).	Diltiazem	117-126	interleukin 6	Homo sapiens	67-71
10404732-2	1999	A solid-phase extraction method (C18) is described for isolating diltiazem and the metabolites N-demethyl-diltiazem (M(A)), deacetyldiltiazem (M1) and N-demethyl-deacetyl-diltiazem (M2) from human plasma spiked with trans-diltiazem as internal standard.	Diltiazem	65-74	Bardet-Biedl syndrome 9	Homo sapiens	33-36
10363626-3	1999	RESULTS: Diltiazem and verapamil increased the expression of LDLr mRNA in a dose-dependent manner.	Diltiazem	9-18	low density lipoprotein receptor	Homo sapiens	61-65
10363626-6	1999	The LDLr promoter activity assay showed that treatment with 100 micromol/ of diltiazem and verapamil increased LDLr promoter activity by 126.72 +/- 10.68%, and 166.41 +/- 11.41%, respectively, at 24 hours (control as 100%), while treatment with 100 micromol/l of nifedipine had an inhibitory effect on LDLr promoter activity.	Diltiazem	77-86	low density lipoprotein receptor	Homo sapiens	4-8
10363626-6	1999	The LDLr promoter activity assay showed that treatment with 100 micromol/ of diltiazem and verapamil increased LDLr promoter activity by 126.72 +/- 10.68%, and 166.41 +/- 11.41%, respectively, at 24 hours (control as 100%), while treatment with 100 micromol/l of nifedipine had an inhibitory effect on LDLr promoter activity.	Diltiazem	77-86	low density lipoprotein receptor	Homo sapiens	111-115
10363626-6	1999	The LDLr promoter activity assay showed that treatment with 100 micromol/ of diltiazem and verapamil increased LDLr promoter activity by 126.72 +/- 10.68%, and 166.41 +/- 11.41%, respectively, at 24 hours (control as 100%), while treatment with 100 micromol/l of nifedipine had an inhibitory effect on LDLr promoter activity.	Diltiazem	77-86	low density lipoprotein receptor	Homo sapiens	111-115
10363626-10	1999	Signal transduction pathway experiments showed that the calmodulin transduction pathway was involved in LDLr upregulation induced by diltiazem or verapamil.	Diltiazem	133-142	low density lipoprotein receptor	Homo sapiens	104-108
10363626-12	1999	CONCLUSION: These studies show that diltiazem and verapamil increase LDLr gene transcription and expression which is independent of cell proliferation in HMCL.	Diltiazem	36-45	low density lipoprotein receptor	Homo sapiens	69-73
10217527-10	1999	Removal of Ca2+ by the addition of EGTA or application of Ca2+-channel blockers, verapamil, diltiazem, and Ni2+, inhibited the BK-induced IP accumulation and Ca2+ mobilization, indicating that Ca2+ influx was required for the BK-induced responses.	Diltiazem	92-101	kininogen 1	Canis lupus familiaris	127-129
9865510-3	1998	In the presence of diltiazem (10 microM), maximal contraction to vasopressin was reduced to a greater extent in male (65+/-2%) than in female aortae (38+/-1%).	Diltiazem	19-28	arginine vasopressin	Rattus norvegicus	65-76
10385214-12	1999	Diltiazem, erythromycin, nifedipine and cyclosporin (CYP 3A substrates) inhibited halofantrine metabolism.	Diltiazem	0-9	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	53-59
10396583-7	1999	After 6 months, patients treated with captopril and, to a lesser extent, those treated with diltiazem showed statistically significantly decreased steady state plasma glucose concentrations and increased insulin sensitivity index compared to basal values.	Diltiazem	92-101	insulin	Homo sapiens	204-211
10396583-9	1999	We conclude that captopril and, to a lesser extent, diltiazem improve insulin sensitivity in patients with stable coronary artery disease.	Diltiazem	52-61	insulin	Homo sapiens	70-77
9753624-4	1998	The effect of UCN (10(-7)M) was not only blunted by cAMP-dependent protein kinase A (PKA) inhibitor, H-89 (10(-5)M), but also diltiazem (10(-7)M), a voltage-dependent Ca2+ channel blocker.	Diltiazem	126-135	urocortin	Rattus norvegicus	14-17
9877310-6	1998	Diltiazem and the metabolites reduced both SBP and DBP, the effects of diltiazem being most potent.	Diltiazem	0-9	sex hormone-binding globulin	Oryctolagus cuniculus	43-46
9877310-6	1998	Diltiazem and the metabolites reduced both SBP and DBP, the effects of diltiazem being most potent.	Diltiazem	0-9	vitamin D-binding protein	Oryctolagus cuniculus	51-54
9777817-9	1998	RESULTS: Clonidine and diltiazem had consistent response rates regardless of renin profile (76%, 67%, and 80% for low, medium, and high renin, respectively, for clonidine and 83%, 82%, and 83%, respectively, for diltiazem for patients with baseline DBP of 95-99 mm Hg).	Diltiazem	23-32	renin	Homo sapiens	136-141
9787942-11	1998	These findings suggest that CsA induced acute vasoconstriction and renal hypoperfusion are mediated by ET-1 and that diltiazem treatment abolishes these pharmacodynamic effects of CsA despite persistent increase of plasma ET-1 levels.	Diltiazem	117-126	endothelin 1	Homo sapiens	222-226
9765513-1	1998	We examined the effects of the calcium channel blockers nitrendipine, diltiazem, verapamil, bepridil, and mibefradil on the cloned HERG and KvLQT1/IsK K+ channels.	Diltiazem	70-79	potassium voltage-gated channel subfamily H member 2	Homo sapiens	131-135
9765513-1	1998	We examined the effects of the calcium channel blockers nitrendipine, diltiazem, verapamil, bepridil, and mibefradil on the cloned HERG and KvLQT1/IsK K+ channels.	Diltiazem	70-79	potassium voltage-gated channel subfamily Q member 1	Homo sapiens	140-146
9765513-3	1998	When expressed in transfected COS cells, HERG is blocked in a concentration-dependent manner by bepridil (EC50 = 0.55 microM), verapamil (EC50 = 0.83 microM), and mibefradil (EC50 = 1.43 microM), whereas nitrendipine and diltiazem have negligible effects.	Diltiazem	221-230	potassium voltage-gated channel subfamily H member 2	Homo sapiens	41-45
9741502-4	1998	METHODS: In this pilot study, 59 patients with an AMI treated with tissue-type plasminogen activator (t-PA) were randomized, double blinded, to intravenous diltiazem or placebo for 48 h, followed by oral therapy for 4 weeks.	Diltiazem	156-165	plasminogen activator, tissue type	Homo sapiens	67-100
9741502-14	1998	CONCLUSIONS: A protective effect for clinical events related to early postinfarction ischemia and reinfarction was suggested in this study, with diltiazem administered intravenously with t-PA followed by oral therapy for 1 month, with no effect on coronary artery patency and left ventricular function and perfusion.	Diltiazem	145-154	plasminogen activator, tissue type	Homo sapiens	187-191
9782065-9	1998	Mg as well as diltiazem similarly affected the plasma ET-1 by reducing ET-1 release during the first hour of the reperfusion period.	Diltiazem	14-23	endothelin 1	Homo sapiens	54-58
9782065-9	1998	Mg as well as diltiazem similarly affected the plasma ET-1 by reducing ET-1 release during the first hour of the reperfusion period.	Diltiazem	14-23	endothelin 1	Homo sapiens	71-75
9782065-11	1998	Ability of Mg, diltiazem and leumedins to decrease the ET-1 plasma level may have direct clinical implications for the use of these agents in patients with coronary artery disease.	Diltiazem	15-24	endothelin 1	Homo sapiens	55-59
9544975-7	1998	Mg or diltiazem similarly affects the plasma Fn, reducing its release during the entire reperfusion period, and did not influence the plasma Fn in the absence of myocardial injury.	Diltiazem	6-15	fibronectin 1	Homo sapiens	45-47
9688645-10	1998	The L-type Ca2+ channel blocker diltiazem (10 microM) and the Ca2+ chelator EGTA (1 mM) significantly inhibited BB-stimulated secretin release by 64% and 59%, respectively, and inhibited PACAP-stimulated release by 75% and 55%, respectively.	Diltiazem	32-41	adenylate cyclase activating polypeptide 1	Rattus norvegicus	187-192
9765513-5	1998	Similarly, KvLQT1/IsK is inhibited by bepridil (EC50 = 10.0 microM) and mibefradil (EC50 = 11.8 microM), while being insensitive to nitrendipine, diltiazem, or verapamil.	Diltiazem	146-155	potassium voltage-gated channel subfamily Q member 1	Homo sapiens	11-17
9765513-5	1998	Similarly, KvLQT1/IsK is inhibited by bepridil (EC50 = 10.0 microM) and mibefradil (EC50 = 11.8 microM), while being insensitive to nitrendipine, diltiazem, or verapamil.	Diltiazem	146-155	potassium voltage-gated channel subfamily E regulatory subunit 1	Homo sapiens	18-21
9667821-5	1998	Previously we have demonstrated that the calcium channel blockers verapamil and diltiazem, as well as dantrolene, an agent that blocks the release of calcium from its cytoplasmic stores, inhibits tumor necrosis factor-a (TNF-alpha) and augments interleukin-10 (IL-10) plasma levels in endotoxemic BALB/c mice.	Diltiazem	80-89	tumor necrosis factor	Mus musculus	221-230
9663178-12	1998	CONCLUSIONS: Both verapamil and diltiazem considerably increase plasma buspirone concentrations, probably by inhibiting its CYP3A4-mediated first-pass metabolism.	Diltiazem	32-41	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	124-130
9625031-6	1998	RESULTS: An interesting effect on proinflammatory monokines was observed: in this study, we demonstrate that the calcium antagonist diltiazem enhances interleukin-1beta and slightly reduces interleukin-6 production in MLC, but it has no effect on tumor necrosis factor-alpha levels.	Diltiazem	132-141	interleukin 1 beta	Homo sapiens	151-168
9625031-6	1998	RESULTS: An interesting effect on proinflammatory monokines was observed: in this study, we demonstrate that the calcium antagonist diltiazem enhances interleukin-1beta and slightly reduces interleukin-6 production in MLC, but it has no effect on tumor necrosis factor-alpha levels.	Diltiazem	132-141	interleukin 6	Homo sapiens	190-203
9625031-6	1998	RESULTS: An interesting effect on proinflammatory monokines was observed: in this study, we demonstrate that the calcium antagonist diltiazem enhances interleukin-1beta and slightly reduces interleukin-6 production in MLC, but it has no effect on tumor necrosis factor-alpha levels.	Diltiazem	132-141	modulator of VRAC current 1	Homo sapiens	218-221
9625031-6	1998	RESULTS: An interesting effect on proinflammatory monokines was observed: in this study, we demonstrate that the calcium antagonist diltiazem enhances interleukin-1beta and slightly reduces interleukin-6 production in MLC, but it has no effect on tumor necrosis factor-alpha levels.	Diltiazem	132-141	tumor necrosis factor	Homo sapiens	247-274
9544975-10	1998	Ability of Mg, diltiazem, and leumedins to modulate plasma Fn level may have direct clinical implications for the use of these agents in patients with coronary artery disease.	Diltiazem	15-24	fibronectin 1	Homo sapiens	59-61
9531253-8	1998	In addition, inhibition of protein kinase C by staurosporine (10 nmol/L) and blockade of L-type Ca2+ channels by diltiazem (1 micromol/L) significantly decreased the sustained phase of ADM-induced increase in developed tension.	Diltiazem	113-122	adrenomedullin	Rattus norvegicus	185-188
9514900-3	1998	In both cardiac SLM and SR, the felodipine fluorescence was sensitive to conformational changes of the DHPR, as diltiazem that binds to DHPR at a separate site altered the values of both the Kd and the Hill coefficient characteristic for felodipine binding.	Diltiazem	112-121	calcium voltage-gated channel subunit alpha1 S	Homo sapiens	103-107
9514900-3	1998	In both cardiac SLM and SR, the felodipine fluorescence was sensitive to conformational changes of the DHPR, as diltiazem that binds to DHPR at a separate site altered the values of both the Kd and the Hill coefficient characteristic for felodipine binding.	Diltiazem	112-121	calcium voltage-gated channel subunit alpha1 S	Homo sapiens	136-140
9528676-3	1998	The cardioactive drugs verapamil, quinidine, diltiazem, nifedipine, and a series of digitalis analogs, interacted directly with Pgp as shown on ATPase in both systems.	Diltiazem	45-54	ATP binding cassette subfamily B member 1	Homo sapiens	128-131
9591927-4	1998	RESULT AND CONCLUSIONS: Diltiazem caused significant venodilation at a dose of 0.01 microg x min(-1) or more, while verapamil and nicardipine only caused this effect at 1 microg x min(-1) or more.	Diltiazem	24-33	CD59 molecule (CD59 blood group)	Homo sapiens	93-99
9591927-4	1998	RESULT AND CONCLUSIONS: Diltiazem caused significant venodilation at a dose of 0.01 microg x min(-1) or more, while verapamil and nicardipine only caused this effect at 1 microg x min(-1) or more.	Diltiazem	24-33	CD59 molecule (CD59 blood group)	Homo sapiens	180-186
9545159-3	1998	A possible drug interaction occurred in a 45-year-old woman who was taking cisapride for gastroesophageal reflux disorder and diltiazem, an agent that has inhibitory effect on CYP3A4, for hypertension.	Diltiazem	126-135	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	176-182
9528676-3	1998	The cardioactive drugs verapamil, quinidine, diltiazem, nifedipine, and a series of digitalis analogs, interacted directly with Pgp as shown on ATPase in both systems.	Diltiazem	45-54	dynein axonemal heavy chain 8	Homo sapiens	144-150
10366993-10	1998	Both phenobarbital and DTZ decreased SBP and DBP significantly without affecting the HR.	Diltiazem	23-26	sex hormone-binding globulin	Oryctolagus cuniculus	37-40
9405282-10	1998	Inhibition of Type-I and -IV Ca2+ influxes by their respective inhibitors, diltiazem and nifedipine, resulted in abolition of phospholipase A2 activation induced by the respective receptor agonists, in agreement with the notion that Ca2+ influx via these routes is responsible for receptor-mediated phospholipase A2 activation.	Diltiazem	75-84	phospholipase A2 group IB	Homo sapiens	126-142
9405282-10	1998	Inhibition of Type-I and -IV Ca2+ influxes by their respective inhibitors, diltiazem and nifedipine, resulted in abolition of phospholipase A2 activation induced by the respective receptor agonists, in agreement with the notion that Ca2+ influx via these routes is responsible for receptor-mediated phospholipase A2 activation.	Diltiazem	75-84	phospholipase A2 group IB	Homo sapiens	299-315
10366993-10	1998	Both phenobarbital and DTZ decreased SBP and DBP significantly without affecting the HR.	Diltiazem	23-26	vitamin D-binding protein	Oryctolagus cuniculus	45-48
9431849-7	1997	Administrations of 10(-6) mol/l diltiazem and 10(-7) mol/l nitrendipine decreased Ang II-elicited [Ca2+]i responses and normalized basal [Ca2+]i in SHR cells.	Diltiazem	32-41	angiogenin	Rattus norvegicus	82-85
9816701-7	1998	The treatment of burn-injured rats with the calcium antagonist diltiazem abrogated enhanced Ca2+ and protein kinase C signaling and superoxide generation.	Diltiazem	63-72	carbonic anhydrase 2	Rattus norvegicus	92-95
9437739-6	1998	Both nifedipine (1-50 microM) and diltiazem (1-50 microM) inhibited substance P-evoked Ca2+ responses in a dose-dependent manner.	Diltiazem	34-43	tachykinin precursor 1	Homo sapiens	68-79
9370178-6	1997	Diltiazem reduced the dose of CsA required to maintain target blood levels (479 +/- 189 mg/d v 576 +/- 178 mg/d at 14 days; P = 0.015).	Diltiazem	0-9	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	30-33
9481610-6	1997	L-CHANNEL CALCIUM ANTAGONISTS: Depending on their pharmacodynamic characteristics, L-channel calcium antagonists of the dihydropyridine, verapamil or diltiazem type reflexly activate the sympathetic nervous system and blunt beta-adrenoceptor-mediated calcium influx, thus eliciting negative inotropy and activation of the renin-angiotensin system.	Diltiazem	150-159	renin	Homo sapiens	322-327
9223567-7	1997	CYP3A4 in lymphoblastoid cell microsomes catalyzed DTZ N-demethylation but CYP2C8 and CYP2C9 were also active (approximately 20% and 10% of the activity supported by CYP3A4); seven other CYPs produced little or no N-desmethyl DTZ from DTZ.	Diltiazem	51-54	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	0-6
9352390-16	1997	This model is additionally supported by the finding that the shape of the hysteresis is dependent on the absorption rate of diltiazem, calculated as mean input time according to MIT = MRT - 1/lambda z.	Diltiazem	124-133	sorting nexin 27	Homo sapiens	184-191
9282941-8	1997	Inhibitors of L-type VDCCs (diltiazem, nifedipine, and verapamil), but not N- or P- or Q-type VDCCs, resulted in a decrease in AChE expression.	Diltiazem	28-37	acetylcholinesterase (Cartwright blood group)	Homo sapiens	127-131
15739506-2	1997	Diltiazem and diazepam (internal standard) in serum were extracted with hexane-chloroform-isopropanol (60:40:5, V/V), and then measured by HPLC using a Spherisorb C18 column as stationary phase and a methanol-water triethylamine as mobile phase.	Diltiazem	0-9	Bardet-Biedl syndrome 9	Homo sapiens	163-166
9292328-8	1997	Diltiazem infusion resulted in diminished ET-1 (34.5%), fibronectin (23.2%), and TxB2 (35.6%); and elevated Protein C (29.3%) when compared with controls.	Diltiazem	0-9	endothelin-1	Sus scrofa	42-46
9211801-7	1997	Furthermore, blocking Ca2+ influx by using the Ca2+ channel blocker diltiazem (10 nM), or a Ca2+-depleted medium prevented the suppression of stretch-induced ANP secretion by glibenclamide.	Diltiazem	68-77	natriuretic peptide A	Rattus norvegicus	158-161
9223567-8	1997	The CYP3A4 inhibitors ketoconazole and troleandomycin decreased microsomal DTZ oxidation, but inhibitors or substrates of CYP2C, CYP2D and CYP2E1 produced no inhibition.	Diltiazem	75-78	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	4-10
9223567-10	1997	In further experiments, the capacities of DTZ and three metabolites to modulate human CYP 1A2, 2E1, 2C9 and 3A4 activities were evaluated in vitro.	Diltiazem	42-45	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	86-93
9223567-11	1997	DTZ and its N-desmethyl and N,N-didesmethyl metabolites selectively inhibited CYP3A4 activity, whereas O-desmethyl DTZ was not inhibitory.	Diltiazem	0-3	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	78-84
9223567-12	1997	The IC50 value of DTZ against CYP3A4-mediated testosterone 6beta-hydroxylation (substrate concentration, 50 microM) was 120 microM.	Diltiazem	18-21	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	30-36
9223567-15	1997	CYP3A4 inhibition was enhanced when DTZ and N-desmethyl DTZ underwent biotransformation in NADPH-supplemented hepatic microsomes in vitro, supporting the contention that inhibitory metabolites may be generated in situ.	Diltiazem	36-39	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	0-6
9223567-16	1997	These findings suggest that N-demethylated metabolites of DTZ may contribute to CYP3A4 inhibition in vivo, especially under conditions in which N-desmethyl DTZ accumulates, such as during prolonged DTZ therapy.	Diltiazem	58-61	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	80-86
9223567-16	1997	These findings suggest that N-demethylated metabolites of DTZ may contribute to CYP3A4 inhibition in vivo, especially under conditions in which N-desmethyl DTZ accumulates, such as during prolonged DTZ therapy.	Diltiazem	156-159	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	80-86
9223891-3	1997	The prophylactic intravenous diltiazem infusion (1.0 micrograms.kg-1.min-1) was started immediately after induction of general anesthesia or epidural analgesia and continued until the end of operation.	Diltiazem	29-38	CD59 molecule (CD59 blood group)	Homo sapiens	69-74
9145926-6	1997	To explore the molecular basis for the sharp distinction in state-dependent inhibition by diltiazem, we constructed chimeric channels from alpha1C and alpha1A and localized the structural determinants for state dependence to repeats III and IV of alpha1C, which have been found to contain the structures required for benzothiazepine binding.	Diltiazem	90-99	calcium voltage-gated channel subunit alpha1 A	Homo sapiens	151-158
9185464-3	1997	In the diltiazem group continuous intravenous infusion of diltiazem (1-3mcg.kg-1.min-1) was started when the patient"s heart rate remained over 110.min-1 without any predisposing factor.	Diltiazem	58-67	CD59 molecule (CD59 blood group)	Homo sapiens	81-86
9185464-3	1997	In the diltiazem group continuous intravenous infusion of diltiazem (1-3mcg.kg-1.min-1) was started when the patient"s heart rate remained over 110.min-1 without any predisposing factor.	Diltiazem	58-67	CD59 molecule (CD59 blood group)	Homo sapiens	148-153
9299207-6	1997	Diltiazem and nifedipine blocked the amphetamine induced facilitation of FSA, while verapamil blocked both amphetamine as well as physostigmine induced facilitation of FSA.	Diltiazem	0-9	RIKEN cDNA 4932438A13 gene	Mus musculus	73-76
8968370-0	1996	Enhanced inhibition of microsomal cytochrome P450 3A2 in rat liver during diltiazem biotransformation.	Diltiazem	74-83	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	34-53
9146848-11	1997	Inhibition of CYP3A isozyme by diltiazem may explain the observed pharmacokinetic interaction.	Diltiazem	31-40	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	14-19
9110418-2	1997	Here we investigated the effects of verapamil and diltiazem, two calcium entry blockers, on endotoxin (bacterial lipopolysaccharide, LPS)-induced production of pro- and anti-inflammatory cytokines and of nitric oxide in mice.	Diltiazem	50-59	toll-like receptor 4	Mus musculus	133-136
9110418-3	1997	LPS-induced interleukin-10 plasma levels were significantly enhanced, and circulating tumor necrosis factor-alpha concentrations were significantly suppressed in animals pretreated intraperitoneally with verapamil (10 mg/kg) or diltiazem (20 mg/kg).	Diltiazem	228-237	toll-like receptor 4	Mus musculus	0-3
9110418-3	1997	LPS-induced interleukin-10 plasma levels were significantly enhanced, and circulating tumor necrosis factor-alpha concentrations were significantly suppressed in animals pretreated intraperitoneally with verapamil (10 mg/kg) or diltiazem (20 mg/kg).	Diltiazem	228-237	interleukin 10	Mus musculus	12-26
