PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
11284996-2	2001	In the present study we aimed to investigate plasma levels of CGRP during headache induced by the NO donor glyceryl trinitrate (GTN) in 16 patients with chronic tension-type headache and 16 healthy controls.	Nitroglycerin	107-126	calcitonin related polypeptide alpha	Homo sapiens	62-66
11179059-7	2001	Vessels from eNOS KO animals were less sensitive to ANP after GTN pretreatment, an effect that was reversed in the presence of an sGC inhibitor.	Nitroglycerin	62-65	sarcoglycan beta	Homo sapiens	130-133
11240977-3	2001	METHODS: In 9 healthy male subjects, increasing doses (0.5-128 ng/min) of nitroglycerin were infused into the dorsal hand vein pretreated with 0 (control), 0.3, or 1 ng/min of angiotensin II.	Nitroglycerin	74-87	angiotensinogen	Homo sapiens	176-190
11240977-4	2001	In 8 healthy male subjects, angiotensin II (0.3 and 1 ng/min) was infused into the vein dilated by nitroglycerin with and without pretreatment with losartan and with diltiazem.	Nitroglycerin	99-112	angiotensinogen	Homo sapiens	28-42
11240977-6	2001	RESULTS: The venodilator response of nitroglycerin was significantly suppressed by the pretreatment with angiotensin II; The maximum venodilator effect was dose-dependently decreased, and the infusion rate producing half-maximum response was dose-dependently increased.	Nitroglycerin	37-50	angiotensinogen	Homo sapiens	105-119
11240977-7	2001	The venodilation caused by nitroglycerin was decreased by angiotensin II, and this effect was attenuated by pretreatment with losartan.	Nitroglycerin	27-40	angiotensinogen	Homo sapiens	58-72
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.	Nitroglycerin	117-130	angiotensinogen	Homo sapiens	53-67
11240977-0	2001	Effect of angiotensin II on venodilator response to nitroglycerin.	Nitroglycerin	52-65	angiotensinogen	Homo sapiens	10-24
11240977-1	2001	OBJECTIVE: An enhanced circulatory angiotensin II level that results from the administration of nitroglycerin may contribute to the development of nitrate tolerance.	Nitroglycerin	96-109	angiotensinogen	Homo sapiens	35-49
11284996-2	2001	In the present study we aimed to investigate plasma levels of CGRP during headache induced by the NO donor glyceryl trinitrate (GTN) in 16 patients with chronic tension-type headache and 16 healthy controls.	Nitroglycerin	128-131	calcitonin related polypeptide alpha	Homo sapiens	62-66
11284996-8	2001	Both in patients and controls, CGRP levels changed significantly over time, on both the GTN and placebo days (P < 0.05).	Nitroglycerin	88-91	calcitonin related polypeptide alpha	Homo sapiens	31-35
11298663-0	2001	Investigations into migraine pathogenesis: time course for effects of m-CPP, BW723C86 or glyceryl trinitrate on appearance of Fos-like immunoreactivity in rat trigeminal nucleus caudalis (TNC).	Nitroglycerin	89-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-129
11741519-0	2001	Involvement of calcitonin gene-related peptide in nitroglycerin induced improvement of preservation with cardioplegic solution.	Nitroglycerin	50-63	calcitonin-related polypeptide alpha	Rattus norvegicus	15-46
11741519-1	2001	AIM: To study improvement of preservation with cardioplegic solution induced by nitroglycerin was related to stimulation of calcitonin gene-related peptide (CG RP) release.	Nitroglycerin	80-93	calcitonin-related polypeptide alpha	Rattus norvegicus	124-155
11741519-1	2001	AIM: To study improvement of preservation with cardioplegic solution induced by nitroglycerin was related to stimulation of calcitonin gene-related peptide (CG RP) release.	Nitroglycerin	80-93	calcitonin-related polypeptide alpha	Rattus norvegicus	157-162