9110418-3	1997	LPS-induced interleukin-10 plasma levels were significantly enhanced, and circulating tumor necrosis factor-alpha concentrations were significantly suppressed in animals pretreated intraperitoneally with verapamil (10 mg/kg) or diltiazem (20 mg/kg).	Diltiazem	228-237	tumor necrosis factor	Mus musculus	86-113
9232324-5	1997	Nifedipine, isradipine, diltiazem, and verapamil dose-dependently inhibited the basic fibroblast growth factor (bFGF)-induced [3H]thymidine incorporation.	Diltiazem	24-33	fibroblast growth factor 2	Homo sapiens	80-110
9232324-5	1997	Nifedipine, isradipine, diltiazem, and verapamil dose-dependently inhibited the basic fibroblast growth factor (bFGF)-induced [3H]thymidine incorporation.	Diltiazem	24-33	fibroblast growth factor 2	Homo sapiens	112-116
9232324-6	1997	Fifty micromolars of nifedipine, isradipine, diltiazem, and verapamil completely inhibited bFGF-induced proliferation of HUAEC.	Diltiazem	45-54	fibroblast growth factor 2	Homo sapiens	91-95
9096261-4	1997	Ca2+ channel blockers affected the endothelin-1 induced response in different ways: diltiazem and nifedipine partially blocked the endothelin-1 induced response, whereas verapamil did not influence this endothelin-1 induced effect.	Diltiazem	84-93	endothelin 1	Rattus norvegicus	35-47
9096261-4	1997	Ca2+ channel blockers affected the endothelin-1 induced response in different ways: diltiazem and nifedipine partially blocked the endothelin-1 induced response, whereas verapamil did not influence this endothelin-1 induced effect.	Diltiazem	84-93	endothelin 1	Rattus norvegicus	131-143
9096261-4	1997	Ca2+ channel blockers affected the endothelin-1 induced response in different ways: diltiazem and nifedipine partially blocked the endothelin-1 induced response, whereas verapamil did not influence this endothelin-1 induced effect.	Diltiazem	84-93	endothelin 1	Rattus norvegicus	131-143
8978594-8	1997	Calcium channel blockers, verapamil and diltiazem, could alleviate both the TNF-mediated 45Ca2+-uptake and killing activity.	Diltiazem	40-49	tumor necrosis factor	Mus musculus	76-79
9223567-0	1997	Role of CYP3A4 in human hepatic diltiazem N-demethylation: inhibition of CYP3A4 activity by oxidized diltiazem metabolites.	Diltiazem	32-41	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	8-14
9223567-0	1997	Role of CYP3A4 in human hepatic diltiazem N-demethylation: inhibition of CYP3A4 activity by oxidized diltiazem metabolites.	Diltiazem	101-110	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	73-79
9223567-1	1997	The antihypertensive agent diltiazem (DTZ) impairs hepatic drug metabolism by inhibition of cytochrome P450 (CYP).	Diltiazem	27-36	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	92-107
9223567-1	1997	The antihypertensive agent diltiazem (DTZ) impairs hepatic drug metabolism by inhibition of cytochrome P450 (CYP).	Diltiazem	27-36	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	109-112
9223567-1	1997	The antihypertensive agent diltiazem (DTZ) impairs hepatic drug metabolism by inhibition of cytochrome P450 (CYP).	Diltiazem	38-41	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	92-107
9223567-1	1997	The antihypertensive agent diltiazem (DTZ) impairs hepatic drug metabolism by inhibition of cytochrome P450 (CYP).	Diltiazem	38-41	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	109-112
9223567-3	1997	Thus, DTZ metabolites may contribute to CYP inhibition.	Diltiazem	6-9	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	40-43
9223567-4	1997	This study assessed the role of human CYPs in microsomal DTZ oxidation and the capacity of DTZ metabolites to inhibit specific CYP activities.	Diltiazem	57-60	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	38-41
9223567-6	1997	DTZ oxidation was correlated with testosterone 6beta-hydroxylation (r = 0.82) and, to a lesser extent, tolbutamide hydroxylation (r = 0.59) but not with activities mediated by CYP1A2 or CYP2E1.	Diltiazem	0-3	cytochrome P450 family 2 subfamily E member 1	Homo sapiens	186-192
9030825-9	1997	Twelve weeks" treatment with diltiazem led to a slight but significant increase in phi1; however, neither diltiazem nor quinapril had significant effects on S(I) or S(G).	Diltiazem	29-38	protein phosphatase 1 regulatory inhibitor subunit 14B	Homo sapiens	83-87
9030825-12	1997	However, treatment with diltiazem led to a significant increase in beta-cell sensitivity to glucose; this is of particular interest, given the importance of phi1 for peripheral glucose uptake.	Diltiazem	24-33	protein phosphatase 1 regulatory inhibitor subunit 14B	Homo sapiens	157-161
9049653-9	1997	The increase in cytosolic Ca2+ concentration occurred via the influx of extracellular Ca2+ independent of L-type Ca2+ channels blocked by verapamil or diltiazem.	Diltiazem	151-160	carbonic anhydrase 2	Homo sapiens	26-29
8968370-4	1996	The principal finding to emerge was that the N-demethylated metabolite of DTZ was a more potent competitive inhibitor than DTZ of CYP3A2-dependent testosterone 6 beta-hydroxylation.	Diltiazem	74-77	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	130-136
8968370-4	1996	The principal finding to emerge was that the N-demethylated metabolite of DTZ was a more potent competitive inhibitor than DTZ of CYP3A2-dependent testosterone 6 beta-hydroxylation.	Diltiazem	123-126	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	130-136
9014219-4	1996	Pretreatment of aortic rings with different doses (10(-9) M and 10(-6) M) of diltiazem (voltage-sensitive L-type calcium channel blocker) produced significant inhibition of ET-1- and PDBu-induced contractions and PGI2 release.	Diltiazem	77-86	endothelin 1	Rattus norvegicus	173-177
8920958-4	1996	The maximal IL-6-induced increase in IGFBP-1 was comparable to that observed with dexamethasone, and this increase was attenuated by diltiazem or dantrolene, both of which are known to reduce the cytosolic Ca2+ concentration.	Diltiazem	133-142	interleukin 6	Homo sapiens	12-16
9772618-1	1996	Comparative study on effect of refined Xuefu capsule, Xuefu Zhuyu capsule and diltiazem on mRNA expression of nitric oxide synthase (NOS) and release of LDH-L, CK, GOT of hypoxic hypoglycemic cultured myocytes were studied by using the serum pharmacological method, reverse transcriptase-polymerase chain reaction (RT-PCR) and Northen blotting.	Diltiazem	78-87	nitric oxide synthase 2	Homo sapiens	110-131
8783330-2	1996	Recent suggestions that calcium (Ca2+) acts as a signal not only for TNF alpha release but also for TNF alpha action at distant sites led us to hypothesize that the calcium channel blocker diltiazem could inhibit TNF alpha release in acute pancreatitis, ameliorating the severity of the disease and improving overall survival.	Diltiazem	189-198	tumor necrosis factor	Rattus norvegicus	69-78
8783330-2	1996	Recent suggestions that calcium (Ca2+) acts as a signal not only for TNF alpha release but also for TNF alpha action at distant sites led us to hypothesize that the calcium channel blocker diltiazem could inhibit TNF alpha release in acute pancreatitis, ameliorating the severity of the disease and improving overall survival.	Diltiazem	189-198	tumor necrosis factor	Rattus norvegicus	100-109
8783330-2	1996	Recent suggestions that calcium (Ca2+) acts as a signal not only for TNF alpha release but also for TNF alpha action at distant sites led us to hypothesize that the calcium channel blocker diltiazem could inhibit TNF alpha release in acute pancreatitis, ameliorating the severity of the disease and improving overall survival.	Diltiazem	189-198	tumor necrosis factor	Rattus norvegicus	100-109
8863516-4	1996	In contrast, lactate dehydrogenase (LDH) release and trypan blue exclusion, which are indices of cell death, start 3 days after exposure to high concentrations of A beta and are blocked by Ca2+ channel blockers such as Co2+, nicardipine, and diltiazem.	Diltiazem	242-251	amyloid beta precursor protein	Homo sapiens	163-169
8898087-5	1996	The galectin-3-induced effect is insensitive to voltage-gated Ca2+ channel antagonists such as prenylamine, nifedipine and diltiazem and to pertussis toxin but is inhibited by cholera toxin.	Diltiazem	123-132	galectin 3	Homo sapiens	4-14
8958561-6	1996	Compared to controls, Mg and diltiazem infusion diminished endothelin 1 (32.9 vs. 34.5%) and fibronectin.	Diltiazem	29-38	endothelin-1	Sus scrofa	59-71
8843778-11	1996	The synergistic effect of bombesin with PACAP was abolished by diltiazem and BAPTA-AM but not by downregulation of protein kinase C, whereas KCl remained synergistic with PACAP after these treatments.	Diltiazem	63-72	adenylate cyclase activating polypeptide 1	Mus musculus	40-45
8899153-13	1996	Mg and diltiazem therapy was associated with the slight elevation of plasma AT-III.	Diltiazem	7-16	serpin family C member 1	Sus scrofa	76-82
8752192-5	1996	Diltiazem induced a systemic vasodilation (cardiac index: 3.4 +/- 1.0 to 4.0 +/- 1.0 L x min(-1) x m(-2), p = 0.003; aortic systolic pressure: 116 +/- 16 to 107 +/- 19 mm Hg, p = 0.007; systemic resistance index: 676 +/- 235 to 532 +/- 193 dynes x s x cm(-5) x m(-2), p = 0.006), not associated with changes in the LV outflow tract gradient.	Diltiazem	0-9	CD59 molecule (CD59 blood group)	Homo sapiens	89-95
8759071-4	1996	METHODS AND RESULTS: Both endothelin antagonists and diltiazem applied intradermally induced vasodilation in CAD patients, which was more pronounced with the ETA/ETB antagonist than with the ETA antagonist or diltiazem.	Diltiazem	53-62	endothelin receptor type A	Homo sapiens	158-161
8759071-4	1996	METHODS AND RESULTS: Both endothelin antagonists and diltiazem applied intradermally induced vasodilation in CAD patients, which was more pronounced with the ETA/ETB antagonist than with the ETA antagonist or diltiazem.	Diltiazem	53-62	endothelin receptor type B	Homo sapiens	162-165
8759071-4	1996	METHODS AND RESULTS: Both endothelin antagonists and diltiazem applied intradermally induced vasodilation in CAD patients, which was more pronounced with the ETA/ETB antagonist than with the ETA antagonist or diltiazem.	Diltiazem	53-62	endothelin receptor type A	Homo sapiens	191-194
8869861-9	1996	Separate analyses for nifedipine (RR 1.00; 95% CI 0.68-1.48), and diltiazem (RR 1.55; 95% CI 1.04-2.32) showed an increased risk of death associated with the latter.	Diltiazem	66-75	ribonucleotide reductase catalytic subunit M1	Homo sapiens	77-81
9772618-1	1996	Comparative study on effect of refined Xuefu capsule, Xuefu Zhuyu capsule and diltiazem on mRNA expression of nitric oxide synthase (NOS) and release of LDH-L, CK, GOT of hypoxic hypoglycemic cultured myocytes were studied by using the serum pharmacological method, reverse transcriptase-polymerase chain reaction (RT-PCR) and Northen blotting.	Diltiazem	78-87	lactate dehydrogenase A like 6B	Homo sapiens	153-158
9772618-2	1996	It was shown that the three drugs can reduce release of LDH-L,CK,GOT of myocytes (P < 0.01), the effect of refined Xuefu capsule and diltiazem were obvious than that of Xuefu Zhuyu capsule in reducing LDH-L release and NOS mRNA expression (P < 0.01), and effect of refined Xuefu capsule was the strongest (P < 0.01).	Diltiazem	136-145	lactate dehydrogenase A like 6B	Homo sapiens	204-209
8796364-3	1996	Similarly, chemotaxis towards 10(-7) M FMLP and phagocytosis were significantly lower in patients receiving nifedipine compared with controls and were only slightly reduced in patients receiving diltiazem or verapamil.	Diltiazem	195-204	formyl peptide receptor 1	Homo sapiens	39-43
8740208-2	1996	The possibility that attenuation of nociceptive messages from the cornea by diltiazem reduced Fos-like immunoreactivity of spinal trigeminal neurons was also examined.	Diltiazem	76-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-97
8632425-8	1996	Given the acetylation at C-3 in diltiazem, the 3-monoacetate (8) and diacetate (3) derivatives of 2 were prepared.	Diltiazem	32-41	complement C3	Homo sapiens	25-28
8770786-2	1995	Left guinea pig atria exposed to diltiazem become desensitised to neurotensin.	Diltiazem	33-42	neurotensin/neuromedin N	Cavia porcellus	66-77
8762016-8	1996	The additional application of diltiazem reduced NAG excretion and histological damage without affecting creatinine clearance.	Diltiazem	30-39	O-GlcNAcase	Rattus norvegicus	48-51
8779971-7	1996	To evaluate whether this increase in [Ca2+]i was due to release of Ca2+ or influx of Ca2+, cells were treated with the L-type calcium channel blocker, diltiazem, which inhibited isoproterenol-stimulated CCK secretion.	Diltiazem	151-160	cholecystokinin	Homo sapiens	203-206
8838433-12	1996	Diltiazem (n = 14) lowered day systolic blood pressure by 13 +/- 2 mmHg, diastolic blood pressure by 11 +/- 2 mmHg and heart rate by 10 +/- 2 beats min-1.	Diltiazem	0-9	CD59 molecule (CD59 blood group)	Homo sapiens	148-153
8866640-4	1996	RESULTS: The average plasma concentration of nortriptyline at steady state (Css) divided by the amount of nortriptyline administered per time rose significantly in a patient with concomitant administration of diltiazem, suggesting increased bioavailability and/or decreased clearance of nortriptyline.	Diltiazem	209-218	cytidine monophosphate N-acetylneuraminic acid synthetase	Homo sapiens	76-79
8699220-4	1996	Diltiazem at doses of 5, 20, and 40 micrograms/kg/min also increased tumor rCBF in a dose-dependent manner (27.9 +/- 12.5%, p < 0.001, 52.0 +/- 21.8%, p-AN 0.001 and 54.5 +/- 18.4%, p < 0.001, respectively).	Diltiazem	0-9	CCAAT/enhancer binding protein zeta	Rattus norvegicus	75-79
8649655-6	1996	There was a trend for intact PTH to be higher on diltiazem (324 +/- 47 pg/ml) than on felodipine (246 +/- 55) or in control condition (305 +/- 49) and 1,25-dihydroxyvitamin D was higher indeed on diltiazem (6.70 +/- 0.92 pg/ml) than on felodipine (4.75 +/- 0.91, P < 0.02) or control (3.87 +/- 0.62, P < 0.05).	Diltiazem	49-58	parathyroid hormone	Homo sapiens	29-32
8649655-6	1996	There was a trend for intact PTH to be higher on diltiazem (324 +/- 47 pg/ml) than on felodipine (246 +/- 55) or in control condition (305 +/- 49) and 1,25-dihydroxyvitamin D was higher indeed on diltiazem (6.70 +/- 0.92 pg/ml) than on felodipine (4.75 +/- 0.91, P < 0.02) or control (3.87 +/- 0.62, P < 0.05).	Diltiazem	196-205	parathyroid hormone	Homo sapiens	29-32
8649655-7	1996	Area under the curve PTH over the first 60 min of dialysis was higher by 16 +/- 7% on diltiazem than on felodipine (P < 0.05).	Diltiazem	86-95	parathyroid hormone	Homo sapiens	21-24
7488286-2	1995	METHODS: Diltiazem, 240-480 mg/day, was given to 4 patients with idiopathic or CREST-related (calcinosis, Raynaud"s phenomenon, esophageal dysmotility, sclerodactyly, telangiectasias) calcinosis for 1-12 years.	Diltiazem	9-18	SS18L1 subunit of BAF chromatin remodeling complex	Homo sapiens	79-84
9346617-6	1995	Diltiazem appears to be well tolerated in children and allows for substantial dose reductions of CSA without apparent effects on liver graft function.	Diltiazem	0-9	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	97-100
7840211-3	1995	L-Phenylalanine-induced secretion of CCK was inhibited by the calcium channel blocker diltiazem (10 microM).	Diltiazem	86-95	cholecystokinin	Homo sapiens	37-40
7655416-6	1995	The contraction in response to NPY per se or in 20 mM K+ was effectively attenuated by Ca2+ antagonists such as d-cis-diltiazem, and in a Ca(2+)-free medium.	Diltiazem	112-127	neuropeptide Y	Canis lupus familiaris	31-34
7615340-4	1995	The Ca2+ channel antagonists nifedipine and diltiazem attenuated the increase in GFAP immunoreactivity.	Diltiazem	44-53	glial fibrillary acidic protein	Rattus norvegicus	81-85
7781712-3	1995	Ca2+ channel antagonists such as d-cis-diltiazem (10 mM) abolished both [Ca2+]cyt and tension augmented by neuropeptide Y.	Diltiazem	33-48	neuropeptide Y	Canis lupus familiaris	107-121
8523457-7	1995	Verapamil (< or = 1 microM) and diltiazem (< or = 1 microM) inhibited the contractile responses to secretin (20 nM) and VIP (20 nM) significantly, and in a concentration-dependent manner, but did not inhibit the contractile response to CGRP.	Diltiazem	35-44	vasoactive intestinal peptide	Homo sapiens	126-129
8523457-7	1995	Verapamil (< or = 1 microM) and diltiazem (< or = 1 microM) inhibited the contractile responses to secretin (20 nM) and VIP (20 nM) significantly, and in a concentration-dependent manner, but did not inhibit the contractile response to CGRP.	Diltiazem	35-44	calcitonin related polypeptide alpha	Homo sapiens	242-246
7750316-7	1995	However, plasma renin activity and aldosterone levels were significantly higher in the diltiazem-treated group with the same changes in plasma atrial natriuretic peptide levels.	Diltiazem	87-96	renin	Homo sapiens	16-21
7776513-6	1995	Diltiazem infusion of 4 mcg.kg-1.min-1 decreased the vecuronium infusion rate by 45% compared with 2 other groups.	Diltiazem	0-9	CD59 molecule (CD59 blood group)	Homo sapiens	33-38
7776513-7	1995	Plasma diltiazem concentrations in patients receiving 4 mcg.kg-1.min-1 were significantly higher than those receiving 2 mcg.kg-1.min-1.	Diltiazem	7-16	CD59 molecule (CD59 blood group)	Homo sapiens	65-70
7776513-8	1995	In conclusion diltiazem 4 mcg.kg-1.min-1 potentiates the neuromuscular blockade of vecuronium and it relates with the plasma diltiazem concentration.	Diltiazem	14-23	CD59 molecule (CD59 blood group)	Homo sapiens	35-40
7776513-8	1995	In conclusion diltiazem 4 mcg.kg-1.min-1 potentiates the neuromuscular blockade of vecuronium and it relates with the plasma diltiazem concentration.	Diltiazem	125-134	CD59 molecule (CD59 blood group)	Homo sapiens	35-40
7776852-3	1995	Overall beneficial effects on mortality, liver necrosis score, and plasma alanine aminotransferase (ALT) activity were found in diltiazem-treated mice 24 h after acetaminophen overdose.	Diltiazem	128-137	glutamic pyruvic transaminase, soluble	Mus musculus	74-98
7776852-3	1995	Overall beneficial effects on mortality, liver necrosis score, and plasma alanine aminotransferase (ALT) activity were found in diltiazem-treated mice 24 h after acetaminophen overdose.	Diltiazem	128-137	glutamic pyruvic transaminase, soluble	Mus musculus	100-103
8001364-12	1995	CONCLUSIONS: The observation that quinacrine and preshock diltiazem limited the extent of shock-induced mucosal injury and bacterial translocation indicate that calcium and phospholipase A2 are involved in the pathogenesis of shock-induced mucosal injury and bacterial translocation.	Diltiazem	58-67	phospholipase A2 group IB	Rattus norvegicus	173-189
11850643-5	1995	A 1- and 3-hour lag time in diltiazem absorption was noted following the administration of Dilacor XR and Cardizem CD, respectively.	Diltiazem	28-37	BCL2 related protein A1	Homo sapiens	0-3
11850643-5	1995	A 1- and 3-hour lag time in diltiazem absorption was noted following the administration of Dilacor XR and Cardizem CD, respectively.	Diltiazem	91-101	BCL2 related protein A1	Homo sapiens	0-3
11850643-5	1995	A 1- and 3-hour lag time in diltiazem absorption was noted following the administration of Dilacor XR and Cardizem CD, respectively.	Diltiazem	106-117	BCL2 related protein A1	Homo sapiens	0-3
7712014-15	1995	The biphasic increases in [Ca2+]i and tension induced by 10-5 M ET-3 and by 1O-7M ET-1 were significantly inhibited by pretreatment with 10-5 M of the Ca2+ entry blocker, diltiazem, although the inhibition of the first component of ET-l-induced [Ca2+]i increase was partial.5.	Diltiazem	171-180	endothelin 3	Homo sapiens	64-68
7712014-15	1995	The biphasic increases in [Ca2+]i and tension induced by 10-5 M ET-3 and by 1O-7M ET-1 were significantly inhibited by pretreatment with 10-5 M of the Ca2+ entry blocker, diltiazem, although the inhibition of the first component of ET-l-induced [Ca2+]i increase was partial.5.	Diltiazem	171-180	endothelin 1	Homo sapiens	82-86
7962276-2	1994	The present study was conducted to determine whether 1) the nondihydropyridine calcium channel blocker diltiazem also reduces circulating insulin levels in humans, and 2) a reduction in circulating insulin with a calcium channel blocker is associated with a rise in serum DHEA-S concentrations in women as well as men.	Diltiazem	103-112	insulin	Homo sapiens	138-145
7742265-0	1994	Diltiazem inhibits DNA synthesis and Ca2+ uptake induced by insulin, IGF-I, and PDGF in vascular smooth muscle cells.	Diltiazem	0-9	insulin-like growth factor 1	Rattus norvegicus	69-74
7742265-4	1994	In this study we have evaluated the effects of diltiazem, a 1,5-benzothiazepine-derived Ca2+ channel blocker, on [3H]thymidine incorporation into DNA stimulated by insulin, insulinlike growth factor I (IGF-I), or PDGF in cultured VSMC from rat aorta.	Diltiazem	47-56	insulin-like growth factor 1	Rattus norvegicus	173-200
7742265-4	1994	In this study we have evaluated the effects of diltiazem, a 1,5-benzothiazepine-derived Ca2+ channel blocker, on [3H]thymidine incorporation into DNA stimulated by insulin, insulinlike growth factor I (IGF-I), or PDGF in cultured VSMC from rat aorta.	Diltiazem	47-56	insulin-like growth factor 1	Rattus norvegicus	202-207
7962102-15	1994	LN-induced neurite growth, like that induced by N-cadherin, is insensitive to diltiazem and conotoxin, but is highly sensitive to Ni2+ inhibition.	Diltiazem	78-87	laminin, beta 2 (laminin S)	Gallus gallus	0-2
7943324-5	1994	Glucose-mediated release of CCK, as well as the increase in cytosolic calcium, was inhibited by the calcium channel blocker diltiazem (10 microM).	Diltiazem	124-133	cholecystokinin	Homo sapiens	28-31
7962276-2	1994	The present study was conducted to determine whether 1) the nondihydropyridine calcium channel blocker diltiazem also reduces circulating insulin levels in humans, and 2) a reduction in circulating insulin with a calcium channel blocker is associated with a rise in serum DHEA-S concentrations in women as well as men.	Diltiazem	103-112	insulin	Homo sapiens	198-205
7962276-5	1994	Diltiazem treatment was associated with reductions in fasting serum insulin levels in both the men (from 91 +/- 14 to 56 +/- 12 pmol/L; P < 0.03) and women (from 92 +/- 20 to 48 +/- 9 pmol/L; P = 0.05).	Diltiazem	0-9	insulin	Homo sapiens	68-75
7982265-7	1994	Ca2+ influx was required for the changes in [Ca2+]i, since Ca(2+)-channel blockers, diltiazem, verapamil, and Ni2+, decreased both the initial and sustained elevation of [Ca2+]i in response to BDK.	Diltiazem	84-93	kininogen 1	Canis lupus familiaris	193-196
7952059-6	1994	The limits of quantitation (LOQ) are 2.5 and 2 ng ml-1 for diltiazem and the metabolites in human plasma, respectively.	Diltiazem	59-68	interleukin 17F	Homo sapiens	50-54
7952059-7	1994	Linearity between concentrations and detector response for diltiazem and metabolites ranged from 10-200 and 5-100 ng ml-1 in human plasma, respectively.	Diltiazem	59-68	interleukin 17F	Homo sapiens	117-121
7939378-4	1994	Treatment with diltiazem induced a non-significant reduction in heart rate with 3 beats min-1 and decreased blood pressure (-11/-9 mm Hg, p < 0.001).	Diltiazem	15-24	CD59 molecule (CD59 blood group)	Homo sapiens	88-93
7516710-6	1994	Ca2+ efflux was induced by Na+, Li+ and K+ through a diltiazem-insensitive reaction.	Diltiazem	53-62	carbonic anhydrase 2	Homo sapiens	0-3
7801783-6	1994	Diltiazem prevented partially from reduction of ventricular fibrillation threshold, eliminated completely the vasopressor response and limited the extension of myocardial necrosis induced by endothelin-1.	Diltiazem	0-9	endothelin 1	Rattus norvegicus	191-203
8188659-5	1994	The IL-4-induced [Ca2+]i rise required extracellular Ca2+ influx, since the response was prevented by LaCl3, and voltage-gated Ca2+ channel blockers, although the IL-4 effect was more sensitive to nicardipine and nifedipine than to diltiazem.	Diltiazem	232-241	interleukin 4	Mus musculus	4-8
8188659-5	1994	The IL-4-induced [Ca2+]i rise required extracellular Ca2+ influx, since the response was prevented by LaCl3, and voltage-gated Ca2+ channel blockers, although the IL-4 effect was more sensitive to nicardipine and nifedipine than to diltiazem.	Diltiazem	232-241	carbonic anhydrase 2	Mus musculus	18-21
8188659-5	1994	The IL-4-induced [Ca2+]i rise required extracellular Ca2+ influx, since the response was prevented by LaCl3, and voltage-gated Ca2+ channel blockers, although the IL-4 effect was more sensitive to nicardipine and nifedipine than to diltiazem.	Diltiazem	232-241	carbonic anhydrase 2	Mus musculus	53-56
8188659-5	1994	The IL-4-induced [Ca2+]i rise required extracellular Ca2+ influx, since the response was prevented by LaCl3, and voltage-gated Ca2+ channel blockers, although the IL-4 effect was more sensitive to nicardipine and nifedipine than to diltiazem.	Diltiazem	232-241	carbonic anhydrase 2	Mus musculus	53-56
8188659-5	1994	The IL-4-induced [Ca2+]i rise required extracellular Ca2+ influx, since the response was prevented by LaCl3, and voltage-gated Ca2+ channel blockers, although the IL-4 effect was more sensitive to nicardipine and nifedipine than to diltiazem.	Diltiazem	232-241	interleukin 4	Mus musculus	163-167
8045269-5	1994	The genistein-induced increase in immunoreactive ANP secretion was completely blocked by diltiazem (P < 0.001) while KN-62 delayed (P < 0.02) the increase of immunoreactive ANP concentration in the perfusate.	Diltiazem	89-98	natriuretic peptide A	Rattus norvegicus	49-52
8015171-7	1994	Balanced anesthesia with analgesics, vecuronium bromide and calcium blocker (diltiazem 0.5 microgram.kg-1.min-1) had been advocated to maintain the stable circulatory state.	Diltiazem	77-86	CD59 molecule (CD59 blood group)	Homo sapiens	106-111
8022139-15	1994	It also seemed that DIL was able to enhance the immunosuppressive effect of CsA, therefore CsA dosage could be reduced when DIL was coadministered.	Diltiazem	20-23	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	76-79
8022139-15	1994	It also seemed that DIL was able to enhance the immunosuppressive effect of CsA, therefore CsA dosage could be reduced when DIL was coadministered.	Diltiazem	20-23	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	91-94
8060463-8	1994	The preventive effect of diltiazem against the cyclosporin A-induced hypersensitivity to angiotensin II supports the hypothesis of increased calcium influx during cyclosporin A therapy.	Diltiazem	25-34	angiotensinogen	Rattus norvegicus	89-103
8198928-6	1994	The area under the midazolam concentration-time curve was increased from 12 +/- 1 microgram ml-1 min to 45 +/- 5 micrograms ml-1 min by diltiazem (P < 0.001) and to 35 +/- 5 micrograms ml-1 min by verapamil (P < 0.001).	Diltiazem	136-145	interleukin 17F	Homo sapiens	92-96
8058116-10	1994	Very high concentrations of nifedipine (10(-6) mol/l), verapamil (5 x 10(-6) mol/l) and diltiazem (5 x 10(-6) mol/l) almost suppressed the tonic effect evoked by the activation of AT1-receptors.	Diltiazem	88-97	angiotensin II receptor, type 1a	Rattus norvegicus	180-183
8198928-6	1994	The area under the midazolam concentration-time curve was increased from 12 +/- 1 microgram ml-1 min to 45 +/- 5 micrograms ml-1 min by diltiazem (P < 0.001) and to 35 +/- 5 micrograms ml-1 min by verapamil (P < 0.001).	Diltiazem	136-145	interleukin 17F	Homo sapiens	124-128
8198928-6	1994	The area under the midazolam concentration-time curve was increased from 12 +/- 1 microgram ml-1 min to 45 +/- 5 micrograms ml-1 min by diltiazem (P < 0.001) and to 35 +/- 5 micrograms ml-1 min by verapamil (P < 0.001).	Diltiazem	136-145	interleukin 17F	Homo sapiens	124-128
8135875-0	1994	Calmodulin antagonistic action of new 1,5-benzothiazepines derived from diltiazem.	Diltiazem	72-81	calmodulin 1	Rattus norvegicus	0-10
7905278-3	1994	IFN-gamma caused a rapid concentration-dependent rise in [Ca2+]i, which was partly inhibited by diltiazem, a calcium channel blocker, TMB-8, an inhibitor of intracellular calcium redistribution, and in calcium-free medium.	Diltiazem	96-105	interferon gamma	Homo sapiens	0-9
7905278-3	1994	IFN-gamma caused a rapid concentration-dependent rise in [Ca2+]i, which was partly inhibited by diltiazem, a calcium channel blocker, TMB-8, an inhibitor of intracellular calcium redistribution, and in calcium-free medium.	Diltiazem	96-105	carbonic anhydrase 2	Homo sapiens	58-61
8027928-1	1994	Pretreatment with diltiazem at a dose of 2 mg kg-1 intravenously protected against sudden death induced by intravenous administration of endothelin-1 (ET-1, 5 nmol kg-1), with an apparent decrease in the plasma immunoreactive-ET-1 (IR-ET-1) in mice.	Diltiazem	18-27	endothelin 1	Mus musculus	137-149
8027928-1	1994	Pretreatment with diltiazem at a dose of 2 mg kg-1 intravenously protected against sudden death induced by intravenous administration of endothelin-1 (ET-1, 5 nmol kg-1), with an apparent decrease in the plasma immunoreactive-ET-1 (IR-ET-1) in mice.	Diltiazem	18-27	endothelin 1	Mus musculus	151-155
8027928-1	1994	Pretreatment with diltiazem at a dose of 2 mg kg-1 intravenously protected against sudden death induced by intravenous administration of endothelin-1 (ET-1, 5 nmol kg-1), with an apparent decrease in the plasma immunoreactive-ET-1 (IR-ET-1) in mice.	Diltiazem	18-27	endothelin 1	Mus musculus	226-230
8027928-1	1994	Pretreatment with diltiazem at a dose of 2 mg kg-1 intravenously protected against sudden death induced by intravenous administration of endothelin-1 (ET-1, 5 nmol kg-1), with an apparent decrease in the plasma immunoreactive-ET-1 (IR-ET-1) in mice.	Diltiazem	18-27	endothelin 1	Mus musculus	226-230
8027928-4	1994	Furthermore, in anaesthetized rats, diltiazem inhibited ET-1-induced decreases in renal blood flow and increased renal accumulation of IR-ET-1.	Diltiazem	36-45	endothelin 1	Rattus norvegicus	56-60
8027928-4	1994	Furthermore, in anaesthetized rats, diltiazem inhibited ET-1-induced decreases in renal blood flow and increased renal accumulation of IR-ET-1.	Diltiazem	36-45	endothelin 1	Mus musculus	138-142
8027928-5	1994	These results indicate that part of the clearance of ET-1 from the bloodstream occurs in the kidney, and that diltiazem enhances the elimination of the peptide, presumably by improvement in the renal circulation, this action leading to alleviation of the toxic effects of ET-1.	Diltiazem	110-119	endothelin 1	Rattus norvegicus	272-276
7538432-8	1994	APP expression in H-35 and HepG2 cells, stimulated by interleukin 1 (IL-1), IL-6, and dexamethasone, was inhibited by diltiazem or verapamil but not SOD.	Diltiazem	118-127	interleukin 6	Homo sapiens	76-80
8135875-2	1994	Some compounds possessing the benzoyloxy moieties at position 4 of 1,5-benzothiazepine ring of diltiazem showed a dose-dependent inhibitory action with the potencies comparable to that of a calmodulin antagonist, N-(6-aminohexyl)-5-chloro-1-naphthalene-sulfonamide (W-7).	Diltiazem	95-104	calmodulin 1	Rattus norvegicus	190-200
7506699-7	1994	The effects of insulin were almost completely inhibited by diltiazem, staurosporine, calphostin C, and thapsigargin.	Diltiazem	59-68	insulin	Homo sapiens	15-22
8201843-7	1994	The effect of pinaverium was equivalent to that of diltiazem in the inhibition of CCK-8- or gastrin-induced contractions.	Diltiazem	51-60	cholecystokinin	Oryctolagus cuniculus	82-85
8084214-1	1994	The effects of calcium channel blockers, verapamil, nifedipine and diltiazem, on CCl4-induced liver damage were determined.	Diltiazem	67-76	C-C motif chemokine ligand 4	Homo sapiens	81-85
8084214-6	1994	When the calcium channel blockers were administered 2 hr prior to and 7 hr after the administration of the toxic agent at doses of 25 mg/kg (diltiazem) and 10 mg/kg (nifedipine and verapamil), the liver showed a significant reestablishment of several of these parameters: a considerable reduction in liver calcium content, a decrease in AST and ALT levels, and a significant increase in protein synthesis rate.	Diltiazem	141-150	solute carrier family 17 member 5	Homo sapiens	337-340
8201843-7	1994	The effect of pinaverium was equivalent to that of diltiazem in the inhibition of CCK-8- or gastrin-induced contractions.	Diltiazem	51-60	gastrin	Oryctolagus cuniculus	92-99
7693284-17	1993	The results indicate that in addition to possessing affinity for the NK1 receptor, the non-peptide antagonist, CP-96,345, displays high affinity for [3H]-diltiazem binding sites on L-type calcium channels.The functional effect that may be observed in integrated models will be a consequence of either property, or be a composite effect of NK1 receptor antagonism and L-channel blockade.	Diltiazem	154-163	tachykinin receptor 1	Rattus norvegicus	339-351
8111804-4	1993	Diltiazem, in doses of 90 mg BID and 180 mg BID, was statistically superior to placebo with respect to increasing total exercise time.	Diltiazem	0-9	BH3 interacting domain death agonist	Homo sapiens	29-32
8111804-4	1993	Diltiazem, in doses of 90 mg BID and 180 mg BID, was statistically superior to placebo with respect to increasing total exercise time.	Diltiazem	0-9	BH3 interacting domain death agonist	Homo sapiens	44-47
8293761-5	1993	Chronic treatment with diltiazem alone did not affect the responsiveness to any of the drugs tested, but the augmentation of contractions to angiotensin II (10(-9) to 10(-6) M) after treatment with cyclosporin, was prevented by co-treatment with diltiazem.	Diltiazem	23-32	angiotensinogen	Rattus norvegicus	141-155
8293761-5	1993	Chronic treatment with diltiazem alone did not affect the responsiveness to any of the drugs tested, but the augmentation of contractions to angiotensin II (10(-9) to 10(-6) M) after treatment with cyclosporin, was prevented by co-treatment with diltiazem.	Diltiazem	246-255	angiotensinogen	Rattus norvegicus	141-155
8293761-8	1993	Co-treatment with diltiazem normalized the response to CGRP.	Diltiazem	18-27	calcitonin-related polypeptide alpha	Rattus norvegicus	55-59
8395510-5	1993	Half-logarithmic plots were linear with rate constants of 0.0058, 0.011, 0.015, and 0.020 min-1 when 3, 10, 30, and 50 microM (+)-cis-diltiazem was added, respectively.	Diltiazem	126-143	CD59 molecule (CD59 blood group)	Homo sapiens	90-95
8473401-1	1993	The impact of two calcium channel blockers of different structure, diltiazem and felodipine, on PTH secretion was studied under hyper- and hypocalcemic conditions.	Diltiazem	67-76	parathyroid hormone	Homo sapiens	96-99
8473401-8	1993	In addition, PTH secretion was less suppressed on diltiazem than on felodipine therapy or during the control period (P < 0.04).	Diltiazem	50-59	parathyroid hormone	Homo sapiens	13-16
8473401-12	1993	These data demonstrate that diltiazem, but not felodipine, stimulates PTH secretion in vivo in man, with a maximal effect observed under hypocalcemic conditions.	Diltiazem	28-37	parathyroid hormone	Homo sapiens	70-73
8094079-5	1993	Increased mdr-1 mRNA was also seen with two other calcium channel blockers, nicardipine and diltiazem, but not with the Pgp antagonists, quinidine and chlorpromazine.	Diltiazem	92-101	ATP binding cassette subfamily B member 1	Homo sapiens	10-15
7700857-4	1994	Furthermore, CCK release induced by glucose was inhibited by the calcium channel blocker diltiazem.	Diltiazem	89-98	cholecystokinin	Mus musculus	13-16
8334915-13	1993	The ACE inhibitors and calcium antagonists of the verapamil and diltiazem groups have demonstrated superior efficacy for preservation of renal function over conventional therapy.	Diltiazem	64-73	angiotensin I converting enzyme	Homo sapiens	4-7
7689399-0	1993	Effects of KRN2391, nicorandil and diltiazem on the changes in the electrocardiogram caused by endothelin-1 in anaesthetized rats.	Diltiazem	35-44	endothelin 1	Rattus norvegicus	95-107
8500860-1	1993	Calcium entry blockers, particularly diltiazem, have been shown to lower not only systemic blood pressure but also improve proteinuria in non-insulin-dependent diabetic patients.	Diltiazem	37-46	insulin	Homo sapiens	142-149
8377279-5	1993	3) Epo alone substantially stimulated 45Ca uptake, leading to an increase in [Ca2+]i, which effect was not seen in Ca2+ deficient medium, and was partially inhibited with diltiazem but not with TMB-8.	Diltiazem	171-180	erythropoietin	Homo sapiens	3-6
8329674-5	1993	With diltiazem (10(-5) M) in the bathing media, 10(-8) M AII caused an abrupt rise and decline in SMC [Ca2+]i in AA, but a sustained elevation in EA (P < 0.02).	Diltiazem	5-14	angiotensinogen	Rattus norvegicus	57-60
8316231-3	1993	When endotoxin-injected rats were treated with the calcium channel-blocker diltiazem, the anisotropy and microviscosity values were comparable to those obtained from control rats (rs = 0.152 +/- 0.003, eta = 1.00 +/- 0.003, n = 6).	Diltiazem	75-84	endothelin receptor type A	Rattus norvegicus	202-205
8382636-3	1993	Verapamil as well as diltiazem inhibited vasopressin-stimulated Mn2+ influx in a dose-dependent manner up to 60% at concentrations of 200-400 microM.	Diltiazem	21-30	arginine vasopressin	Rattus norvegicus	41-52
8430823-4	1993	Vasoconstriction to ANG II was significantly inhibited by diltiazem (29 +/- 12 vs. 67 +/- 31%; P < 0.02) in AA.	Diltiazem	58-67	angiotensinogen	Rattus norvegicus	20-26
8428211-7	1993	Diltiazem (10 nM-0.1 mM) partially inhibited both the increases in [Ca2+]i and tension.	Diltiazem	0-9	carbonic anhydrase 2	Rattus norvegicus	68-71
8428211-10	1993	In the presence of diltiazem the sarafotoxin-induced [Ca2+]i-force relationship was shifted even further to the left.	Diltiazem	19-28	carbonic anhydrase 2	Rattus norvegicus	54-57
8434130-5	1993	Pretreatment of mice with the phospholipase A2 (PLA2) inhibitors chlorpromazine or diltiazem one hour prior to APAP administration inhibits loss of mitochondrial Ca2+ homeostasis, prevents nuclear damage, and inhibits APAP hepatotoxicity as indicated by serum alanine aminotransferase activity and electron microscopic studies.	Diltiazem	83-92	phospholipase A2, group IB, pancreas	Mus musculus	30-46
8434130-5	1993	Pretreatment of mice with the phospholipase A2 (PLA2) inhibitors chlorpromazine or diltiazem one hour prior to APAP administration inhibits loss of mitochondrial Ca2+ homeostasis, prevents nuclear damage, and inhibits APAP hepatotoxicity as indicated by serum alanine aminotransferase activity and electron microscopic studies.	Diltiazem	83-92	phospholipase A2, group IB, pancreas	Mus musculus	48-52
1472072-5	1992	Ca2+ channel blockers, Nifedipine, Diltiazem and Verapamil (5 microM), reduced ET-1 chemotaxsis more than 60% (P < 0.001).	Diltiazem	35-44	endothelin 1	Homo sapiens	79-83
1507210-0	1992	Synthesis, characterization, and Ca2+ antagonistic activity of diltiazem metabolites.	Diltiazem	63-72	carbonic anhydrase 2	Homo sapiens	33-36
1490588-6	1992	The vasorelaxant effect of ANP on AT II-induced contraction was significantly increased in Ca(2+)-free medium containing 3 mM ethylene glycol bis(beta-aminoethyl ether) N,N,N",N"-tetraacetic acid (EGTA-Ringer) or by pretreatment with the calcium antagonist, diltiazem (DIL).	Diltiazem	258-267	natriuretic peptide A	Homo sapiens	27-30
1490588-6	1992	The vasorelaxant effect of ANP on AT II-induced contraction was significantly increased in Ca(2+)-free medium containing 3 mM ethylene glycol bis(beta-aminoethyl ether) N,N,N",N"-tetraacetic acid (EGTA-Ringer) or by pretreatment with the calcium antagonist, diltiazem (DIL).	Diltiazem	258-267	angiotensinogen	Homo sapiens	34-39
1490588-6	1992	The vasorelaxant effect of ANP on AT II-induced contraction was significantly increased in Ca(2+)-free medium containing 3 mM ethylene glycol bis(beta-aminoethyl ether) N,N,N",N"-tetraacetic acid (EGTA-Ringer) or by pretreatment with the calcium antagonist, diltiazem (DIL).	Diltiazem	269-272	natriuretic peptide A	Homo sapiens	27-30
1490588-6	1992	The vasorelaxant effect of ANP on AT II-induced contraction was significantly increased in Ca(2+)-free medium containing 3 mM ethylene glycol bis(beta-aminoethyl ether) N,N,N",N"-tetraacetic acid (EGTA-Ringer) or by pretreatment with the calcium antagonist, diltiazem (DIL).	Diltiazem	269-272	angiotensinogen	Homo sapiens	34-39
1452374-7	1992	Diltiazem also tended to decrease plasma bradykinin, thromboxane B2, and 6-keto-prostaglandin F1 alpha levels.	Diltiazem	0-9	kininogen 1	Homo sapiens	41-51
1452374-9	1992	Further, bradykinin was significantly decreased by diltiazem only in patients with exercise-induced silent ischemia or no exercise-induced ischemia, while the thromboxane B2/6-keto-prostaglandin F1 alpha ratio was unaffected by the administration of diltiazem.	Diltiazem	51-60	kininogen 1	Homo sapiens	9-19
1280721-0	1992	Diltiazem potentiates angiotensin II-mediated renal prostacyclin synthesis.	Diltiazem	0-9	angiotensinogen	Rattus norvegicus	22-36
1280721-11	1992	We conclude that DIL enhances AII-induced renal prostacyclin synthesis and that this is functionally relevant.	Diltiazem	17-20	angiotensinogen	Rattus norvegicus	30-33
1497067-3	1992	The source of the luteinizing hormone-releasing hormone induced increase in intracellular Ca++ was investigated with various calcium channel blockers (verapamil, diltiazem, and nifedipine), high K+ buffer, and perifusion with media lacking Ca++.	Diltiazem	162-171	gonadotropin releasing hormone 1	Rattus norvegicus	18-55
1377295-12	1992	Plasma levels of soluble interleukin-2 receptors decreased significantly during diltiazem treatment.	Diltiazem	80-89	interleukin 2	Homo sapiens	25-38
1415641-9	1992	Also, vasopressin-induced increase in hepatocyte cytosolic [Ca2+] in diltiazem-treated septic rats was significantly greater than that observed in untreated septic rats.	Diltiazem	69-78	arginine vasopressin	Rattus norvegicus	6-17
1495189-5	1992	Diltiazem was administered i. v. at a rate of 3 micrograms.kg-1.min-1 before induction of anesthesia.	Diltiazem	0-9	CD59 molecule (CD59 blood group)	Homo sapiens	64-69
1495189-9	1992	Hypertension during the manipulation of the tumor was controlled by increasing the inspired concentration of enflurane or by increasing the infusion rate of diltiazem to 5 micrograms.kg-1.min-1.	Diltiazem	157-166	CD59 molecule (CD59 blood group)	Homo sapiens	188-193
1397005-6	1992	Diltiazem, verapamil and nifedipine only reduced veratrine-induced contracture at concentrations much higher than those producing a negative inotropic effect, giving them negative NIE/VIC ratios of 0.31, 0.08 and 0.08 respectively.	Diltiazem	0-9	endothelin 2	Rattus norvegicus	184-187
1623657-7	1992	Diltiazem CD lowered DBP and SBP throughout the dosing interval.	Diltiazem	0-9	selenium binding protein 1	Homo sapiens	29-32
1730694-6	1992	Nifedipine and diltiazem inhibited the normal increase in [Ca2+]i from aggregated IgG binding to FcR and also prevented formyl-methionyl-leucyl-phenyl-alanine (fMLP)-induced [Ca2+]i rise.	Diltiazem	15-24	formyl peptide receptor 1	Homo sapiens	160-164
1566911-8	1992	Decrease in the force of contraction by verapamil as well as diltiazem indicates activation of voltage-dependent calcium channels during 5-HT-mediated contraction and perhaps during amplification of the vasoconstrictor activity of ET-1 by 5-HT.	Diltiazem	61-70	endothelin 1	Rattus norvegicus	231-235
1318127-4	1992	In the present study, the effect of nifedipine and diltiazem on AII- and PDGF-BB-induced vascular smooth muscle cell proliferation was examined.	Diltiazem	51-60	angiotensinogen	Homo sapiens	64-67