11741519-5	2001	The protection induced by nitroglycerin was abolished by CGRP(8-37), the selective CGRP receptor antagonist, or pretreatment wit h capsaicin to deplete sensory nerves neurotransmitter content, but was unaltered by treatment w ith glibenclamide, the blocker of the ATP-sensitive potassium channel (KATP).	Nitroglycerin	26-39	calcitonin-related polypeptide alpha	Rattus norvegicus	57-61
11741519-5	2001	The protection induced by nitroglycerin was abolished by CGRP(8-37), the selective CGRP receptor antagonist, or pretreatment wit h capsaicin to deplete sensory nerves neurotransmitter content, but was unaltered by treatment w ith glibenclamide, the blocker of the ATP-sensitive potassium channel (KATP).	Nitroglycerin	26-39	calcitonin-related polypeptide alpha	Rattus norvegicus	83-87
11741519-7	2001	Levels of CGRP-LI in the coronary effluent were significantly increased in the hearts treated with nitroglycerin.	Nitroglycerin	99-112	calcitonin-related polypeptide alpha	Rattus norvegicus	10-14
11741519-8	2001	However, the elevated level of CGRP-LI by nitroglycerin was abolished by pretreatment with capsaicin.	Nitroglycerin	42-55	calcitonin-related polypeptide alpha	Rattus norvegicus	31-35
11741519-9	2001	CONCLUSION: The improvement of preservation with cardioplegic solution induced by nitroglycerin was related to stimulation of CGRP release in the rat heart, and the effect is not related to the activation of the KATP channel.	Nitroglycerin	82-95	calcitonin-related polypeptide alpha	Rattus norvegicus	126-130
11137083-4	2001	The purpose of this investigation was to verify in vivo and in vitro vasoreactivity to bradykinin (BK) and serotonin (5-hydroxytryptamine; 5-HT) (endothelial dependent agonists) as well as to nitroglycerin (NTG) (exogenous nitric oxide donor) at different times after oversized balloon angioplasty intervention ranging from 1 h to 12 weeks, in normal porcine coronary arteries.	Nitroglycerin	192-205	kininogen 1	Homo sapiens	87-97
11255792-4	2001	To assess the mechanism of abortion and fetal death in rabbits given G-CSF, 125I-labeled NTG was given intravenously on Day 18 of pregnancy after repeated administration of cold NTG on Days 6 through 17 of pregnancy, and the feto-maternal distribution of radioactivity was examined.	Nitroglycerin	89-92	colony stimulating factor 3	Homo sapiens	69-74
11137083-4	2001	The purpose of this investigation was to verify in vivo and in vitro vasoreactivity to bradykinin (BK) and serotonin (5-hydroxytryptamine; 5-HT) (endothelial dependent agonists) as well as to nitroglycerin (NTG) (exogenous nitric oxide donor) at different times after oversized balloon angioplasty intervention ranging from 1 h to 12 weeks, in normal porcine coronary arteries.	Nitroglycerin	207-210	kininogen 1	Homo sapiens	87-97
11201500-0	2001	YC-1 enhances the responsiveness of tolerant vascular smooth muscle to glyceryl trinitrate.	Nitroglycerin	71-90	RNA binding motif single stranded interacting protein 1	Homo sapiens	0-4
11201500-4	2001	Treatment with YC-1 (3 microM) produced a left shift of the GTN concentration-response curve and decreased the EC50 value for GTN-induced relaxation in both GTN-tolerant and non-tolerant RARs (P < 0.05).	Nitroglycerin	126-129	RNA binding motif single stranded interacting protein 1	Homo sapiens	15-19
11201500-5	2001	Intravascular cGMP elevation induced by GTN was enhanced in the presence of YC-1 in GTN-tolerant and non-tolerant RARs (P < 0.05).	Nitroglycerin	40-43	RNA binding motif single stranded interacting protein 1	Homo sapiens	76-80