1318127-7	1992	Both AII- and PDGF-BB-induced DNA synthesis was significantly blunted by diltiazem and nifedipine in a concentration of 10 microM, while no significant influence was seen with concentrations from 10 nM up to 1 microM.	Diltiazem	73-82	angiotensinogen	Homo sapiens	5-8
1738105-9	1992	In contrast, the contractile effect to ET-1 was reduced markedly by removal of extracellular calcium or by the voltage-dependent calcium channel blockers nicardipine and diltiazem.	Diltiazem	170-179	endothelin-1	Cavia porcellus	39-43
1730694-8	1992	Consistent with this, nifedipine and diltiazem inhibited fMLP-stimulated phagocytosis (which is dependent on an increase in [Ca2+]i) when PMN had repleted intracellular stores.	Diltiazem	37-46	formyl peptide receptor 1	Homo sapiens	57-61
1306705-13	1992	Several studies have demonstrated elevated CsA blood concentrations during concomitant treatment with verapamil and diltiazem but not with the dihydropyridine class of calcium antagonists.	Diltiazem	116-125	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	43-46
1305062-3	1992	In spite of the fact that diltiazem protracted electrocardiographic QT interval from 0.16 +/- 0.008 to 0.18 +/- 0.009 s. (p < 0.01), QaT from 0.29 +/- 0.007 to 0.31 +/- 0.008 s. (p < 0.05), QeT from 0.35 +/- 0.009 to 0.37 +/- 0.009 s. (p < 0.01), it did not affect Kg in any significant way, nor did it affect the glycosylated protein levels, insulin and C-peptide secretion, nor the secretion of adrenaline, noradrenaline, dopamine, cortisol and growth hormone.	Diltiazem	26-35	insulin	Homo sapiens	352-359
1305062-3	1992	In spite of the fact that diltiazem protracted electrocardiographic QT interval from 0.16 +/- 0.008 to 0.18 +/- 0.009 s. (p < 0.01), QaT from 0.29 +/- 0.007 to 0.31 +/- 0.008 s. (p < 0.05), QeT from 0.35 +/- 0.009 to 0.37 +/- 0.009 s. (p < 0.01), it did not affect Kg in any significant way, nor did it affect the glycosylated protein levels, insulin and C-peptide secretion, nor the secretion of adrenaline, noradrenaline, dopamine, cortisol and growth hormone.	Diltiazem	26-35	growth hormone 1	Homo sapiens	456-470
1356961-7	1992	Moreover, responses to ME (an alpha 1A-agonist) were blocked by diltiazem as well as by bunazosin and WB4101, while CEC had no blocking effect on ME-induced responses.	Diltiazem	64-73	adrenoceptor alpha 1A	Canis lupus familiaris	30-38
1490655-0	1992	Effects of prolonged treatment with diltiazem on pituitary secretion of luteinizing hormone, follicle-stimulating hormone, thyrotropin and prolactin.	Diltiazem	36-45	prolactin	Homo sapiens	139-148
1309615-5	1992	Further, the (+)-cis isomer was approximately 50 times more effective than the (-)-cis isomer in blocking the Ca2+ spikes, indicating that diltiazem action on the rdgB eye is mediated by means of blocking voltage-sensitive Ca2+ channels, rather than by blocking the light-sensitive channels.	Diltiazem	139-148	retinal degeneration B	Drosophila melanogaster	163-167
1309615-6	1992	Application of the Ca(2+)-channel blockers (+)-cis-diltiazem and verapamil hydrochloride to the eyes of rdgB flies over a 7-day period largely inhibited light-dependent degeneration of the photoreceptor cells.	Diltiazem	43-60	retinal degeneration B	Drosophila melanogaster	104-108
1380721-12	1992	Plasma levels of soluble interleukin-2 receptors decreased significantly during diltiazem treatment.	Diltiazem	80-89	interleukin 2	Homo sapiens	25-38
1667291-18	1991	Pentobarbitone also prevented the diltiazem-induced epileptiform bursting only at a concentration (100 microM) that also reduced the control CA1 synaptic transmission.	Diltiazem	34-43	carbonic anhydrase 1	Rattus norvegicus	141-144
1810605-13	1991	A Ca2+ channel blocking drug such as diltiazem abolished the increase in [Ca2+]i and partially attenuated the mechanical potentiation produced by a small amount of ET-1 in combination with 5-HT.7.	Diltiazem	37-46	endothelin-1	Sus scrofa	164-168
1748812-4	1991	It was partly attenuated by diltiazem, a potent Ca++ entry blocker, but not affected by alpha-adrenoceptor antagonist phentolamine, indicating that endothelin-1 causes vasoconstriction by either the extracellular Ca++ entry or intracellular movement of Ca++ from the cytosolic storage site.	Diltiazem	28-37	endothelin 1	Homo sapiens	148-160
1819708-5	1991	Results (triplicate experiments, * P less than 0.05 vs buffer, P less than 0.05 vs thrombin) demonstrate that pre-incubation with calcium channel blocker markedly inhibits thrombin-induced PAF production (verapamil:buffer 273 +/- 122, thrombin 10,735 +/- 1524*, thrombin + verapamil 178 +/- 91 cpm/plate; diltiazem:buffer 1097 +/- 581, thrombin 15,283 +/- 2661*, thrombin + diltiazem 280 +/- 56 cpm/plate).	Diltiazem	305-314	coagulation factor II, thrombin	Homo sapiens	172-180
1819708-5	1991	Results (triplicate experiments, * P less than 0.05 vs buffer, P less than 0.05 vs thrombin) demonstrate that pre-incubation with calcium channel blocker markedly inhibits thrombin-induced PAF production (verapamil:buffer 273 +/- 122, thrombin 10,735 +/- 1524*, thrombin + verapamil 178 +/- 91 cpm/plate; diltiazem:buffer 1097 +/- 581, thrombin 15,283 +/- 2661*, thrombin + diltiazem 280 +/- 56 cpm/plate).	Diltiazem	305-314	coagulation factor II, thrombin	Homo sapiens	172-180
1819708-5	1991	Results (triplicate experiments, * P less than 0.05 vs buffer, P less than 0.05 vs thrombin) demonstrate that pre-incubation with calcium channel blocker markedly inhibits thrombin-induced PAF production (verapamil:buffer 273 +/- 122, thrombin 10,735 +/- 1524*, thrombin + verapamil 178 +/- 91 cpm/plate; diltiazem:buffer 1097 +/- 581, thrombin 15,283 +/- 2661*, thrombin + diltiazem 280 +/- 56 cpm/plate).	Diltiazem	305-314	coagulation factor II, thrombin	Homo sapiens	172-180
1819708-5	1991	Results (triplicate experiments, * P less than 0.05 vs buffer, P less than 0.05 vs thrombin) demonstrate that pre-incubation with calcium channel blocker markedly inhibits thrombin-induced PAF production (verapamil:buffer 273 +/- 122, thrombin 10,735 +/- 1524*, thrombin + verapamil 178 +/- 91 cpm/plate; diltiazem:buffer 1097 +/- 581, thrombin 15,283 +/- 2661*, thrombin + diltiazem 280 +/- 56 cpm/plate).	Diltiazem	305-314	coagulation factor II, thrombin	Homo sapiens	172-180
1819708-5	1991	Results (triplicate experiments, * P less than 0.05 vs buffer, P less than 0.05 vs thrombin) demonstrate that pre-incubation with calcium channel blocker markedly inhibits thrombin-induced PAF production (verapamil:buffer 273 +/- 122, thrombin 10,735 +/- 1524*, thrombin + verapamil 178 +/- 91 cpm/plate; diltiazem:buffer 1097 +/- 581, thrombin 15,283 +/- 2661*, thrombin + diltiazem 280 +/- 56 cpm/plate).	Diltiazem	305-314	coagulation factor II, thrombin	Homo sapiens	172-180
1819708-5	1991	Results (triplicate experiments, * P less than 0.05 vs buffer, P less than 0.05 vs thrombin) demonstrate that pre-incubation with calcium channel blocker markedly inhibits thrombin-induced PAF production (verapamil:buffer 273 +/- 122, thrombin 10,735 +/- 1524*, thrombin + verapamil 178 +/- 91 cpm/plate; diltiazem:buffer 1097 +/- 581, thrombin 15,283 +/- 2661*, thrombin + diltiazem 280 +/- 56 cpm/plate).	Diltiazem	374-383	coagulation factor II, thrombin	Homo sapiens	172-180
1819708-5	1991	Results (triplicate experiments, * P less than 0.05 vs buffer, P less than 0.05 vs thrombin) demonstrate that pre-incubation with calcium channel blocker markedly inhibits thrombin-induced PAF production (verapamil:buffer 273 +/- 122, thrombin 10,735 +/- 1524*, thrombin + verapamil 178 +/- 91 cpm/plate; diltiazem:buffer 1097 +/- 581, thrombin 15,283 +/- 2661*, thrombin + diltiazem 280 +/- 56 cpm/plate).	Diltiazem	374-383	coagulation factor II, thrombin	Homo sapiens	172-180
1819708-5	1991	Results (triplicate experiments, * P less than 0.05 vs buffer, P less than 0.05 vs thrombin) demonstrate that pre-incubation with calcium channel blocker markedly inhibits thrombin-induced PAF production (verapamil:buffer 273 +/- 122, thrombin 10,735 +/- 1524*, thrombin + verapamil 178 +/- 91 cpm/plate; diltiazem:buffer 1097 +/- 581, thrombin 15,283 +/- 2661*, thrombin + diltiazem 280 +/- 56 cpm/plate).	Diltiazem	374-383	coagulation factor II, thrombin	Homo sapiens	172-180
1819708-5	1991	Results (triplicate experiments, * P less than 0.05 vs buffer, P less than 0.05 vs thrombin) demonstrate that pre-incubation with calcium channel blocker markedly inhibits thrombin-induced PAF production (verapamil:buffer 273 +/- 122, thrombin 10,735 +/- 1524*, thrombin + verapamil 178 +/- 91 cpm/plate; diltiazem:buffer 1097 +/- 581, thrombin 15,283 +/- 2661*, thrombin + diltiazem 280 +/- 56 cpm/plate).	Diltiazem	374-383	coagulation factor II, thrombin	Homo sapiens	172-180
1819708-5	1991	Results (triplicate experiments, * P less than 0.05 vs buffer, P less than 0.05 vs thrombin) demonstrate that pre-incubation with calcium channel blocker markedly inhibits thrombin-induced PAF production (verapamil:buffer 273 +/- 122, thrombin 10,735 +/- 1524*, thrombin + verapamil 178 +/- 91 cpm/plate; diltiazem:buffer 1097 +/- 581, thrombin 15,283 +/- 2661*, thrombin + diltiazem 280 +/- 56 cpm/plate).	Diltiazem	374-383	coagulation factor II, thrombin	Homo sapiens	172-180
1819708-7	1991	Diltiazem also inhibited bradykinin (10(-8) M) induced PAF synthesis.	Diltiazem	0-9	kininogen 1	Homo sapiens	25-35
1819708-7	1991	Diltiazem also inhibited bradykinin (10(-8) M) induced PAF synthesis.	Diltiazem	0-9	PCNA clamp associated factor	Homo sapiens	55-58
1782723-0	1991	Calcium-channel blocking agents verapamil and diltiazem are inhibitors of vasopressin-induced human platelet activation.	Diltiazem	46-55	arginine vasopressin	Homo sapiens	74-85
1782723-2	1991	This study investigated the influences of calcium-channel blocking agents verapamil and diltiazem on platelet responses induced by arginine vasopressin (AVP) and lysine vasopressin (LVP).	Diltiazem	88-97	arginine vasopressin	Homo sapiens	140-151
1782723-2	1991	This study investigated the influences of calcium-channel blocking agents verapamil and diltiazem on platelet responses induced by arginine vasopressin (AVP) and lysine vasopressin (LVP).	Diltiazem	88-97	arginine vasopressin	Homo sapiens	169-180
1782723-10	1991	Our data provide evidence that the effects of verapamil and diltiazem on vasopressin-induced platelet responses may be directly related to inhibition of extracellular calcium entry.	Diltiazem	60-69	arginine vasopressin	Homo sapiens	73-84
1766117-11	1991	In conclusion, our data show that induced hypotension by diltiazem activates the renin-angiotensin-sympathetic nervous system.	Diltiazem	57-66	LOW QUALITY PROTEIN: renin	Oryctolagus cuniculus	81-86
1928878-0	1991	The effect of CPR on plasma diltiazem concentrations in dogs.	Diltiazem	28-37	cytochrome p450 oxidoreductase	Canis lupus familiaris	14-17
1928878-1	1991	STUDY OBJECTIVE: To determine the effect of cardiac arrest with CPR on diltiazem concentrations in dogs.	Diltiazem	71-80	cytochrome p450 oxidoreductase	Canis lupus familiaris	64-67
1928878-9	1991	The mean diltiazem concentration rose 70% during CPR in the group that received diltiazem before cardiac arrest.	Diltiazem	9-18	cytochrome p450 oxidoreductase	Canis lupus familiaris	49-52
1928878-9	1991	The mean diltiazem concentration rose 70% during CPR in the group that received diltiazem before cardiac arrest.	Diltiazem	80-89	cytochrome p450 oxidoreductase	Canis lupus familiaris	49-52
1928878-10	1991	The group that received diltiazem during CPR had concentrations five times greater than expected during sinus rhythm.	Diltiazem	24-33	cytochrome p450 oxidoreductase	Canis lupus familiaris	41-44
1928878-11	1991	CONCLUSION: Increased diltiazem concentrations are observed during CPR and are probably related to altered distribution encountered during CPR.	Diltiazem	22-31	cytochrome p450 oxidoreductase	Canis lupus familiaris	67-70
1928878-11	1991	CONCLUSION: Increased diltiazem concentrations are observed during CPR and are probably related to altered distribution encountered during CPR.	Diltiazem	22-31	cytochrome p450 oxidoreductase	Canis lupus familiaris	139-142
1679346-7	1991	Total inhibition of photolabeling of the P-glycoprotein was observed with verapamil, nifedipine, diltiazem, and vinbalastine, and partial inhibition was observed with colchicine and cytochalasin B.	Diltiazem	97-106	ATP binding cassette subfamily B member 1	Homo sapiens	41-55
1650153-6	1991	Inhibition of protein synthesis by cycloheximide blocked the PAF-enhanced NK cell activity after preincubation for 18 h. Extracellular Ca2+ was also needed for the action of PAF as suggested by the effects of Ca2+ chelation with ethyleneglycol-bis-(beta-aminoethyl ether)-N,N"-tetraacetic acid (EGTA) and inhibition of Ca2+ entry into the cells with verapamil and diltiazem, all of which abrogated the action of PAF.	Diltiazem	364-373	PCNA clamp associated factor	Rattus norvegicus	61-64
1650153-6	1991	Inhibition of protein synthesis by cycloheximide blocked the PAF-enhanced NK cell activity after preincubation for 18 h. Extracellular Ca2+ was also needed for the action of PAF as suggested by the effects of Ca2+ chelation with ethyleneglycol-bis-(beta-aminoethyl ether)-N,N"-tetraacetic acid (EGTA) and inhibition of Ca2+ entry into the cells with verapamil and diltiazem, all of which abrogated the action of PAF.	Diltiazem	364-373	PCNA clamp associated factor	Rattus norvegicus	174-177
1650153-6	1991	Inhibition of protein synthesis by cycloheximide blocked the PAF-enhanced NK cell activity after preincubation for 18 h. Extracellular Ca2+ was also needed for the action of PAF as suggested by the effects of Ca2+ chelation with ethyleneglycol-bis-(beta-aminoethyl ether)-N,N"-tetraacetic acid (EGTA) and inhibition of Ca2+ entry into the cells with verapamil and diltiazem, all of which abrogated the action of PAF.	Diltiazem	364-373	PCNA clamp associated factor	Rattus norvegicus	174-177
1907699-0	1991	Diltiazem restores IL-2, IL-3, IL-6, and IFN-gamma synthesis and decreases host susceptibility to sepsis following hemorrhage.	Diltiazem	0-9	interleukin 2	Mus musculus	19-23
1907699-0	1991	Diltiazem restores IL-2, IL-3, IL-6, and IFN-gamma synthesis and decreases host susceptibility to sepsis following hemorrhage.	Diltiazem	0-9	interleukin 3	Mus musculus	25-29
1907699-0	1991	Diltiazem restores IL-2, IL-3, IL-6, and IFN-gamma synthesis and decreases host susceptibility to sepsis following hemorrhage.	Diltiazem	0-9	interleukin 6	Mus musculus	31-35
1907699-0	1991	Diltiazem restores IL-2, IL-3, IL-6, and IFN-gamma synthesis and decreases host susceptibility to sepsis following hemorrhage.	Diltiazem	0-9	interferon gamma	Mus musculus	41-50
1907699-7	1991	However, diltiazem (400 but not 2400 micrograms/kg) treatment after hemorrhage restored lymphocyte capacity to produce IL-2, IL-3, IL-6, and IFN-gamma (P less than 0.05).	Diltiazem	9-18	interleukin 2	Mus musculus	119-123
1907699-7	1991	However, diltiazem (400 but not 2400 micrograms/kg) treatment after hemorrhage restored lymphocyte capacity to produce IL-2, IL-3, IL-6, and IFN-gamma (P less than 0.05).	Diltiazem	9-18	interleukin 3	Mus musculus	125-129
1907699-7	1991	However, diltiazem (400 but not 2400 micrograms/kg) treatment after hemorrhage restored lymphocyte capacity to produce IL-2, IL-3, IL-6, and IFN-gamma (P less than 0.05).	Diltiazem	9-18	interleukin 6	Mus musculus	131-135
1907699-7	1991	However, diltiazem (400 but not 2400 micrograms/kg) treatment after hemorrhage restored lymphocyte capacity to produce IL-2, IL-3, IL-6, and IFN-gamma (P less than 0.05).	Diltiazem	9-18	interferon gamma	Mus musculus	141-150
1871801-5	1991	Concentrations of diltiazem which blocked the proliferation of PHA-stimulated human peripheral blood mononuclear cells, or prevented activation-associated accumulation of interleukin-2 mRNA, or p50- and p70-IL-2 receptor mRNA exceeded pharmacological concentrations by more than 100-fold.	Diltiazem	18-27	interleukin 2	Homo sapiens	171-184
1871801-5	1991	Concentrations of diltiazem which blocked the proliferation of PHA-stimulated human peripheral blood mononuclear cells, or prevented activation-associated accumulation of interleukin-2 mRNA, or p50- and p70-IL-2 receptor mRNA exceeded pharmacological concentrations by more than 100-fold.	Diltiazem	18-27	nuclear factor kappa B subunit 1	Homo sapiens	194-197
1871801-5	1991	Concentrations of diltiazem which blocked the proliferation of PHA-stimulated human peripheral blood mononuclear cells, or prevented activation-associated accumulation of interleukin-2 mRNA, or p50- and p70-IL-2 receptor mRNA exceeded pharmacological concentrations by more than 100-fold.	Diltiazem	18-27	interleukin 2	Homo sapiens	207-211
1871801-6	1991	Both, CsA and high doses of diltiazem caused an increase of IL-6 mRNA.	Diltiazem	28-37	interleukin 6	Homo sapiens	60-64
1871801-7	1991	In contrast to these findings, the IL-6 plasma concentrations were comparable in both groups, whereas the serum concentration of soluble IL-2 receptors was decreased in patients treated with diltiazem.	Diltiazem	191-200	interleukin 2	Homo sapiens	137-141
1775187-3	1991	It was demonstrated that the angiotensin II-induced increase in slowly exchanging 45Ca2+ in rat aorta was incompletely (by approximately 60%-70%) inhibited by the organic Ca2+ entry blockers nifedipine, verapamil and diltiazem and by other Ca2+ entry blocking compounds like CoCl2 and chlorpromazine.	Diltiazem	217-226	angiotensinogen	Rattus norvegicus	29-43
1994656-5	1991	The diltiazem:placebo Cox hazard ratio (95% confidence limits) for the trial primary end point (cardiac death or nonfatal reinfarction, whichever occurred first) was: first non-Q-wave AMI-0.48 (0.26, 0.89); first inferior Q-wave AMI-0.66 (0.40, 1.09); first anterior Q-wave AMI-0.82 (0.51, 1.31); and prior AMI-1.11 (0.85, 1.44).	Diltiazem	4-13	cytochrome c oxidase subunit 8A	Homo sapiens	22-25
1942082-3	1991	The inotropic effect of AII was markedly inhibited by 1 microM saralasin or 1 microM diltiazem.	Diltiazem	85-94	angiotensinogen	Homo sapiens	24-27
2283645-6	1990	Moreover, BP control (sitting DBP less than 90 mmHg) was achieved in a greater proportion of patients treated with diltiazem (63 vs 44%).	Diltiazem	115-124	D-box binding PAR bZIP transcription factor	Homo sapiens	30-33
1666033-5	1991	The percent control of CDP formation were decreased by up to 76.7% in 5 microM and 44.3% in 50 microM of diltiazem.	Diltiazem	105-114	cut-like homeobox 1	Mus musculus	23-26
1846113-6	1991	Both the GRF-dependent increase in [Ca2+]i and GH release were blocked by incubation in low Ca2+ medium and by the organic Ca2+ antagonists nifedipine and diltiazem.	Diltiazem	155-164	growth hormone releasing hormone	Rattus norvegicus	9-12
2055416-2	1991	In rat hippocampal slices, the lowering of the calcium concentration (from 2 to 1 mM) or diltiazem (200 microM) or CdCl2 (50 microM) significantly (P less than 0.01) increased the amplitude and shifted the stimulus-response curve of the secondary population spikes, due to paired pulse CA1 stimulation to the left.	Diltiazem	89-98	carbonic anhydrase 1	Rattus norvegicus	286-289
1715719-2	1991	Systemic administration of VSCC antagonists, i.e. nimodipine, nifedipine, verapamil and diltiazem, resulted in a marked suppression of the nighttime pineal NAT activity.	Diltiazem	88-97	N-acetyltransferase 1	Rattus norvegicus	156-159
1822207-10	1991	The absolute recoveries of the drugs are about 90% and the limit of detection for diltiazem is 0.8 ng ml-1.	Diltiazem	82-91	interleukin 17F	Homo sapiens	102-106
20504713-5	1991	Nifedipine, a dihydropyridine Ca(2+) channel antagonist and diltiazem, a benzothiazepine that also inhibits dihydropyridine sensitive Ca(2+) channels, decreased Bay K 8644-induced somatostatin release in a dose-dependent manner with IC(50)s of 0.39 +/- 0.05 ?M and 66+/-0.07 ?M.	Diltiazem	60-69	somatostatin	Homo sapiens	180-192
1706050-8	1990	The hepatocytes of rats treated with both diltiazem and CCl4 revealed fewer Ca granules than those treated with CCl4 alone.	Diltiazem	42-51	C-C motif chemokine ligand 4	Rattus norvegicus	112-116
1706050-10	1990	The Ca staining in liver cells in CCl4-treated rats was decreased by diltiazem.	Diltiazem	69-78	C-C motif chemokine ligand 4	Rattus norvegicus	34-38
1983065-3	1990	The vasoconstrictor response to UK14304 in the presence of vasopressin was antagonized by idazoxan (1 microM) but was not affected by prazosin (10 nM), indicating that it was due to activation of alpha 2-adrenoceptors, and it was reduced by diltiazem (10 microM) and abolished when perfusion was done with a Ca2(+)-free solution, suggesting that the effect depends on the influx of Ca2+.	Diltiazem	241-250	arginine vasopressin	Rattus norvegicus	59-70
2256111-4	1990	Removal of Ca2+ from the media or pretreating the cells with diltiazem (10(-5) M), a calcium channel blocker, delayed the onset and reduced the magnitude of the drop in pHi.	Diltiazem	61-70	glucose-6-phosphate isomerase	Rattus norvegicus	169-172
2125563-3	1990	The calcium antagonists nifedipine, diltiazem and verapamil partially inhibited endothelin-induced t-PA release, but had no effect on endothelin-induced vWF release.	Diltiazem	36-45	plasminogen activator, tissue type	Rattus norvegicus	99-103
2257435-2	1990	Using front-surface fluorometry with fura-2-loaded porcine coronary arterial strips, we simultaneously measured effects of a Ca2+ antagonist, diltiazem, on cytosolic Ca2+ concentrations [( Ca2+]i) and on tension development.	Diltiazem	142-151	carbonic anhydrase 2	Homo sapiens	125-128
2257435-8	1990	Diltiazem, 10(-8)M to 10(-5)M, concentration-dependently inhibited the second component of [Ca2+]i elevation and tension development induced by histamine (10(-5) M).	Diltiazem	0-9	carbonic anhydrase 2	Homo sapiens	92-95
2257435-9	1990	Only at higher concentrations (over 10(-5) M) did diltiazem inhibit the first component of increases in [Ca2+]i and tension development induced by histamine, both in the presence and absence of extracellular Ca2+.	Diltiazem	50-59	carbonic anhydrase 2	Homo sapiens	105-108
2257435-11	1990	Diltiazem (10(-6) M) inhibited increases in [Ca2+]i and tension development induced by cumulative applications of extracellular Ca2+ during K(+)-depolarization.	Diltiazem	0-9	carbonic anhydrase 2	Homo sapiens	45-48
2257435-11	1990	Diltiazem (10(-6) M) inhibited increases in [Ca2+]i and tension development induced by cumulative applications of extracellular Ca2+ during K(+)-depolarization.	Diltiazem	0-9	carbonic anhydrase 2	Homo sapiens	128-131
2257435-12	1990	The curve of [Ca2+]i against tension of these Ca2(+)-induced contractions obtained in diltiazem-treated strips overlapped with that obtained in untreated strips.	Diltiazem	86-95	carbonic anhydrase 2	Homo sapiens	14-17
2257435-12	1990	The curve of [Ca2+]i against tension of these Ca2(+)-induced contractions obtained in diltiazem-treated strips overlapped with that obtained in untreated strips.	Diltiazem	86-95	carbonic anhydrase 2	Homo sapiens	46-49
2257435-15	1990	In contrast, the histamine-induced Ca2(+)-tension curve (second component) was shifted in parallel to the left by diltiazem.	Diltiazem	114-123	carbonic anhydrase 2	Homo sapiens	35-38
2257435-17	1990	We conclude that diltiazem, at therapeutic concentrations, specifically inhibits extracellular Ca2+- dependent increases in [Ca2 +]i, with no effects on the release of Ca2 + from intracellular store sites or on Ca2 +-sensitivity of the contractile elements involved in the contractions induced by elevations of [Ca2 +]i.	Diltiazem	17-26	carbonic anhydrase 2	Homo sapiens	95-98
2257435-17	1990	We conclude that diltiazem, at therapeutic concentrations, specifically inhibits extracellular Ca2+- dependent increases in [Ca2 +]i, with no effects on the release of Ca2 + from intracellular store sites or on Ca2 +-sensitivity of the contractile elements involved in the contractions induced by elevations of [Ca2 +]i.	Diltiazem	17-26	carbonic anhydrase 2	Homo sapiens	125-128
2257435-17	1990	We conclude that diltiazem, at therapeutic concentrations, specifically inhibits extracellular Ca2+- dependent increases in [Ca2 +]i, with no effects on the release of Ca2 + from intracellular store sites or on Ca2 +-sensitivity of the contractile elements involved in the contractions induced by elevations of [Ca2 +]i.	Diltiazem	17-26	carbonic anhydrase 2	Homo sapiens	125-128
2257435-17	1990	We conclude that diltiazem, at therapeutic concentrations, specifically inhibits extracellular Ca2+- dependent increases in [Ca2 +]i, with no effects on the release of Ca2 + from intracellular store sites or on Ca2 +-sensitivity of the contractile elements involved in the contractions induced by elevations of [Ca2 +]i.	Diltiazem	17-26	carbonic anhydrase 2	Homo sapiens	125-128
2257435-17	1990	We conclude that diltiazem, at therapeutic concentrations, specifically inhibits extracellular Ca2+- dependent increases in [Ca2 +]i, with no effects on the release of Ca2 + from intracellular store sites or on Ca2 +-sensitivity of the contractile elements involved in the contractions induced by elevations of [Ca2 +]i.	Diltiazem	17-26	carbonic anhydrase 2	Homo sapiens	125-128
1884720-8	1991	In the diltiazem group, supine BP was reduced by 10 (11)/10 (6) mmHg (SBP/DBP) at the highest dose level, and the corresponding values for the metoprolol group were 7 (16)/8 (9) mmHg (SBP/DBP).	Diltiazem	7-16	selenium binding protein 1	Homo sapiens	70-73
1884720-8	1991	In the diltiazem group, supine BP was reduced by 10 (11)/10 (6) mmHg (SBP/DBP) at the highest dose level, and the corresponding values for the metoprolol group were 7 (16)/8 (9) mmHg (SBP/DBP).	Diltiazem	7-16	D-box binding PAR bZIP transcription factor	Homo sapiens	74-77
1884720-8	1991	In the diltiazem group, supine BP was reduced by 10 (11)/10 (6) mmHg (SBP/DBP) at the highest dose level, and the corresponding values for the metoprolol group were 7 (16)/8 (9) mmHg (SBP/DBP).	Diltiazem	7-16	selenium binding protein 1	Homo sapiens	184-187
1884720-8	1991	In the diltiazem group, supine BP was reduced by 10 (11)/10 (6) mmHg (SBP/DBP) at the highest dose level, and the corresponding values for the metoprolol group were 7 (16)/8 (9) mmHg (SBP/DBP).	Diltiazem	7-16	D-box binding PAR bZIP transcription factor	Homo sapiens	188-191
2148481-2	1990	Verapamil and diltiazem (0.01 to 5 mM) inhibited both (Ca2+ + Mg2+)-ATPase activity and initial rates of 45Ca2+ net uptake analogously.	Diltiazem	14-23	carbonic anhydrase 2	Homo sapiens	55-58
2148481-2	1990	Verapamil and diltiazem (0.01 to 5 mM) inhibited both (Ca2+ + Mg2+)-ATPase activity and initial rates of 45Ca2+ net uptake analogously.	Diltiazem	14-23	dynein axonemal heavy chain 8	Homo sapiens	68-74
2148481-5	1990	Verapamil and diltiazem inhibited the calmodulin-Ca2+ transport concentration-effect relationship by changing its apparent affinity as well as the maximal velocity of the process.	Diltiazem	14-23	carbonic anhydrase 2	Homo sapiens	49-52
2148481-8	1990	Our results suggest that verapamil, diltiazem and bepridil (0.01 to 0.3 mM), but not nifedipine (1 nM to 0.01 mM), in relatively high concentrations can antagonize the calmodulin-stimulated Ca2(+)-pump, i.e. the ATPase as well as the transport process.	Diltiazem	36-45	carbonic anhydrase 2	Homo sapiens	190-193
2148481-8	1990	Our results suggest that verapamil, diltiazem and bepridil (0.01 to 0.3 mM), but not nifedipine (1 nM to 0.01 mM), in relatively high concentrations can antagonize the calmodulin-stimulated Ca2(+)-pump, i.e. the ATPase as well as the transport process.	Diltiazem	36-45	dynein axonemal heavy chain 8	Homo sapiens	212-218
2095401-9	1990	The results suggest that the dimethylaminoethyl group of diltiazem is oxidized to an aldehyde group by microsomal cytochrome P-450 in the liver.	Diltiazem	57-66	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	114-130
2176795-0	1990	Effects of diltiazem on renin-aldosterone and ACTH-adrenocortical function during upper abdominal surgery.	Diltiazem	11-20	proopiomelanocortin	Homo sapiens	46-50
2176795-1	1990	STUDY OBJECTIVE: To observe the effects of continuous intravenous infusion of diltiazem on the renin-aldosterone system and ACTH-adrenocortical axis responses during surgical stimulation.	Diltiazem	78-87	renin	Homo sapiens	95-100
2176795-10	1990	Adrenocorticotropic hormone was significantly lower in the diltiazem group compared with that in the control group 60 minutes after the start of surgery (p less than 0.05).	Diltiazem	59-68	proopiomelanocortin	Homo sapiens	0-27
2145465-7	1990	It is concluded that 1,4-dihydropyridines and verapamil and diltiazem did differently influence Ca2(+)-mediated increase in force of contraction.	Diltiazem	60-69	carbonic anhydrase 2	Homo sapiens	96-99
2077185-6	1990	Nifedipine, diltiazem and verapamil showed a slight preventive effect on the cholesterol accumulation and on the reduction of elastin content in the aorta without a cholesterol lowering effect in the serum.	Diltiazem	12-21	elastin	Mus musculus	126-133
2169937-7	1990	Nicergoline and other Ca2+ antagonists dose-dependently blocked the T-type Ca2+ channel with an order of potency nicardipine greater than nicergoline greater than diltiazem.	Diltiazem	163-172	carbonic anhydrase 2	Rattus norvegicus	22-25
2169937-7	1990	Nicergoline and other Ca2+ antagonists dose-dependently blocked the T-type Ca2+ channel with an order of potency nicardipine greater than nicergoline greater than diltiazem.	Diltiazem	163-172	carbonic anhydrase 2	Rattus norvegicus	75-78
2169937-9	1990	The L-type Ca2+ channel was also blocked in the order nicardipine greater than nicergoline greater than diltiazem, although the T-type Ca2+ channel was more sensitive to nicergoline.	Diltiazem	104-113	carbonic anhydrase 2	Rattus norvegicus	11-14
2382217-10	1990	However, both doses of diltiazem significantly improved peritoneal macrophage antigen presentation, Ia expression, and IL-1 synthesis.	Diltiazem	23-32	interleukin 1 complex	Mus musculus	119-123
2382217-11	1990	IL-6 synthesis was only increased with high doses of diltiazem, whereas both diltiazem doses decreased TNF production.	Diltiazem	53-62	interleukin 6	Mus musculus	0-4
2382217-11	1990	IL-6 synthesis was only increased with high doses of diltiazem, whereas both diltiazem doses decreased TNF production.	Diltiazem	77-86	tumor necrosis factor	Mus musculus	103-106
2232165-7	1990	The marked reduction of stimulation-evoked pressor responses and norepinephrine release by diltiazem suggests that enhanced Ca2(+)-dependent adrenergic transmission may contribute to the exaggerated vascular sympathetic tone in salt-dependent hypertension.	Diltiazem	91-100	carbonic anhydrase 2	Rattus norvegicus	124-127
2159405-6	1990	Inhibition of voltage-dependent calcium influx by diltiazem also antagonized the effect of EGF.	Diltiazem	50-59	epidermal growth factor	Gallus gallus	91-94
2166422-1	1990	We previously showed that the calcium channel blocker diltiazem raises cytosolic Ca2+ and inhibits PTH release in bovine parathyroid cells.	Diltiazem	54-63	parathyroid hormone	Bos taurus	99-102
2166422-3	1990	Like diltiazem, TA-3090 (10(-6)-10(-4] produced a dose-dependent inhibition of immunoreactive PTH release at 0.5 mM Ca2+ and raised the cytosolic Ca2+ concentration by 25-50% in fura-2-loaded parathyroid cells in the presence but not in the absence of extracellular Ca2+, suggesting that it activated rather than inhibited Ca2+ channels.	Diltiazem	5-14	parathyroid hormone	Bos taurus	94-97
2140394-5	1990	IFN-gamma caused a rapid and concentration-dependent increase in [Ca2+]i, which was partly inhibited by calcium-free medium, diltiazem, and TMB-8.	Diltiazem	125-134	interferon gamma	Homo sapiens	0-9
2159347-6	1990	Other calcium antagonists such as diltiazem, nifedipine, nitrendipine or amphiphilic drugs such as phenothiazines and propranolol also enhanced HDL3 uptake by Hep G2 cells.	Diltiazem	34-43	HDL3	Homo sapiens	144-148
2353130-4	1990	ALT remained close to control values 48 hours after the administration of the 24 mg/kg dose of diltiazem.	Diltiazem	95-104	glutamic pyruvic transaminase, soluble	Mus musculus	0-3
2353130-6	1990	Diltiazem (24 mg/kg) reduced the increase in ALT induced by 1.1 mg/kg of phalloidine by 58% (4460 +/- 317 U/mL v.s.	Diltiazem	0-9	glutamic pyruvic transaminase, soluble	Mus musculus	45-48
2184913-16	1990	Two out of five diltiazem-treated dogs died of ventricular fibrillation with a mean time to death of 20 min following treatment with ET-1 (300 kg- 1).	Diltiazem	16-25	endothelin 1	Canis lupus familiaris	133-137
1706010-7	1990	Sustained-release diltiazem is effective as monotherapy at single daily doses of 300 mg as evidenced by an effect/dose study in 105 patients: DBP = -17 mm Hg with 300 mg (72% of the patients responded to this dosage).	Diltiazem	18-27	D-box binding PAR bZIP transcription factor	Homo sapiens	142-145
1706014-3	1990	In the groups treated with diltiazem, enalapril, or the combination of both, the drop in arterial blood pressure was 20, 11, and 19 mm Hg for supine diastolic blood pressure (supine DBP): 18, 12, and 19 mm Hg for standing diastolic blood pressure (standing DBP); 22, 20, and 23 mm Hg for supine systolic blood pressure (supine SBP); and 21, 19, and 24 mm Hg for standing systolic blood pressure (standing SBP), respectively.	Diltiazem	27-36	D-box binding PAR bZIP transcription factor	Homo sapiens	182-185
1706014-3	1990	In the groups treated with diltiazem, enalapril, or the combination of both, the drop in arterial blood pressure was 20, 11, and 19 mm Hg for supine diastolic blood pressure (supine DBP): 18, 12, and 19 mm Hg for standing diastolic blood pressure (standing DBP); 22, 20, and 23 mm Hg for supine systolic blood pressure (supine SBP); and 21, 19, and 24 mm Hg for standing systolic blood pressure (standing SBP), respectively.	Diltiazem	27-36	D-box binding PAR bZIP transcription factor	Homo sapiens	257-260
1706014-3	1990	In the groups treated with diltiazem, enalapril, or the combination of both, the drop in arterial blood pressure was 20, 11, and 19 mm Hg for supine diastolic blood pressure (supine DBP): 18, 12, and 19 mm Hg for standing diastolic blood pressure (standing DBP); 22, 20, and 23 mm Hg for supine systolic blood pressure (supine SBP); and 21, 19, and 24 mm Hg for standing systolic blood pressure (standing SBP), respectively.	Diltiazem	27-36	selenium binding protein 1	Homo sapiens	327-330
1706014-3	1990	In the groups treated with diltiazem, enalapril, or the combination of both, the drop in arterial blood pressure was 20, 11, and 19 mm Hg for supine diastolic blood pressure (supine DBP): 18, 12, and 19 mm Hg for standing diastolic blood pressure (standing DBP); 22, 20, and 23 mm Hg for supine systolic blood pressure (supine SBP); and 21, 19, and 24 mm Hg for standing systolic blood pressure (standing SBP), respectively.	Diltiazem	27-36	selenium binding protein 1	Homo sapiens	405-408
1706014-4	1990	The reduction in DBP was significantly more pronounced in the group treated with sustained-release diltiazem 300 mg than in the group treated with enalapril 20 mg. Cardiac tolerance was good for patients treated with sustained-release diltiazem 300 mg alone or the combination therapy: no orthostatic hypotension or lengthening of the PR interval in the electrocardiogram was observed.	Diltiazem	99-108	D-box binding PAR bZIP transcription factor	Homo sapiens	17-20
1706014-4	1990	The reduction in DBP was significantly more pronounced in the group treated with sustained-release diltiazem 300 mg than in the group treated with enalapril 20 mg. Cardiac tolerance was good for patients treated with sustained-release diltiazem 300 mg alone or the combination therapy: no orthostatic hypotension or lengthening of the PR interval in the electrocardiogram was observed.	Diltiazem	235-244	D-box binding PAR bZIP transcription factor	Homo sapiens	17-20
1706015-9	1990	Moreover, on day 90, blood pressure values were maintained in the diuretic-treated group, whereas an additional significant reduction in supine DBP (p less than 0.002) was noted in the sustained-release diltiazem 300 mg-treated group (-4.8 mm Hg).	Diltiazem	203-212	D-box binding PAR bZIP transcription factor	Homo sapiens	144-147
2184938-7	1990	ACE inhibitors may apparently enhance the effectiveness of diltiazem in normotensive patients with angina pectoris and it may be assumed that it will have an even more potent effect in concurrent hypertension or left ventricular dysfunction.	Diltiazem	59-68	angiotensin I converting enzyme	Homo sapiens	0-3
2184913-0	1990	The effect of diltiazem on the coronary haemodynamic and cardiac functional effects produced by intracoronary administration of endothelin-1 in the anaesthetized dog.	Diltiazem	14-23	endothelin 1	Canis lupus familiaris	128-140
2184913-15	1990	Although there was a general trend for diltiazem to inhibit the coronary vasoconstrictor responses to ET-1, diltiazem significantly attenuated only the reduction in coronary blood flow produced by 100 ng kg-1 ET-1 by 60% but not the response to 30 or 300 ng kg-1 ET-1.	Diltiazem	39-48	endothelin 1	Canis lupus familiaris	102-106
2184913-15	1990	Although there was a general trend for diltiazem to inhibit the coronary vasoconstrictor responses to ET-1, diltiazem significantly attenuated only the reduction in coronary blood flow produced by 100 ng kg-1 ET-1 by 60% but not the response to 30 or 300 ng kg-1 ET-1.	Diltiazem	108-117	endothelin 1	Canis lupus familiaris	209-213
2184913-15	1990	Although there was a general trend for diltiazem to inhibit the coronary vasoconstrictor responses to ET-1, diltiazem significantly attenuated only the reduction in coronary blood flow produced by 100 ng kg-1 ET-1 by 60% but not the response to 30 or 300 ng kg-1 ET-1.	Diltiazem	108-117	endothelin 1	Canis lupus familiaris	209-213
1967551-7	1990	Modulators of Pgp-MDR also compete with LU-49888 for binding to Pgp: verapamil (82%), diltiazem (73%), quinidine (91%), reserpine (91%), rescinnamine (88%), and trimethoxybenzoylyohimbine (89%).	Diltiazem	86-95	ATP binding cassette subfamily B member 1	Homo sapiens	14-17
1967551-7	1990	Modulators of Pgp-MDR also compete with LU-49888 for binding to Pgp: verapamil (82%), diltiazem (73%), quinidine (91%), reserpine (91%), rescinnamine (88%), and trimethoxybenzoylyohimbine (89%).	Diltiazem	86-95	ATP binding cassette subfamily B member 1	Homo sapiens	64-67
1689966-4	1990	Cellular Ca2+ was modified by adding a Ca2+ agonist (BAY K 8644) and/or Ca2+ antagonists (nifedipine, nitrendipine, diltiazem) to the "load" and "wash" media.	Diltiazem	116-125	carbonic anhydrase 2	Rattus norvegicus	9-12
1970270-9	1990	In the presence of either nitrendipine (10(-6) M) or diltiazem (10(-5) M), NPY (100 nM) did not alter the concentration-response curves to either noradrenaline or phenylephrine.	Diltiazem	53-62	neuropeptide Y	Rattus norvegicus	75-78
1688825-4	1990	We found that three different calcium channel blockers, diltiazem, nifedipine, and verapamil, were able to significantly inhibit [3H]thymidine incorporation into human mesangial cells induced by either PDGF or thrombin.	Diltiazem	56-65	coagulation factor II, thrombin	Homo sapiens	210-218
2279694-4	1990	Results showed that diltiazem inhibits platelet aggregation induced by ADP, arginine vasopressin, adrenaline, collagen, Na arachidonate, thrombin and phorbol ester PMA in a dose-dependent way.	Diltiazem	20-29	arginine vasopressin	Homo sapiens	85-96
2279694-4	1990	Results showed that diltiazem inhibits platelet aggregation induced by ADP, arginine vasopressin, adrenaline, collagen, Na arachidonate, thrombin and phorbol ester PMA in a dose-dependent way.	Diltiazem	20-29	coagulation factor II, thrombin	Homo sapiens	137-145
2279694-6	1990	Diltiazem decreased also beta-thromboglobulin release and Thromboxane B2 production from stimulated platelets.	Diltiazem	0-9	pro-platelet basic protein	Homo sapiens	25-45
1688546-3	1990	When cardiocytes were treated with the calcium channel blockers diltiazem, nifedipine, or verapamil, both ANF synthesis and secretion fell to 25-40% of control values.	Diltiazem	64-73	natriuretic peptide A	Rattus norvegicus	106-109
2405151-11	1990	The pressor effects of ET-1 were reduced by diltiazem, nitrendipine, verapamil or cromakalim and unchanged after BW 755c, desipramine, enalapril, indomethacin, methysergide, phentolamine or SK&F 100273.	Diltiazem	44-53	endothelin 1	Rattus norvegicus	23-27
35203062-9	2022	The suppression of ANP secretion by CORM-2 was attenuated by pretreatment with 5-hydroxydecanoic acid, paxilline, and 1H-(1,2,4) oxadiazolo (4,3-a) quinoxalin-1-one, but not by diltiazem, wortmannin, LY-294002, or NG-nitro-L-arginine methyl ester.	Diltiazem	177-186	natriuretic peptide A	Rattus norvegicus	19-22
34503976-6	2021	Further pharmacokinetic studies of diltiazem, a typical substrate of CES2A, confirmed the loss of function of CES2A both in vivo and in vitro.	Diltiazem	35-44	carboxylesterase 2A	Rattus norvegicus	69-74
34503976-6	2021	Further pharmacokinetic studies of diltiazem, a typical substrate of CES2A, confirmed the loss of function of CES2A both in vivo and in vitro.	Diltiazem	35-44	carboxylesterase 2A	Rattus norvegicus	110-115
34276002-0	2021	Diltiazem Inhibits Coronary Spasm via Inhibition of Cav1.2Phosphorylation and Protein Kinase C Activation in a Mouse Model of Coronary Spastic Angina.	Diltiazem	0-9	calcium channel, voltage-dependent, L type, alpha 1C subunit	Mus musculus	52-58
34276002-6	2021	DL treatment significantly inhibited Cav1.2 phosphorylation and PKC activity.	Diltiazem	0-2	calcium channel, voltage-dependent, L type, alpha 1C subunit	Mus musculus	37-43
34276002-6	2021	DL treatment significantly inhibited Cav1.2 phosphorylation and PKC activity.	Diltiazem	0-2	protein kinase C, gamma	Rattus norvegicus	64-67
34276002-7	2021	Although total Cav1.2 expression was similar between WT and PLC-TG mice treated with TM, DL treatment significantly increased its expression in PLC-TG mice.	Diltiazem	89-91	calcium channel, voltage-dependent, L type, alpha 1C subunit	Mus musculus	15-21
34276002-9	2021	DL and PKC inhibitor suppressed intracellular calcium response to acetylcholine in cultured rat aortic smooth muscle cells transfected with variant PLC-delta1.These results indicate that enhanced PLC activity causes coronary spasm, presumably via enhanced Cav1.2 phosphorylation and PKC activity, both of which were inhibited by DL.	Diltiazem	329-331	protein kinase C, gamma	Rattus norvegicus	7-10
34276002-9	2021	DL and PKC inhibitor suppressed intracellular calcium response to acetylcholine in cultured rat aortic smooth muscle cells transfected with variant PLC-delta1.These results indicate that enhanced PLC activity causes coronary spasm, presumably via enhanced Cav1.2 phosphorylation and PKC activity, both of which were inhibited by DL.	Diltiazem	329-331	phospholipase C, delta 1	Rattus norvegicus	148-158
34276002-9	2021	DL and PKC inhibitor suppressed intracellular calcium response to acetylcholine in cultured rat aortic smooth muscle cells transfected with variant PLC-delta1.These results indicate that enhanced PLC activity causes coronary spasm, presumably via enhanced Cav1.2 phosphorylation and PKC activity, both of which were inhibited by DL.	Diltiazem	329-331	calcium channel, voltage-dependent, L type, alpha 1C subunit	Mus musculus	256-262