11201500-2	2001	Recently, 3-(5"-hydroxymethyl-2"-furyl)-1-benzylindazole (YC-1) was shown to potentiate vascular smooth muscle responsiveness to glyceryl trinitrate (GTN), sodium nitroprusside, and the nitric oxide donor NOC 18, in organic nitrate-naive vascular smooth muscle.	Nitroglycerin	129-148	RNA binding motif single stranded interacting protein 1	Homo sapiens	58-62
11201500-5	2001	Intravascular cGMP elevation induced by GTN was enhanced in the presence of YC-1 in GTN-tolerant and non-tolerant RARs (P < 0.05).	Nitroglycerin	84-87	RNA binding motif single stranded interacting protein 1	Homo sapiens	76-80
11201500-6	2001	These observations indicate that YC-1, or similarly acting drugs, may be useful in overcoming the tolerance that develops during sustained GTN therapy, and that its mechanism may involve enhanced cGMP formation.	Nitroglycerin	139-142	RNA binding motif single stranded interacting protein 1	Homo sapiens	33-37
11201500-2	2001	Recently, 3-(5"-hydroxymethyl-2"-furyl)-1-benzylindazole (YC-1) was shown to potentiate vascular smooth muscle responsiveness to glyceryl trinitrate (GTN), sodium nitroprusside, and the nitric oxide donor NOC 18, in organic nitrate-naive vascular smooth muscle.	Nitroglycerin	150-153	RNA binding motif single stranded interacting protein 1	Homo sapiens	58-62
11201500-3	2001	We used GTN-tolerant rabbit aortic rings (RARs) to test the hypothesis that a non-vasorelaxant concentration of YC-1 enhances the ability of the prototypical organic nitrate GTN to relax vascular smooth muscle and elevate intravascular cGMP under conditions of GTN tolerance.	Nitroglycerin	8-11	RNA binding motif single stranded interacting protein 1	Homo sapiens	112-116
11201500-3	2001	We used GTN-tolerant rabbit aortic rings (RARs) to test the hypothesis that a non-vasorelaxant concentration of YC-1 enhances the ability of the prototypical organic nitrate GTN to relax vascular smooth muscle and elevate intravascular cGMP under conditions of GTN tolerance.	Nitroglycerin	174-177	RNA binding motif single stranded interacting protein 1	Homo sapiens	112-116
11201500-3	2001	We used GTN-tolerant rabbit aortic rings (RARs) to test the hypothesis that a non-vasorelaxant concentration of YC-1 enhances the ability of the prototypical organic nitrate GTN to relax vascular smooth muscle and elevate intravascular cGMP under conditions of GTN tolerance.	Nitroglycerin	174-177	RNA binding motif single stranded interacting protein 1	Homo sapiens	112-116
11201500-4	2001	Treatment with YC-1 (3 microM) produced a left shift of the GTN concentration-response curve and decreased the EC50 value for GTN-induced relaxation in both GTN-tolerant and non-tolerant RARs (P < 0.05).	Nitroglycerin	60-63	RNA binding motif single stranded interacting protein 1	Homo sapiens	15-19
11201500-4	2001	Treatment with YC-1 (3 microM) produced a left shift of the GTN concentration-response curve and decreased the EC50 value for GTN-induced relaxation in both GTN-tolerant and non-tolerant RARs (P < 0.05).	Nitroglycerin	126-129	RNA binding motif single stranded interacting protein 1	Homo sapiens	15-19
11193508-7	2000	The value of urine NAG in the TNG group was larger than that in the NIC or PGE1 group.	Nitroglycerin	30-33	NBAS subunit of NRZ tethering complex	Homo sapiens	19-22
11156122-7	2000	Nearly 200% vasodilation was observed with calcium antagonist in combination with NTG in AII-precontracted vessels.	Nitroglycerin	82-85	angiotensinogen	Homo sapiens	89-92