34276002-9	2021	DL and PKC inhibitor suppressed intracellular calcium response to acetylcholine in cultured rat aortic smooth muscle cells transfected with variant PLC-delta1.These results indicate that enhanced PLC activity causes coronary spasm, presumably via enhanced Cav1.2 phosphorylation and PKC activity, both of which were inhibited by DL.	Diltiazem	329-331	protein kinase C, gamma	Rattus norvegicus	283-286
25661249-0	2015	Protective effects of diltiazem against vascular endothelial cell injury induced by angiotensin-II and hypoxia.	Diltiazem	22-31	angiotensinogen	Rattus norvegicus	84-98
25661249-4	2015	Our study showed that AngII and hypoxia decreased the mitochondrial membrane potential in VEC, which was significantly inhibited by diltiazem.	Diltiazem	132-141	angiotensinogen	Rattus norvegicus	22-27
25661249-5	2015	Diltiazem protected against VEC injury induced by the increased concentration of intracellular free calcium, which was associated with AngII and hypoxia.	Diltiazem	0-9	angiotensinogen	Rattus norvegicus	135-140
25661249-9	2015	Diltiazem, a calcium channel blocker, protected VEC from AngII- and hypoxia-induced injury.	Diltiazem	0-9	angiotensinogen	Rattus norvegicus	57-62
1808624-2	1991	Our results showed that diltiazem inhibits collagen- and thrombin-induced platelet aggregation and TXB2 production from PRP.	Diltiazem	24-33	coagulation factor II, thrombin	Homo sapiens	57-65
1808624-3	1991	Since no significant interference with conversion of arachidonate to thromboxane A2 was demonstrated, inhibition of phospholipase A2 activity may be the prevailing mechanism of the diltiazem effect.	Diltiazem	181-190	phospholipase A2 group IB	Homo sapiens	116-132
35502121-2	2022	METHODS: A retrospective new-user cohort study design was used to identify (N=160828) patients who concurrently initiated CYP3A4-inhibitors (diltiazem, ketoconazole, clarithromycin, others) and CYP3A4-metabolized statins (statin DDI exposed, n = 104774) vs. other statins (unexposed to statin DDI, n = 56054) from the MarketScan Commercial claims database (2012 - 2017).	Diltiazem	141-150	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	122-128
35248545-6	2022	In order to scrutinize known Ca2+ channel blockers for their ability to bind at the pore region of TRPC1, 31 known compounds were tested through docking runs and three hits, named as diltiazem impurity B (b3), diltiazem (b5) and felodipine (b6) were selected for detailed binding analysis through MD runs.	Diltiazem	183-192	transient receptor potential cation channel subfamily C member 1	Homo sapiens	99-104
35248545-6	2022	In order to scrutinize known Ca2+ channel blockers for their ability to bind at the pore region of TRPC1, 31 known compounds were tested through docking runs and three hits, named as diltiazem impurity B (b3), diltiazem (b5) and felodipine (b6) were selected for detailed binding analysis through MD runs.	Diltiazem	210-219	transient receptor potential cation channel subfamily C member 1	Homo sapiens	99-104
35176124-3	2022	We found that diltiazem, a blocker of the L-type calcium channel Cav1.2 pore-forming subunit (Cav1.2 alpha1c) and an FDA-approved drug, inhibits the binding and internalization of SARS-CoV-2, and decreases SARS-CoV-2 infection in cells and mouse lung.	Diltiazem	14-23	calcium voltage-gated channel subunit alpha1 C	Homo sapiens	65-71
35386137-2	2022	We set out to compare the risk for hemorrhage following initiation of amiodarone, verapamil, or diltiazem (moderate cytochrome P450 3A4 and/or P-glycoprotein activity) vs metoprolol or amlodipine (weak or no activity), among older adults prescribed DOACs.	Diltiazem	96-105	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	116-135
2686646-2	1989	Potent inhibition of IL-8-induced migration was observed in response to nifedipine (IC50 = 10 nM), verapamil (IC50 = 60 nM) and diltiazem (IC50 = 10 nM).	Diltiazem	128-137	C-X-C motif chemokine ligand 8	Homo sapiens	21-25
2555195-5	1989	When the calcium channel-blocking drugs, either verapamil or diltiazem, were withdrawn or when exogenous Ca2+ was added to the Ca2+-free medium, EBV-induced B cell activation was noted, demonstrating the reversibility of the inhibition.	Diltiazem	61-70	B cell linker	Homo sapiens	157-174
2688978-5	1989	There was a diltiazem-related reduction in cardiac death (Cox hazard ratio, 0.76-0.86) for each of the parameters reflecting good ventricular function, and a significant diltiazem-related increase in cardiac death (Cox hazard ratio, 1.52-1.85) for each of the parameters associated with impaired function.	Diltiazem	12-21	cytochrome c oxidase subunit 8A	Homo sapiens	58-61
2688978-5	1989	There was a diltiazem-related reduction in cardiac death (Cox hazard ratio, 0.76-0.86) for each of the parameters reflecting good ventricular function, and a significant diltiazem-related increase in cardiac death (Cox hazard ratio, 1.52-1.85) for each of the parameters associated with impaired function.	Diltiazem	170-179	cytochrome c oxidase subunit 8A	Homo sapiens	215-218
2597113-0	1989	Inhibition of apolipoprotein B net synthesis and secretion from cultured rat hepatocytes by the calcium-channel blocker diltiazem.	Diltiazem	120-129	apolipoprotein B	Rattus norvegicus	14-30
2597113-2	1989	The effect of the Ca2+-channel blocker diltiazem on hepatic apolipoprotein B (apo B) synthesis and secretion was studied in 12-18 h cultures of collagenase-dispersed rat hepatocytes.	Diltiazem	39-48	apolipoprotein B	Rattus norvegicus	60-76
2597113-2	1989	The effect of the Ca2+-channel blocker diltiazem on hepatic apolipoprotein B (apo B) synthesis and secretion was studied in 12-18 h cultures of collagenase-dispersed rat hepatocytes.	Diltiazem	39-48	apolipoprotein B	Rattus norvegicus	78-83
2597113-4	1989	The presence of diltiazem in the medium decreased apo B secretion by hepatocytes in a concentration-dependent manner.	Diltiazem	16-25	apolipoprotein B	Rattus norvegicus	50-55
2597113-5	1989	At 25 microM, diltiazem inhibited apo B secretion by approx.	Diltiazem	14-23	apolipoprotein B	Rattus norvegicus	34-39
2597113-8	1989	The inhibition of apo B secretion by hepatocytes was significantly correlated with cell-associated diltiazem (r = 0.72, P less than 0.01).	Diltiazem	99-108	apolipoprotein B	Rattus norvegicus	18-23
2569930-6	1989	The photolabeling of P-glycoprotein with N-[benzoyl-3,5-3H]-(+/-)-5-[(3,4-dimethoxyphenetyl)methylamino]-2- (3,4-dimethoxyphenyl)-2-isopropyl-N-p-azidobenzoylphentylamine was significantly blocked by other calcium channel blockers, nicardipine and diltiazem, that have been shown to overcome multidrug resistance.	Diltiazem	248-257	ATP binding cassette subfamily B member 1	Homo sapiens	21-35
2684314-6	1989	Preincubation of tissues for 60 min with diltiazem (1 microM) induced a significant 3 fold rightward shift of concentration-effect curves to ET-1 without affecting maximal responses elicited by 10 nM of this peptide, whereas the same treatment failed to modify concentration-effect curves to [Ala3,11]ET-1.	Diltiazem	41-50	endothelin 1	Rattus norvegicus	141-145
2684314-6	1989	Preincubation of tissues for 60 min with diltiazem (1 microM) induced a significant 3 fold rightward shift of concentration-effect curves to ET-1 without affecting maximal responses elicited by 10 nM of this peptide, whereas the same treatment failed to modify concentration-effect curves to [Ala3,11]ET-1.	Diltiazem	41-50	endothelin 1	Rattus norvegicus	301-305
2504305-10	1989	A calcium channel blocker (diltiazem) blocked the increased levels of GM-CSF mRNA mediated by ouabain, but could not block the stimulation mediated by TNF alpha.	Diltiazem	27-36	colony stimulating factor 2	Homo sapiens	70-76
2553324-14	1989	Effects of low [Ca2+], diltiazem and TMB-8 on renin secretion were all shown to be reversible when superfusion with control buffer was resumed.	Diltiazem	23-32	renin	Rattus norvegicus	46-51
2553324-7	1989	The Ca2+ entry blocking drug diltiazem in a range of concentrations increased renin release and at 10(-5) mol/l diltiazem the mean stimulation was 35% (P less than 0.01).	Diltiazem	29-38	renin	Rattus norvegicus	78-83
2597113-10	1989	The rate of apo B secretion remained linear over 16 h even in the presence of 50 microM-diltiazem.	Diltiazem	88-97	apolipoprotein B	Rattus norvegicus	12-17
2597113-12	1989	At diltiazem concentrations in the medium which were inhibitory for apo B secretion, [14C]acetate incorporation into cellular lipids and [35S]methionine incorporation into protein were enhanced.	Diltiazem	3-12	apolipoprotein B	Rattus norvegicus	68-73
2764137-6	1989	Only at high concentrations did verapamil (IC50 = 8.7 microM) and diltiazem (IC50 = 95.7 microM) inhibit the Ca2+ release from the cellular store sites, as induced by 10 microM histamine.	Diltiazem	66-75	carbonic anhydrase 2	Rattus norvegicus	109-112
2764137-8	1989	From these results, we conclude that verapamil and diltiazem strongly inhibit the histamine-mediated, extracellular Ca2+-dependent intracellular [Ca2+] increase.	Diltiazem	51-60	carbonic anhydrase 2	Rattus norvegicus	116-119
2764137-8	1989	From these results, we conclude that verapamil and diltiazem strongly inhibit the histamine-mediated, extracellular Ca2+-dependent intracellular [Ca2+] increase.	Diltiazem	51-60	carbonic anhydrase 2	Rattus norvegicus	146-149
2764137-9	1989	In addition, verapamil and diltiazem seem to inhibit the release of Ca2+ from intracellular store sites, only at high concentrations, and probably by competing with histamine for binding to the H1-receptor.	Diltiazem	27-36	carbonic anhydrase 2	Rattus norvegicus	68-71
2519888-6	1989	In decreasing order of potency, the following PAF-acether antagonists inhibited the change in platelet cytosolic free calcium elicited by 10 nM PAF-acether: L-652,731, kadsurenone, triazolam, diltiazem and alprazolam.	Diltiazem	192-201	PCNA clamp associated factor	Homo sapiens	46-49
2597113-14	1989	Diltiazem inhibited the secretion of the apo B variants with a preferential inhibition of the higher-molecular-mass form of apo B (apo BH) over the lower-molecular-mass form (apo BL) at diltiazem concentrations in the medium greater than 25 microM.	Diltiazem	0-9	apolipoprotein B	Rattus norvegicus	41-46
2597113-14	1989	Diltiazem inhibited the secretion of the apo B variants with a preferential inhibition of the higher-molecular-mass form of apo B (apo BH) over the lower-molecular-mass form (apo BL) at diltiazem concentrations in the medium greater than 25 microM.	Diltiazem	0-9	apolipoprotein B	Rattus norvegicus	124-129
2597113-14	1989	Diltiazem inhibited the secretion of the apo B variants with a preferential inhibition of the higher-molecular-mass form of apo B (apo BH) over the lower-molecular-mass form (apo BL) at diltiazem concentrations in the medium greater than 25 microM.	Diltiazem	186-195	apolipoprotein B	Rattus norvegicus	41-46
2510664-10	1989	The decline in both SBP and DBP with diltiazem was significantly related to their control values (r = 0.31 and 0.28 respectively, p less than 0.0001 for both).	Diltiazem	37-46	selenium binding protein 1	Homo sapiens	20-23
2510664-10	1989	The decline in both SBP and DBP with diltiazem was significantly related to their control values (r = 0.31 and 0.28 respectively, p less than 0.0001 for both).	Diltiazem	37-46	D-box binding PAR bZIP transcription factor	Homo sapiens	28-31
2544103-8	1989	In the presence of either verapamil or diltiazem, the effect of ANG II to decrease efferent diameter was sustained (-15 +/- 4%); however, the effect of ANG II on afferent diameter was abolished (-1 +/- 1%).	Diltiazem	39-48	angiotensinogen	Rattus norvegicus	64-70
2570876-3	1989	The positive inotropic effect of SS was accompanied by a significant enhancement of the slow action potentials and was suppressed by diltiazem and phentolamine.	Diltiazem	133-142	somatostatin	Cavia porcellus	33-35
2635255-5	1989	Both diltiazem and atenolol significantly decreased heart rate at peak effort but the decrease was much more pronounced after atenolol (-52 b.min-1) than after diltiazem (-6 b.min-1).	Diltiazem	5-14	CD59 molecule (CD59 blood group)	Homo sapiens	142-147
2635255-5	1989	Both diltiazem and atenolol significantly decreased heart rate at peak effort but the decrease was much more pronounced after atenolol (-52 b.min-1) than after diltiazem (-6 b.min-1).	Diltiazem	5-14	CD59 molecule (CD59 blood group)	Homo sapiens	176-181
2668407-8	1989	The insulin peak was decreased by 13% during diltiazem treatment (P less than 0.05).	Diltiazem	45-54	insulin	Homo sapiens	4-11
2751676-4	1989	The extent of enhancement was different for the two drugs, and up to a 9- to 10-fold increase in harringtonine cytotoxicity occurred in P388/ADM cells, and 14- to 22-fold enhancement in K562/ADM cells with diltiazem or cepharanthine.	Diltiazem	206-215	adrenomedullin	Homo sapiens	186-194
2751676-5	1989	Harringtonine resistance of P388/ADM was circumvented completely, and the resistance of K562/ADM was circumvented partially, by diltiazem or cepharanthine.	Diltiazem	128-137	adrenomedullin	Homo sapiens	88-96
2751676-6	1989	The mechanism of enhanced cytotoxicity by diltiazem and cepharanthine is probably inhibition of active efflux of harringtonine in P388/ADM and K562/ADM cells.	Diltiazem	42-51	adrenomedullin	Homo sapiens	135-138
2751676-6	1989	The mechanism of enhanced cytotoxicity by diltiazem and cepharanthine is probably inhibition of active efflux of harringtonine in P388/ADM and K562/ADM cells.	Diltiazem	42-51	adrenomedullin	Homo sapiens	143-151
2723023-1	1989	PTH secretion is inversely related to the extracellular and cytosolic calcium (Ca2+) concentrations and, therefore, might be affected by calcium channel blockers such as diltiazem.	Diltiazem	170-179	parathyroid hormone	Bos taurus	0-3
2723023-3	1989	Diltiazem lowered serum PTH levels from 1.07 +/- 0.07 to 0.87 +/- 0.07 pg/L (P = 0.001), and increased urinary calcium and decreased urinary phosphate excretion (P less than 0.001 and P less than 0.01, respectively).	Diltiazem	0-9	parathyroid hormone	Bos taurus	24-27
2723023-6	1989	Regression analysis of PTH released vs. the concentration of diltiazem (10(-7)-10(-4) mol/L) revealed a significant negative relationship (P less than 0.01) with 40% inhibition of PTH release at 10(-4) mol/L (P less than 0.01).	Diltiazem	61-70	parathyroid hormone	Bos taurus	180-183
2723023-8	1989	In summary, diltiazem lowered PTH levels in vivo and in vitro, perhaps acting as a Ca2+ channel agonist in the parathyroid cell and inhibiting PTH release through a rise in the cytosolic Ca2+ concentration.	Diltiazem	12-21	parathyroid hormone	Bos taurus	30-33
2723023-8	1989	In summary, diltiazem lowered PTH levels in vivo and in vitro, perhaps acting as a Ca2+ channel agonist in the parathyroid cell and inhibiting PTH release through a rise in the cytosolic Ca2+ concentration.	Diltiazem	12-21	parathyroid hormone	Bos taurus	143-146
2723639-6	1989	On the other hand, diltiazem, which is a more potent blocker of the release of Ca2+ from the mitochondria, inhibited the increasing cytosolic free Ca2+ concentration at the third phase in a concentration-dependent manner.	Diltiazem	19-28	carbonic anhydrase 2	Rattus norvegicus	79-82
2723639-6	1989	On the other hand, diltiazem, which is a more potent blocker of the release of Ca2+ from the mitochondria, inhibited the increasing cytosolic free Ca2+ concentration at the third phase in a concentration-dependent manner.	Diltiazem	19-28	carbonic anhydrase 2	Rattus norvegicus	147-150
9301913-0	1989	[A clinical study of diltiazem administration using cold glucose-insulin-potassium cardioplegic solution--comparison between diltiazem cardioplegia and diltiazem pretreatment].	Diltiazem	21-30	insulin	Homo sapiens	65-72
2519888-6	1989	In decreasing order of potency, the following PAF-acether antagonists inhibited the change in platelet cytosolic free calcium elicited by 10 nM PAF-acether: L-652,731, kadsurenone, triazolam, diltiazem and alprazolam.	Diltiazem	192-201	PCNA clamp associated factor	Homo sapiens	144-147
2713221-0	1989	Effects of atenolol vs diltiazem on the haemodynamic effects of an inhaled beta 2-adrenoceptor agonist.	Diltiazem	23-32	adrenoceptor beta 2	Homo sapiens	75-94
2792166-6	1989	In these 6 volunteers, intake of diltiazem (240 mg daily), concurrently with rifampicin for a week, significantly elevated theophylline half-life to 6.2 h as well as reduced its clearance to 1.03 ml.min-1.kg-1.	Diltiazem	33-42	CD59 molecule (CD59 blood group)	Homo sapiens	199-204
2657057-4	1989	Verapamil increased fasting serum immunoreactive insulin: diltiazem and propranolol tended to reduce it.	Diltiazem	58-67	insulin	Homo sapiens	49-56
2687079-6	1989	These effects of LH-RH were affected by phentolamine and diltiazem but not by propranolol and cold condition.	Diltiazem	57-66	progonadoliberin-1	Cavia porcellus	17-22
2848686-3	1988	The positive inotropic effect of TRH was associated with an augmentation of slow action potentials in high K+ solution and was reduced in the presence of diltiazem, verapamil, and manganese.	Diltiazem	154-163	thyrotropin releasing hormone	Cavia porcellus	33-36
2473323-6	1989	Relaxation of ET-1-induced and NE-induced contractions by diltiazem was not complete (maximal at 58 +/- 6% with 10 microM diltiazem after 6 nM ET-1, and at 70 +/- 3% after 0.1 microM NE), in contrast to that of 80 mM K+-induced contractions, which were potently (IC50 = 0.2 microM) and completely reversed (100% relaxation at 10 microM diltiazem).	Diltiazem	58-67	endothelin 1	Rattus norvegicus	14-18
2853992-0	1988	Release of growth hormone from purified somatotrophs: effects of the calcium channel antagonists diltiazem and nifedipine on release induced by growth hormone-releasing factor.	Diltiazem	97-106	growth hormone releasing hormone	Homo sapiens	144-175
2853992-1	1988	We examined the effect of the voltage-sensitive Ca2+ channel antagonists, diltiazem and nifedipine, on basal and stimulated growth hormone (GH) release from purified somatotrophs.	Diltiazem	74-83	growth hormone 1	Homo sapiens	124-138
2853992-4	1988	The release of GH induced by 29 mM K+ was blocked by diltiazem and nifedipine, at 10(-7) and 10(-8) M, respectively.	Diltiazem	53-62	growth hormone 1	Homo sapiens	15-17
2853992-6	1988	The release of GH induced by growth hormone-releasing factor was significantly reduced by 10(-4) M diltiazem and completely blocked by nifedipine at a concentration of 10(-6) M or greater.	Diltiazem	99-108	growth hormone 1	Homo sapiens	15-17
2853992-6	1988	The release of GH induced by growth hormone-releasing factor was significantly reduced by 10(-4) M diltiazem and completely blocked by nifedipine at a concentration of 10(-6) M or greater.	Diltiazem	99-108	growth hormone releasing hormone	Homo sapiens	29-60
2899840-4	1988	There were 11 percent fewer first recurrent cardiac events (death from cardiac causes or nonfatal reinfarction) in the diltiazem group than in the placebo group (202 vs. 226; Cox hazard ratio, 0.90; 95 percent confidence limits, 0.74 and 1.08).	Diltiazem	119-128	cytochrome c oxidase subunit 8A	Homo sapiens	175-178
3416553-3	1988	We tested the effect of a calcium entry-blocking agent, diltiazem, on AA-PAF-induced platelet aggregation in platelet-rich plasma from seven healthy volunteers.	Diltiazem	56-65	PCNA clamp associated factor	Homo sapiens	73-76
3416553-7	1988	When PAF was used the inhibition of aggregation was obtained at a lower concentration of diltiazem (0.4 to 1 microgram/ml).	Diltiazem	89-98	PCNA clamp associated factor	Homo sapiens	5-8
3416553-10	1988	Diltiazem added in vitro at the clinically attainable concentration of 0.1 microgram/ml produced a complete inhibition of this AA-PAF synergism on platelet aggregation.	Diltiazem	0-9	PCNA clamp associated factor	Homo sapiens	130-133
3207972-8	1988	Verapamil, azelastine, diltiazem and TMB-8 (each 10 microM) significantly attenuated PLA2-induced AH.	Diltiazem	23-32	phospholipase A2 group IB	Rattus norvegicus	85-89
3404443-3	1988	Omission of Ca++ (1.8 mM) or addition of Ca++ channel blockers, diltiazem (60 microM) or nifedipine (1.4 microM), to the perfusion fluid abolished the effects of NPY to promote renal vasoconstriction and PG synthesis.	Diltiazem	64-73	neuropeptide Y	Rattus norvegicus	162-165
3381103-3	1988	The increase was dependent on extracellular calcium and was inhibited by the antagonistic PAF analog CV-3988 and by the calcium-influx blockers prenylamine and diltiazem.	Diltiazem	160-169	PCNA clamp associated factor	Rattus norvegicus	90-93
3383374-1	1988	We investigated the effects of the Ca2+ antagonists diltiazem and verapamil on release of Ca2+ from intracellular store sites of rat aorta vascular smooth muscle cells in primary culture.	Diltiazem	52-61	carbonic anhydrase 2	Rattus norvegicus	90-93
3383374-3	1988	In the presence of 1 mM extracellular Ca2+, both diltiazem (IC50, 0.31 microM) and verapamil (IC50, 0.47 microM) dose-dependently inhibited elevations in the cytosolic Ca2+, as induced by depolarization of the plasma membrane with high extracellular K+.	Diltiazem	49-58	carbonic anhydrase 2	Rattus norvegicus	38-41
3383374-3	1988	In the presence of 1 mM extracellular Ca2+, both diltiazem (IC50, 0.31 microM) and verapamil (IC50, 0.47 microM) dose-dependently inhibited elevations in the cytosolic Ca2+, as induced by depolarization of the plasma membrane with high extracellular K+.	Diltiazem	49-58	carbonic anhydrase 2	Rattus norvegicus	168-171
3260898-5	1988	The calcium channel blocker diltiazem interferes with the ability of PCT-GF to maintain transferrin receptor expression in PCT-GF-dependent cell lines and causes a G1 arrest of the cell population.	Diltiazem	28-37	transferrin receptor	Mus musculus	88-108
3049099-9	1988	Spontaneously hypertensive rats also exhibit progressive arterial Ca2+ overload which responds excellently to the Ca2+ antagonists nifedipine, nimodipine, nisoldipine, nitrendipine, as well as to verapamil and diltiazem.	Diltiazem	210-219	carbonic anhydrase 2	Rattus norvegicus	66-69
3260898-6	1988	When added to a PCT-GF-independent cell line, diltiazem also inhibited transferrin receptor expression and caused G1 arrest.	Diltiazem	46-55	transferrin	Mus musculus	71-82
3381007-0	1988	Effects of calcium antagonist diltiazem on liver calcium content and necrosis of hepatocytes in rats following treatment with CCL4.	Diltiazem	30-39	C-C motif chemokine ligand 4	Rattus norvegicus	126-130
2451639-6	1988	In ganglion-blocked SHR, the smaller dose of diltiazem antagonized by 40 and 80% the pressor effects of norepinephrine and B-HT 920, respectively, but failed to change the vasoconstrictor responses of phenylephrine, epinephrine, or vasopressin, which were, however, reduced by the higher dose of diltiazem.	Diltiazem	45-54	arginine vasopressin	Rattus norvegicus	232-243
3395166-7	1988	In the canine femoral artery tensed up with high K+, all of these 3 CaM antagonists and 3 Ca++ channel blockers produced concentration-dependent vasorelaxation and relative potencies determined on the basis of concentrations producing IC30 were in the descending order: nicardipine greater than diltiazem greater than verapamil greater than calmidazolium greater than or equal to trifluoperazine greater than W-7.	Diltiazem	295-304	calmodulin-3	Cavia porcellus	68-71
3277818-6	1988	Approximately 30 percent of our patients with PPH have been improved on diltiazem treatment.	Diltiazem	72-81	enolase 1	Homo sapiens	46-49
2964236-0	1988	Verapamil, diltiazem and nifedipine interactions with calmodulin stimulated (Ca2+ + Mg2+)-ATPase.	Diltiazem	11-20	calmodulin 1	Homo sapiens	54-64
2964236-1	1988	The functional interactions of the three prototype Ca2+ antagonists, verapamil, diltiazem and nifedipine, were examined in relation to the calmodulin regulated plasma membrane Ca2+ pump ATPase.	Diltiazem	80-89	calmodulin 1	Homo sapiens	139-149
2964236-4	1988	Half-maximal activation by 6 nM calmodulin was antagonized by 10(-3) M verapamil and 10(-3) M diltiazem 25.1 and 12.1% respectively.	Diltiazem	94-103	calmodulin 1	Homo sapiens	32-42
3377372-6	1988	Verapamil and diltiazem stimulate LDL receptor activity in normal fibroblasts, in fibroblasts obtained from a hypercholesterolemic type IIa heterozygous patient, in the human hepatoma cell line HepG2, but not in receptor-negative cells.	Diltiazem	14-23	low density lipoprotein receptor	Homo sapiens	34-46
3280492-10	1988	However, nifedipine, verapamil, and diltiazem in high doses may inhibit liberation of insulin.	Diltiazem	36-45	insulin	Homo sapiens	86-93
2959345-10	1987	When added in Ca2+-containing solutions diltiazem and, to a lesser extent, nicardipine strongly reduced the contractions evoked in Ca2 -free solutions, suggesting that they inhibited the filling of the internal calcium store.	Diltiazem	40-49	carbonic anhydrase 2	Rattus norvegicus	14-17
2891847-4	1988	Diltiazem also inhibited mesenteric vasoconstrictor responses to angiotensin II, vasopressin, prostaglandin F2 alpha and KCl.	Diltiazem	0-9	angiotensinogen	Homo sapiens	65-79
2891847-4	1988	Diltiazem also inhibited mesenteric vasoconstrictor responses to angiotensin II, vasopressin, prostaglandin F2 alpha and KCl.	Diltiazem	0-9	arginine vasopressin	Homo sapiens	81-92
2896538-7	1987	The calcium channel blockers nifedipine and diltiazem both partly inhibit GRF- and TPA-stimulated GH release, showing some component of the calcium necessary for GH release arises from influx across the cell membrane.	Diltiazem	44-53	growth hormone releasing hormone	Rattus norvegicus	74-77
2896538-7	1987	The calcium channel blockers nifedipine and diltiazem both partly inhibit GRF- and TPA-stimulated GH release, showing some component of the calcium necessary for GH release arises from influx across the cell membrane.	Diltiazem	44-53	gonadotropin releasing hormone receptor	Rattus norvegicus	98-100
2959345-10	1987	When added in Ca2+-containing solutions diltiazem and, to a lesser extent, nicardipine strongly reduced the contractions evoked in Ca2 -free solutions, suggesting that they inhibited the filling of the internal calcium store.	Diltiazem	40-49	carbonic anhydrase 2	Rattus norvegicus	131-134
3322825-4	1987	The rise in plasma renin activity following diltiazem 0.02 mg kg-1 or 0.1 mg kg-1 or nifedipine 0.01 mg kg-1 was similar to values in a control group, whereas in those receiving verapamil 0.15 mg kg-1 or 0.6 mg kg-1, or nifedipine 0.05 mg kg-1, the rise was greater.	Diltiazem	44-53	renin	Canis lupus familiaris	19-24
3623678-9	1987	The results suggest that in normal subjects increased DBP responses to ANG II, induced by an increase in sodium intake, are partially mediated by increased extracellular to intracellular calcium movements, since they are blocked by the structurally different calcium channel blocking drugs nifedipine and diltiazem.	Diltiazem	305-314	angiotensinogen	Homo sapiens	71-77
3604896-5	1987	In individuals with pretreatment glomerular filtration rates less than or equal to 80 ml/min/1.73m2, diltiazem monotherapy showed both short-term and long-term improvement in glomerular filtration rate (62%) and effective renal plasma flow (34%).	Diltiazem	101-110	CD59 molecule (CD59 blood group)	Homo sapiens	89-94
3497799-2	1987	DNA synthesis assessed by incorporation of [3H]thymidine into the cells was significantly stimulated by epidermal growth factor (EGF), platelet-derived growth factor (PDGF) or fetal bovine serum (FBS), of which the effects were dose-dependently inhibited by a variety of Ca2+-antagonists, such as verapamil, diltiazem and nicardipine.	Diltiazem	308-317	myotrophin	Rattus norvegicus	114-127
2438500-8	1987	Thus, diltiazem and HCTZ were similar in that the depressor response to each drug activated the renin-angiotensin system, which in turn was accompanied by increased production of PGE2-M.	Diltiazem	6-15	renin	Homo sapiens	96-101
2438147-3	1987	In addition, the inhibitory effect of neurotensin was cancelled when the tissues were incubated in the presence of diltiazem, methoxyverapamil or nifedipine.	Diltiazem	115-124	neurotensin	Rattus norvegicus	38-49
2437403-4	1987	Of eight patients studied, a single dose of 90 mg diltiazem administered 3 h before dipyridamole infusion inhibited dipyridamole-induced ST-segment depression completely in seven (nST = 0) and incompletely in one (nST = from 24 to 5).	Diltiazem	50-59	sulfotransferase family 4A member 1	Homo sapiens	180-183
2437403-4	1987	Of eight patients studied, a single dose of 90 mg diltiazem administered 3 h before dipyridamole infusion inhibited dipyridamole-induced ST-segment depression completely in seven (nST = 0) and incompletely in one (nST = from 24 to 5).	Diltiazem	50-59	sulfotransferase family 4A member 1	Homo sapiens	214-217
2834513-7	1988	The increase in cyclic GMP content caused by treatment of the cells with a high K+ level (50 mM) was completely blocked by voltage-dependent Ca2+ entry blockers, such as verapamil (10 microM), nifedipine (1 microM), and diltiazem (100 microM); however, the PG (10 microM)-induced increase in cyclic GMP content was not affected by such Ca2+ entry blockers.	Diltiazem	220-229	5'-nucleotidase, cytosolic II	Mus musculus	23-26
3038124-3	1987	Of the four Ca2+ entry blockers tested, only verapamil and diltiazem specifically inhibited the calmodulin-stimulated (Ca2+ + Mg2+)-ATPase activity, the basal enzyme activity being unaltered by these drugs.	Diltiazem	59-68	calmodulin 1	Homo sapiens	96-106
3038124-5	1987	Calmodulin concentration effect curves showed the inhibition by verapamil (10(-3) M) and diltiazem (10(-3) M) to be non-competitive.	Diltiazem	89-98	calmodulin 1	Homo sapiens	0-10
2955785-2	1987	This IFN-gamma-induced increase was reduced to 30-40% of basal (Ca2+) by the addition of diltiazem (1 microM) or incubation in Ca2+-free buffer.	Diltiazem	89-98	interferon gamma	Homo sapiens	5-14
2436829-14	1987	Distinct receptors for verapamil and diltiazem are poorly defined, but appear to be allosterically related to the dihydropyridine receptor.	Diltiazem	37-46	calcium voltage-gated channel subunit alpha1 S	Homo sapiens	114-138
3590086-3	1987	Diltiazem and verapamil inhibited aggregation by PAF in a dose-dependent manner with 50% inhibition at 2.8 +/- 1.4 X 10(-5) M diltiazem (mean +/- SD, n = 5) and 4.2 +/- 2.0 X 10(-5) M verapamil.	Diltiazem	0-9	PCNA clamp associated factor	Homo sapiens	49-52
3590086-3	1987	Diltiazem and verapamil inhibited aggregation by PAF in a dose-dependent manner with 50% inhibition at 2.8 +/- 1.4 X 10(-5) M diltiazem (mean +/- SD, n = 5) and 4.2 +/- 2.0 X 10(-5) M verapamil.	Diltiazem	126-135	PCNA clamp associated factor	Homo sapiens	49-52
3590086-4	1987	Both channel blockers also inhibited PAF binding in a dose-dependent manner with 50% inhibition at 4.7 +/- 2.5 X 10(-5) M diltiazem and 6.3 +/- 1.2 X 10(-5) M verapamil.	Diltiazem	122-131	PCNA clamp associated factor	Homo sapiens	37-40
3590086-6	1987	Scatchard analysis of PAF binding in the presence of different fixed concentrations of either diltiazem or verapamil revealed that these agents both increased PAF receptor number and decreased the receptor binding affinity.	Diltiazem	94-103	PCNA clamp associated factor	Homo sapiens	22-25
3590086-6	1987	Scatchard analysis of PAF binding in the presence of different fixed concentrations of either diltiazem or verapamil revealed that these agents both increased PAF receptor number and decreased the receptor binding affinity.	Diltiazem	94-103	PCNA clamp associated factor	Homo sapiens	159-162
3806874-0	1987	Association of diltiazem therapy with increased insulin resistance in a patient with type I diabetes mellitus.	Diltiazem	15-24	insulin	Homo sapiens	48-55
3544786-4	1987	Diltiazem may increase glomerular filtration rate via attenuation of the intrarenal effects of angiotensin II or norepinephrine.	Diltiazem	0-9	angiotensinogen	Homo sapiens	95-109
3102857-2	1987	Although the Ca2+ channel blockers verapamil, nifedipine, and diltiazem induced a dose-dependent inhibition of [3H]-thymidine incorporation by HT-2 cells in response to recombinant human and purified rat IL 2, the stimulation indices of the treated and untreated cells were equivalent.	Diltiazem	62-71	interleukin 2	Rattus norvegicus	204-208
2442519-4	1987	The binding of other calmodulin antagonists and calcium antagonists, including prenylamine, R24571, and diltiazem, to these calcium-binding proteins abolishes the cooperativity between two felodipine-binding sites, resulting in felodipine binding to the remaining site with a 20-25-fold greater affinity.	Diltiazem	104-113	calmodulin 1	Homo sapiens	21-31
3578945-1	1987	An elderly patient, receiving long-term oral diltiazem at the usual dosage, presented a sudden attack of junctional bradycardia at 35 b X min-1; this was badly tolerated by the patient.	Diltiazem	45-54	CD59 molecule (CD59 blood group)	Homo sapiens	138-143
2432398-0	1986	Diltiazem inhibits transferrin receptor expression and causes G1 arrest in normal and neoplastic T cells.	Diltiazem	0-9	transferrin	Homo sapiens	19-30
2432398-7	1986	In contrast, diltiazem prevented the induction of transferrin receptor (mRNA and protein) in normal T cells and caused a progressive loss of transferrin receptor (mRNA and protein) in malignant T cells.	Diltiazem	13-22	transferrin receptor	Homo sapiens	50-70
2432398-7	1986	In contrast, diltiazem prevented the induction of transferrin receptor (mRNA and protein) in normal T cells and caused a progressive loss of transferrin receptor (mRNA and protein) in malignant T cells.	Diltiazem	13-22	transferrin receptor	Homo sapiens	141-161
3718500-1	1986	Human skin fibroblasts incubated in lipoprotein-deficient medium in the presence of 50-100 microM of the calcium channel blockers verapamil or diltiazem incorporated up to 2.5 times more [35S]methionine into immunoprecipitable LDL receptor protein than did control cells.	Diltiazem	143-152	low density lipoprotein receptor	Homo sapiens	227-239
3018407-6	1986	The addition of the calcium channel blocking agent diltiazem (10(-4) M) resulted in a significant increase in renin release (364 to 567 ng X mg-1, p less than .05) which was not blocked by the addition of AP.	Diltiazem	51-60	renin	Rattus norvegicus	110-115
3094310-0	1986	The calcium antagonist diltiazem inhibits calcification enhanced by calcitonin in growth cartilage of rats in ethane-1-hydroxy-1,1-diphosphonate (EHDP)-induced rickets.	Diltiazem	23-32	calcitonin-related polypeptide alpha	Rattus norvegicus	68-78
3094310-3	1986	Diltiazem suppressed, in a dose-dependent manner, the accelerated calcification due to CT in the growth cartilage, as determined by findings on the soft X-ray photos, contact microradiograph and light microscopic histology of the proximal region of the tibia.	Diltiazem	0-9	calcitonin-related polypeptide alpha	Rattus norvegicus	87-89
3094310-5	1986	If it is assumed that diltiazem inhibits the entry of calcium ion into the cells of growth cartilage, in the same manner as seen in case of smooth muscle and myocardial cells, then our results indicate that intracellular concentrations of calcium might play an important role in the occurrence of accelerated calcification due to CT.	Diltiazem	22-31	calcitonin-related polypeptide alpha	Rattus norvegicus	330-332
3752187-8	1986	In the presence of 10(-4) gm/ml of diltiazem, 10(-2) U/ml of oxytocin could not evoke any action potentials but did evoke small and long contractures, while in a high ionized potassium contracture experiment, oxytocin potentiated the tonic phase.	Diltiazem	35-44	oxytocin/neurophysin I prepropeptide	Homo sapiens	61-69
3752187-8	1986	In the presence of 10(-4) gm/ml of diltiazem, 10(-2) U/ml of oxytocin could not evoke any action potentials but did evoke small and long contractures, while in a high ionized potassium contracture experiment, oxytocin potentiated the tonic phase.	Diltiazem	35-44	oxytocin/neurophysin I prepropeptide	Homo sapiens	209-217
3803799-5	1986	Oxygen inhalation produced no significant modifications of haemodynamic variables, whilst a significant (p less than 0.05) decrease of PAPm, pulmonary arteriolar resistance (PAR) and peripheral resistance (TPR) was observed after diltiazem administration (respectively 14%, 23% and 11.6%).	Diltiazem	230-239	translocated promoter region, nuclear basket protein	Homo sapiens	206-209
2944690-0	1986	[Diltiazem-induced changes in plasma beta-thromboglobulin and platelet aggregation in chronic cor pulmonale].	Diltiazem	1-10	pro-platelet basic protein	Homo sapiens	37-57
3760114-6	1986	During the high sodium diet (200 meq Na/day), only diltiazem decreased AII sensitivity, and the reduction was less (P less than 0.05) than that during the low sodium diet.	Diltiazem	51-60	angiotensinogen	Homo sapiens	71-74
3760114-10	1986	The results suggest that in normal subjects, increased plasma aldosterone responses to AII induced by reduction in sodium intake are partially mediated by increased extracellular to intracellular calcium movements, since they are blocked by the structurally different calcium channel-blocking drugs nifedipine and diltiazem.	Diltiazem	314-323	angiotensinogen	Homo sapiens	87-90
3705683-5	1986	Carbohydrate and lipid metabolism including the lipoproteins as well as HGH, cortisol and insulin showed the same behaviour under diltiazem and placebo.	Diltiazem	130-139	insulin	Homo sapiens	90-97
3949375-6	1986	In subjects with pretreatment glomerular filtration rates of 80 ml/min/1.73 m2 or less, diltiazem therapy was associated with marked improvement in glomerular filtration rate (48%) and effective renal plasma flow (36%).	Diltiazem	88-97	CD59 molecule (CD59 blood group)	Homo sapiens	67-72
2419690-8	1986	The rise in plasma catecholamines and plasma renin activity was greatest with nifedipine, least with nitroprusside, and intermediate with diltiazem.	Diltiazem	138-147	renin	Canis lupus familiaris	45-50
3484629-6	1986	The concentrations of unlabeled bepridil, W-7, prenylamine, verapamil and diltiazem producing 50% inhibition (IC50) of the binding of [3H]bepridil to calmodulin were 4 microM, 28 microM, 45 microM, 130 microM and 700 microM, respectively.	Diltiazem	74-83	calmodulin 1	Homo sapiens	150-160
3961730-4	1986	The relative inhibitory effect of four calcium antagonists on [3H]-Paf-acether high affinity binding correlates closely with their respective anti-aggregatory activity against Paf-acether induced responses in human PRP; order of potency being (+)-cis diltiazem greater than (+/-)-verapamil greater than (-)-cis diltiazem greater than nifedipine.	Diltiazem	243-260	prion protein	Homo sapiens	215-218
2933950-4	1985	Diltiazem may increase glomerular filtration rate via attenuation of the intrarenal effects of angiotensin II or norepinephrine.	Diltiazem	0-9	angiotensinogen	Homo sapiens	95-109
3006091-2	1986	The specific binding and internalization of human 125I-labeled LDL are dose-dependently increased in HSF by CA of the verapamil series (verapamil, anipamil, gallopamil, ronipamil, and diltiazem), but neither by CA of the dihydropyridine series (nifedipine, nitrendipine) nor by flunarizine.	Diltiazem	184-193	interleukin 6	Homo sapiens	101-104
3878075-6	1985	Diltiazem increased plasma renin activity but had no influence on plasma aldosterone concentration.	Diltiazem	0-9	renin	Rattus norvegicus	27-32
4056906-7	1985	Diltiazem increased rCBF in marginally ischemic regions.	Diltiazem	0-9	CCAAT/enhancer binding protein zeta	Rattus norvegicus	20-24
3878075-12	1985	Diltiazem opposed angiotensin II-induced responses, such as renal vasoconstriction and reduction of glomerular filtration rate.	Diltiazem	0-9	angiotensinogen	Rattus norvegicus	18-32
3866796-8	1985	pretreatment with diltiazem, diltiazem attenuated the pressor responses to angiotensin II.	Diltiazem	18-27	angiotensinogen	Rattus norvegicus	75-89
3866796-8	1985	pretreatment with diltiazem, diltiazem attenuated the pressor responses to angiotensin II.	Diltiazem	29-38	angiotensinogen	Rattus norvegicus	75-89
6507979-0	1984	Diltiazem for myocardial protection in CPR.	Diltiazem	0-9	cytochrome p450 oxidoreductase	Homo sapiens	39-42
4044600-9	1985	This reactivation of phosphorylase showed saturation kinetics with respect to extracellular [Ca2+], was maximally stimulated within 1 min of vasopressin addition and was inhibited by high concentration of diltiazem.	Diltiazem	205-214	arginine vasopressin	Homo sapiens	141-152
2935663-0	1985	Effect of neuraminidase on diltiazem-mediated alteration of nitrendipine binding in the hog coronary artery.	Diltiazem	27-36	neuraminidase 1	Homo sapiens	10-23
2935663-3	1985	The influences of diltiazem on 3H-NTD bindings differed between NUase treated and untreated preparations.	Diltiazem	18-27	neuraminidase 1	Homo sapiens	64-69
2935663-5	1985	After treatment with NUase, a low dose of diltiazem decreased 3H-NTD (100 pM) binding, and the greatest effect was observed at 10(-9) M with a 50% decrease, while at a high dose of diltiazem (10(-6) M), 80% increase of the binding was observed.	Diltiazem	42-51	neuraminidase 1	Homo sapiens	21-26
2935663-6	1985	Scatchard plot analysis indicated that a high dose of diltiazem (10(-6) M) increased only the affinity of 3H-NTD to the binding site in both the NUase-treated and untreated preparations.	Diltiazem	54-63	neuraminidase 1	Homo sapiens	145-150
2996387-1	1985	When cultured with a Ca2+ antagonist diltiazem, fetal bovine aortic smooth muscle cells showed a cobblestone-like monolayer and a positive factor VIII-related antigen in culture, which are supposed to be specific to the endothelial cells in general.	Diltiazem	37-46	coagulation factor VIII	Bos taurus	139-150
4015695-1	1985	Diltiazem and verapamil were found to be inhibitors of the cytochrome P-450-dependent biotransformation of drugs.	Diltiazem	0-9	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	59-75
2409272-1	1985	Dose-dependent inhibition by three organic calcium channel antagonists, D-600, nisoldipine and diltiazem, of the inward calcium current (iCa) and the delayed, outward potassium current (iK) in single frog atrial cells was examined using a voltage clamp technique.	Diltiazem	95-104	calcium voltage-gated channel subunit alpha1 C	Canis lupus familiaris	137-140
2409272-4	1985	The estimated Kd values for inhibition of iCa and iK, respectively, were 3.7 X 10(-7) M and 8.2 X 10(-4) M for D-600, 1.6 X 10(-8) M and 1.6 X 10(-5) M for nisoldipine and 4.4 X 10(-6) M and 3.3 X 10(-4) M for diltiazem.	Diltiazem	210-219	calcium voltage-gated channel subunit alpha1 C	Canis lupus familiaris	42-45
3898610-5	1985	Both verapamil and diltiazem attenuated the lead-induced renin release in vitro, but only with diltiazem did this attain statistical significance.	Diltiazem	19-28	LOW QUALITY PROTEIN: renin	Oryctolagus cuniculus	57-62
3993799-2	1985	The Ca2+ channel antagonists, diltiazem and verapamil, competitively inhibited adenosine influx (Ki = 158 +/- 17.4 and 13.5 +/- 1.3 microM at 10 microM adenosine, respectively), despite no apparent effect on transport by Ca2+, Mg2+, Na+, or K+.	Diltiazem	30-39	carbonic anhydrase 2	Homo sapiens	4-7
3993799-2	1985	The Ca2+ channel antagonists, diltiazem and verapamil, competitively inhibited adenosine influx (Ki = 158 +/- 17.4 and 13.5 +/- 1.3 microM at 10 microM adenosine, respectively), despite no apparent effect on transport by Ca2+, Mg2+, Na+, or K+.	Diltiazem	30-39	carbonic anhydrase 2	Homo sapiens	221-224
2982480-1	1985	The cytotoxic activity against human tumor cells of toxic conjugates of Pseudomonas exotoxin with anti-transferrin receptor antibody or epidermal growth factor was potentiated up to 10 to 20-fold by the calcium antagonists verapamil, D-600, and diltiazem and by the lysosomotropic agent beta-glycylphenyl-naphthylamide.	Diltiazem	245-254	transferrin	Homo sapiens	103-114
2982480-1	1985	The cytotoxic activity against human tumor cells of toxic conjugates of Pseudomonas exotoxin with anti-transferrin receptor antibody or epidermal growth factor was potentiated up to 10 to 20-fold by the calcium antagonists verapamil, D-600, and diltiazem and by the lysosomotropic agent beta-glycylphenyl-naphthylamide.	Diltiazem	245-254	epidermal growth factor	Homo sapiens	136-159
2578123-3	1985	For verapamil, diltiazem, trifluoperazine, dibucaine, and quinacrine, there is complete agreement between the relative potencies as inhibitors of phospholipase A2 and the two other processes.	Diltiazem	15-24	phospholipase A2 group IB	Rattus norvegicus	146-162
3880562-0	1985	Divergent influences of the structurally dissimilar calcium entry blockers, diltiazem and verapamil, on thyrotropin- and gonadotropin-releasing hormone-stimulated anterior pituitary hormone secretion in man.	Diltiazem	76-85	thyrotropin releasing hormone	Homo sapiens	104-151
6092067-10	1984	(iv) A low-affinity binding site for verapamil and for some other Ca2+ channel blockers is detected by studies of dissociation kinetics of the [3H]verapamil receptor in the presence of high concentrations of verapamil, gallopamil, bepridil and diltiazem.	Diltiazem	244-253	carbonic anhydrase 2	Oryctolagus cuniculus	66-69
6323630-3	1984	The binding site in both brain and heart was highly specific for dihydropyridine calcium antagonists, such as nifedipine, nimodipine, and nisoldipine, since these drugs were several orders of magnitude more potent as inhibitors of [3H]NDP binding than verapamil, methoxyverapamil, or diltiazem.	Diltiazem	284-293	NDP, norrin cystine knot growth factor	Gallus gallus	235-238
6747823-9	1984	Inhibition of superprecipitation by diltiazem was apparent at a concentration of 10(-6) M, was manifest by a rightward shift in the pCa relationship and could be attenuated by exogenous calmodulin.	Diltiazem	36-45	calmodulin 1	Homo sapiens	186-196
6747823-11	1984	However, diltiazem may inhibit Ca++-dependent arterial actin-myosin interactions by a mechanism which is independent of regulation of myosin light chain phosphorylation.	Diltiazem	9-18	myosin heavy chain 14	Homo sapiens	61-67
6375339-5	1984	Plasma renin activity increased slightly, from 0.6 to 0.9 ng/ml/hour during diltiazem treatment, but the change was not significant (p less than 0.10).	Diltiazem	76-85	renin	Homo sapiens	7-12
6324751-3	1984	It is concluded that all three enzymes may be activated by increases in the intramitochondrial concentration of Ca2+ and that the distribution of Ca2+ across the mitochondrial inner membrane is determined, as in rat heart mitochondria, by the relative activities of a uniporter (which transports Ca2+ into mitochondria and is inhibited by Mg2+ and Ruthenium Red) and an antiporter (which allows Ca2+ to leave mitochondria in exchange for Na+ and is inhibited by diltiazem).	Diltiazem	462-471	carbonic anhydrase 2	Rattus norvegicus	146-149
6324751-3	1984	It is concluded that all three enzymes may be activated by increases in the intramitochondrial concentration of Ca2+ and that the distribution of Ca2+ across the mitochondrial inner membrane is determined, as in rat heart mitochondria, by the relative activities of a uniporter (which transports Ca2+ into mitochondria and is inhibited by Mg2+ and Ruthenium Red) and an antiporter (which allows Ca2+ to leave mitochondria in exchange for Na+ and is inhibited by diltiazem).	Diltiazem	462-471	carbonic anhydrase 2	Rattus norvegicus	146-149
6324751-3	1984	It is concluded that all three enzymes may be activated by increases in the intramitochondrial concentration of Ca2+ and that the distribution of Ca2+ across the mitochondrial inner membrane is determined, as in rat heart mitochondria, by the relative activities of a uniporter (which transports Ca2+ into mitochondria and is inhibited by Mg2+ and Ruthenium Red) and an antiporter (which allows Ca2+ to leave mitochondria in exchange for Na+ and is inhibited by diltiazem).	Diltiazem	462-471	carbonic anhydrase 2	Rattus norvegicus	146-149
6376141-0	1984	Diltiazem and verapamil: functional antagonism of exogenous noradrenaline and angiotensin II in man.	Diltiazem	0-9	angiotensinogen	Homo sapiens	60-92
6376141-5	1984	During the administration of diltiazem and verapamil, the increase in blood pressure in response to the infusion of NA and angiotensin II was attenuated; the increase in diastolic pressure was mainly affected.	Diltiazem	29-38	angiotensinogen	Homo sapiens	123-137
6616987-4	1983	PEP/LVET increased slightly after verapamil (+ 15%) and decreased after nifedipin (-5%) and diltiazem (-3%), the changes being not significant.	Diltiazem	92-101	progestagen associated endometrial protein	Homo sapiens	0-3
6662118-0	1983	Comparative effects of nifedipine and diltiazem on vascular responses to norepinephrine and angiotensin II.	Diltiazem	38-47	angiotensinogen	Rattus norvegicus	92-106
6662118-4	1983	At concentrations of 3 X 10(-7) mol l-1 and 10(-6) mol l-1, diltiazem inhibited only the response to angiotensin II without affecting the vasoconstrictor effect of norepinephrine.	Diltiazem	60-69	angiotensinogen	Rattus norvegicus	101-115
6662118-5	1983	Increase in diltiazem concentration to 10(-5) mol l-1 and 10(-4) mol l-1 was associated with a similar inhibition of the response to angiotensin II and norepinephrine.	Diltiazem	12-21	angiotensinogen	Rattus norvegicus	133-147
6411841-5	1983	Incubation of PRP with diltiazem in a pharmacologic range resulted in marked reduction in ionophore A23187-induced potentiation of platelet activity caused by ADP or epinephrine.	Diltiazem	23-32	prion protein	Homo sapiens	14-17
6662118-6	1983	These results demonstrate that at concentration less than 10(-5) mol l-1, diltiazem acts as a selective antagonist of the effect of angiotensin II whilst no such selectivity of action was observed with all concentrations of nifedipine used in the present studies.	Diltiazem	74-83	angiotensinogen	Rattus norvegicus	132-146
6139380-2	1983	Diltiazem was a potent antagonist of phasic responses induced by low concentrations of K+, tetraethylammonium (TEA), the selective alpha 2-adrenoreceptor agonists UK 14304 or TL99 and angiotensin II (AII).	Diltiazem	0-9	angiotensinogen	Rattus norvegicus	184-198
6139380-2	1983	Diltiazem was a potent antagonist of phasic responses induced by low concentrations of K+, tetraethylammonium (TEA), the selective alpha 2-adrenoreceptor agonists UK 14304 or TL99 and angiotensin II (AII).	Diltiazem	0-9	angiotensinogen	Rattus norvegicus	200-203
6350692-6	1983	The activation of the adrenergic and renin angiotension systems seen after nifedipine administration is less pronounced after chronic administration of the drug and is nearly absent after verapamil and diltiazem.	Diltiazem	202-211	renin	Homo sapiens	37-42
34051994-5	2021	The diltiazem samples (5.0-300 ng mL-1) dynamically quenched the fluorescence of 15 mug/mL DICOF in 50 mM phosphate buffer at pH 6.5 at 8.0 min equilibrium; thus, Stern-Volmer plots were linearly constructed for sensing diltiazem with an LOD of 3.4 ng mL-1 and an LOQ of 10.2 ng mL-1.	Diltiazem	4-13	L1 cell adhesion molecule	Mus musculus	34-38
6307716-1	1983	The effect of three calcium antagonists (verapamil, nifedipine and diltiazem) on the calcium-induced activation of phosphodiesterase (a calmodulin dependent process) was investigated.	Diltiazem	67-76	calmodulin 1	Homo sapiens	136-146
6307716-3	1983	In the presence of calmodulin, phosphodiesterase activity was stimulated by calcium in the range 4 X 10(-6)-2.5 X 10(-5) M. Diltiazem (10(-6) M), verapamil (10(-6) M) and nifedipine (10(-7) and 10(-6) M) had no influence on phosphodiesterase activity in the presence or absence of calmodulin at any concentration of calcium employed.	Diltiazem	124-133	calmodulin 1	Homo sapiens	19-29
6847674-3	1983	Hydrophobic ligands including the calmodulin antagonist, R24571 and Ca2+ antagonists, prenylamine and diltiazem, bind to calmodulin and potentiate felodipine binding by as much as 20 fold.	Diltiazem	102-111	calmodulin 1	Homo sapiens	121-131
6299112-3	1983	D600 (200 microM), diltiazem (200 microM), and nifedipine (60 microM) inhibited vasopressin-induced water flow but enhanced adenosine 3",5"-cyclic monophosphate (cAMP)-induced water flow, suggesting that the drugs inhibit cAMP generation in response to vasopressin but enhance the response to exogenous cAMP by inhibiting phosphodiesterase activity.	Diltiazem	19-28	arginine vasopressin	Homo sapiens	80-91
6301463-1	1983	Treatment of Ltk- cells with the calcium antagonists, verapamil and diltiazem, but not nifedipine, causes a 3-fold enhancement of the frequency of transfer of the cloned gene for herpes simplex virus thymidine kinase (HSV-tk).	Diltiazem	68-77	leukocyte receptor tyrosine kinase	Homo sapiens	13-16
535823-9	1979	On the other hand, it was demonstrated that the pressor responses to norepinephrine and angiotensin II in the anesthetized normotensive rats were non-competitively inhibited by intravenous administration of diltiazem at a dose which had no effect on the blood pressure.	Diltiazem	207-216	angiotensinogen	Rattus norvegicus	88-102
582767-7	1979	This constriction may be related to renin-angiotensin system which diltiazem was reported to antagonize.	Diltiazem	67-76	renin	Homo sapiens	36-41
6875846-4	1983	The relaxations produced by these calmodulin antagonists and prenylamine could not be overcome by contractile agonists which release Ca++ from internal stores (histamine and serotonin), whereas the relaxations produced by felodipine, verapamil and diltiazem were readily reversed by either of these agonists.	Diltiazem	248-257	calmodulin 1	Homo sapiens	34-44
6176579-0	1982	Selective inhibition of Na+-induced Ca2+ release from heart mitochondria by diltiazem and certain other Ca2+ antagonist drugs.	Diltiazem	76-85	carbonic anhydrase 2	Oryctolagus cuniculus	36-39
6176579-8	1982	These results indicate that diltiazem and certain other Ca2+ antagonist drugs may be selective inhibitors of the Na+/Ca2+ antiporter in heart mitochondria much like ruthenium red is a selective inhibitor of the Ca2+ uniporter.	Diltiazem	28-37	carbonic anhydrase 2	Oryctolagus cuniculus	117-120
6176579-8	1982	These results indicate that diltiazem and certain other Ca2+ antagonist drugs may be selective inhibitors of the Na+/Ca2+ antiporter in heart mitochondria much like ruthenium red is a selective inhibitor of the Ca2+ uniporter.	Diltiazem	28-37	carbonic anhydrase 2	Oryctolagus cuniculus	117-120
6268911-0	1981	Effect of diltiazem, a calcium antagonist, on renin secretion from rat kidney slices.	Diltiazem	10-19	renin	Rattus norvegicus	46-51
7262036-1	1980	The effect of diltiazem hydrochloride (DTZ), a calcium-antagonist, on pressor and steroidogenic action of angiotensin II (AII), angiotensin III (AIII) and norepinephrine (NE) was studied in 5 normal men.	Diltiazem	14-37	angiotensinogen	Homo sapiens	106-120
7241862-4	1980	Diltiazem also depressed the Ca2+ uptake was not due to an increased permeability for Ca2+, since release of Ca2+ from the microsomes was not significantly affected by either drug.	Diltiazem	0-9	carbonic anhydrase 2	Homo sapiens	29-32
7241862-5	1980	It is proposed that verapamil and diltiazem inhibit Ca2+ transport by interfering with an active process of Ca2+ accumulation in microsomes of the renal cortex.	Diltiazem	34-43	carbonic anhydrase 2	Homo sapiens	52-55
7241862-5	1980	It is proposed that verapamil and diltiazem inhibit Ca2+ transport by interfering with an active process of Ca2+ accumulation in microsomes of the renal cortex.	Diltiazem	34-43	carbonic anhydrase 2	Homo sapiens	108-111
34051994-5	2021	The diltiazem samples (5.0-300 ng mL-1) dynamically quenched the fluorescence of 15 mug/mL DICOF in 50 mM phosphate buffer at pH 6.5 at 8.0 min equilibrium; thus, Stern-Volmer plots were linearly constructed for sensing diltiazem with an LOD of 3.4 ng mL-1 and an LOQ of 10.2 ng mL-1.	Diltiazem	4-13	L1 cell adhesion molecule	Mus musculus	252-256
34051994-5	2021	The diltiazem samples (5.0-300 ng mL-1) dynamically quenched the fluorescence of 15 mug/mL DICOF in 50 mM phosphate buffer at pH 6.5 at 8.0 min equilibrium; thus, Stern-Volmer plots were linearly constructed for sensing diltiazem with an LOD of 3.4 ng mL-1 and an LOQ of 10.2 ng mL-1.	Diltiazem	4-13	L1 cell adhesion molecule	Mus musculus	252-256
34051994-5	2021	The diltiazem samples (5.0-300 ng mL-1) dynamically quenched the fluorescence of 15 mug/mL DICOF in 50 mM phosphate buffer at pH 6.5 at 8.0 min equilibrium; thus, Stern-Volmer plots were linearly constructed for sensing diltiazem with an LOD of 3.4 ng mL-1 and an LOQ of 10.2 ng mL-1.	Diltiazem	220-229	L1 cell adhesion molecule	Mus musculus	34-38
34051994-6	2021	According to the plots, 30 ng mL-1 diltiazem solutions that were diluted from 30 mg-specified tablets had an average measured concentration of 29.5 ng mL-1 (sigma = 1.3% and n = 5).	Diltiazem	35-44	L1 cell adhesion molecule	Mus musculus	30-34
34051994-6	2021	According to the plots, 30 ng mL-1 diltiazem solutions that were diluted from 30 mg-specified tablets had an average measured concentration of 29.5 ng mL-1 (sigma = 1.3% and n = 5).	Diltiazem	35-44	L1 cell adhesion molecule	Mus musculus	151-155
34051994-7	2021	In addition to application as fluorescent sensors, DICOFs (30 mg) could be used as dispersive extractants to recover 95.2% of 0.6 ng mL-1 diltiazem from 25 mL phosphate buffer with quadruplicate uses of 0.5 mL methanol/acetic acid (v/v = 9/1) as the eluent.	Diltiazem	138-147	L1 cell adhesion molecule	Mus musculus	133-137
34032727-15	2021	A multivariate logistic regression analysis will be performed A P-value < .05 will be considered significant.The direct indices (CMR and coronary angiographic TIMI blood flow grade) may improve after adding diltiazem or nicorandil during routine drug treatments (such as aspirin, statins, and nitrates) in PMVA patients, and indirect indices (homocysteine and von Willebrand factor levels) may be reduced.	Diltiazem	207-216	von Willebrand factor	Homo sapiens	360-381
33581123-4	2021	IL-4-stimulated eotaxin-3 secretion was measured by ELISA after treatment with omeprazole, SCH 28080 (potassium-competitive acid blocker), EGTA-AM (calcium chelator), 2-APB (inhibitor of endoplasmic reticulum calcium release), verapamil and diltiazem (L-type calcium channel inhibitors).	Diltiazem	241-250	interleukin 4	Homo sapiens	0-4
33581123-4	2021	IL-4-stimulated eotaxin-3 secretion was measured by ELISA after treatment with omeprazole, SCH 28080 (potassium-competitive acid blocker), EGTA-AM (calcium chelator), 2-APB (inhibitor of endoplasmic reticulum calcium release), verapamil and diltiazem (L-type calcium channel inhibitors).	Diltiazem	241-250	C-C motif chemokine ligand 26	Homo sapiens	16-25
33581123-9	2021	IL-4 increased intracellular calcium transients, and IL-4-stimulated eotaxin-3 secretion was blocked by EGTA-AM, 2-APB, verapamil, and diltiazem.	Diltiazem	135-144	interleukin 4	Homo sapiens	0-4
33581123-9	2021	IL-4 increased intracellular calcium transients, and IL-4-stimulated eotaxin-3 secretion was blocked by EGTA-AM, 2-APB, verapamil, and diltiazem.	Diltiazem	135-144	interleukin 4	Homo sapiens	53-57
33581123-9	2021	IL-4 increased intracellular calcium transients, and IL-4-stimulated eotaxin-3 secretion was blocked by EGTA-AM, 2-APB, verapamil, and diltiazem.	Diltiazem	135-144	C-C motif chemokine ligand 26	Homo sapiens	69-78
33898141-9	2021	However, treatments of the rats with metoprolol, pilocarpine, and diltiazem significantly prevented prolongation of the QTc interval as compared to the insulin + saline group (p<0.005, p<0.005, and p<0.01, respectively).	Diltiazem	66-75	insulin	Homo sapiens	152-159
32803289-1	2021	PURPOSE: To evaluate the role of diltiazem on tacrolimus sparing in pediatric primary nephrotic syndrome (PNS) and its relation to CYP3A4, CYP3A5, ABCB1, and SLCO1B3 polymorphisms.	Diltiazem	33-42	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	131-137
33482177-0	2021	T1143 Essential for CaV1.2 Inhibition by Diltiazem.	Diltiazem	41-50	calcium voltage-gated channel subunit alpha1 C	Homo sapiens	20-26
33666764-6	2021	Data has established the calcium channel blockers, namely, diltiazem and verapamil, as potent inhibitors of CYP3A4, and the majority of significant drug interactions involving antihypertensives are attributable to these two agents.	Diltiazem	59-68	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	108-114
33666142-0	2021	Investigations of the molecular mechanism of diltiazem binding to human serum albumin in the presence of metal ions, glucose and urea.	Diltiazem	45-54	albumin	Homo sapiens	72-85
33666142-1	2021	The molecular mechanism and thermodynamic properties of the interaction between diltiazem (DTZ) and human serum albumin (HSA), has been studied in vitro using spectroscopic techniques (UV-Vis, fluorescence, FTIR), and molecular docking methods.	Diltiazem	80-89	albumin	Homo sapiens	106-119
33666142-1	2021	The molecular mechanism and thermodynamic properties of the interaction between diltiazem (DTZ) and human serum albumin (HSA), has been studied in vitro using spectroscopic techniques (UV-Vis, fluorescence, FTIR), and molecular docking methods.	Diltiazem	91-94	albumin	Homo sapiens	106-119
32803289-1	2021	PURPOSE: To evaluate the role of diltiazem on tacrolimus sparing in pediatric primary nephrotic syndrome (PNS) and its relation to CYP3A4, CYP3A5, ABCB1, and SLCO1B3 polymorphisms.	Diltiazem	33-42	solute carrier organic anion transporter family member 1B3	Homo sapiens	158-165
32803289-8	2021	CONCLUSION: Moderate effect of diltiazem on tacrolimus sparing, which might relate to the polymorphisms of CYP3A4, CYP3A5, ABCB1, and SLCO1B3, was documented.	Diltiazem	31-40	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	107-113
32803289-8	2021	CONCLUSION: Moderate effect of diltiazem on tacrolimus sparing, which might relate to the polymorphisms of CYP3A4, CYP3A5, ABCB1, and SLCO1B3, was documented.	Diltiazem	31-40	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	115-121
32803289-8	2021	CONCLUSION: Moderate effect of diltiazem on tacrolimus sparing, which might relate to the polymorphisms of CYP3A4, CYP3A5, ABCB1, and SLCO1B3, was documented.	Diltiazem	31-40	ATP binding cassette subfamily B member 1	Homo sapiens	123-128
32803289-8	2021	CONCLUSION: Moderate effect of diltiazem on tacrolimus sparing, which might relate to the polymorphisms of CYP3A4, CYP3A5, ABCB1, and SLCO1B3, was documented.	Diltiazem	31-40	solute carrier organic anion transporter family member 1B3	Homo sapiens	134-141
33011221-0	2020	Diltiazem potentiates the cytotoxicity of gemcitabine and 5-fluorouracil in PANC-1 human pancreatic cancer cells through inhibition of P-glycoprotein.	Diltiazem	0-9	ATP binding cassette subfamily B member 1	Homo sapiens	135-149
33011221-3	2020	Diltiazem, a calcium channel blocker, is a P-gp inhibitor.	Diltiazem	0-9	ATP binding cassette subfamily B member 1	Homo sapiens	43-47
33011221-4	2020	In the current study, we investigated the hypothesis that targeting of P-gp by diltiazem can enhance the cytotoxicity of gemcitabine and 5-FU against human pancreatic cancer cells.	Diltiazem	79-88	ATP binding cassette subfamily B member 1	Homo sapiens	71-75
33011221-9	2020	In addition, diltiazem co-treatment decreased the expressions of stem cell markers CD24 and CD44, increased the expressions of Bax and cleaved caspase 3, enhanced DNA fragmentation, and attenuated cyclin D1 and P-gp expressions as compared to cells treated with either gemcitabine or 5-FU alone.	Diltiazem	13-22	CD24 molecule	Homo sapiens	83-87
33011221-9	2020	In addition, diltiazem co-treatment decreased the expressions of stem cell markers CD24 and CD44, increased the expressions of Bax and cleaved caspase 3, enhanced DNA fragmentation, and attenuated cyclin D1 and P-gp expressions as compared to cells treated with either gemcitabine or 5-FU alone.	Diltiazem	13-22	CD44 molecule (Indian blood group)	Homo sapiens	92-96
33011221-9	2020	In addition, diltiazem co-treatment decreased the expressions of stem cell markers CD24 and CD44, increased the expressions of Bax and cleaved caspase 3, enhanced DNA fragmentation, and attenuated cyclin D1 and P-gp expressions as compared to cells treated with either gemcitabine or 5-FU alone.	Diltiazem	13-22	BCL2 associated X, apoptosis regulator	Homo sapiens	127-130
33011221-9	2020	In addition, diltiazem co-treatment decreased the expressions of stem cell markers CD24 and CD44, increased the expressions of Bax and cleaved caspase 3, enhanced DNA fragmentation, and attenuated cyclin D1 and P-gp expressions as compared to cells treated with either gemcitabine or 5-FU alone.	Diltiazem	13-22	caspase 3	Homo sapiens	143-152
33011221-9	2020	In addition, diltiazem co-treatment decreased the expressions of stem cell markers CD24 and CD44, increased the expressions of Bax and cleaved caspase 3, enhanced DNA fragmentation, and attenuated cyclin D1 and P-gp expressions as compared to cells treated with either gemcitabine or 5-FU alone.	Diltiazem	13-22	cyclin D1	Homo sapiens	197-206
33011221-9	2020	In addition, diltiazem co-treatment decreased the expressions of stem cell markers CD24 and CD44, increased the expressions of Bax and cleaved caspase 3, enhanced DNA fragmentation, and attenuated cyclin D1 and P-gp expressions as compared to cells treated with either gemcitabine or 5-FU alone.	Diltiazem	13-22	ATP binding cassette subfamily B member 1	Homo sapiens	211-215