11291271-6	2000	The high incidence of serious side-effects of vasopressin, even with nitroglycerin, has limited its application and decreased the use of this drug, with its abandonment in Europe.	Nitroglycerin	69-82	arginine vasopressin	Homo sapiens	46-57
11053225-0	2000	Endothelial nitric oxide synthase is a site of superoxide synthesis in endothelial cells treated with glyceryl trinitrate.	Nitroglycerin	102-121	nitric oxide synthase 3	Homo sapiens	0-33
11053225-11	2000	In conclusion, endothelial NOS is a site of O(2)(*-) synthesis in endothelial cells activated by GTN.	Nitroglycerin	97-100	nitric oxide synthase 3	Homo sapiens	15-30
11046091-1	2000	There is evidence that increased endothelial production of endothelin-1 (ET-1) may contribute to glyceryl trinitrate (GTN) tolerance.	Nitroglycerin	97-116	endothelin 1	Rattus norvegicus	59-71
11046091-1	2000	There is evidence that increased endothelial production of endothelin-1 (ET-1) may contribute to glyceryl trinitrate (GTN) tolerance.	Nitroglycerin	118-121	endothelin 1	Rattus norvegicus	59-71
11501035-5	2000	Drug-induced preconditioning, such as by nitroglycerin, may be related to stimulated release of CGRP.	Nitroglycerin	41-54	calcitonin related polypeptide alpha	Homo sapiens	96-100
10930383-4	2000	METHODS & RESULTS: Both NTG and SNAP induced a dose-dependent decrease in PDGF-induced DNA synthesis and cell migration, which was associated with a decrease in PDGF-induced intracellular Ca(2+) increase and extracellular signal-regulated kinase (ERK) activity.	Nitroglycerin	28-31	mitogen-activated protein kinase 1	Homo sapiens	212-249
11012561-2	2000	METHODS: Four patients received a GTN tape following intravenous administration of 0.1 microg kg-1 min-1 GTN, and the other four patients received two GTN tapes following intravenous administration of 0.2 microg kg-1 min-1 GTN.	Nitroglycerin	34-37	CD59 molecule (CD59 blood group)	Homo sapiens	99-104
11043526-0	2000	Systemic nitroglycerin increases nNOS levels in rat trigeminal nucleus caudalis.	Nitroglycerin	9-22	nitric oxide synthase 1	Rattus norvegicus	33-37
11043526-2	2000	Subcutaneous nitroglycerin (10 mg/kg) produced a significant increase of nitric oxide synthase (NOS)- and c-fos-immunoreactive neurons in the cervical part of trigeminal nucleus caudalis in rats after 4 h. This effect was not observed in the thoracic dorsal horn.	Nitroglycerin	13-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
11026640-10	2000	Both nitroglycerin and nicorandil exhibited an increase in vasodilation in the presence of an ACE inhibitor containing a sulfhydryl group.	Nitroglycerin	5-18	angiotensin I converting enzyme	Homo sapiens	94-97
12206003-11	2000	CONCLUSION: The AMs from patients with asthma exacerbation secrete a large quantity of NO and ET because of the increasing expression of iNOS-mRNA, ET-mRNA; DXM can inhibit the expression of iNOS-mRNA and ET-mRNA, and decrease NO and ET level, but the NO and ET level are still abnormal; NTG can improve directly the production of NO and inhibit significantly the expression of iNOS-mRNA and ET-mRNA as well as decrease the ET level.	Nitroglycerin	288-291	inositol-3-phosphate synthase 1	Homo sapiens	191-195
12206003-11	2000	CONCLUSION: The AMs from patients with asthma exacerbation secrete a large quantity of NO and ET because of the increasing expression of iNOS-mRNA, ET-mRNA; DXM can inhibit the expression of iNOS-mRNA and ET-mRNA, and decrease NO and ET level, but the NO and ET level are still abnormal; NTG can improve directly the production of NO and inhibit significantly the expression of iNOS-mRNA and ET-mRNA as well as decrease the ET level.	Nitroglycerin	288-291	inositol-3-phosphate synthase 1	Homo sapiens	191-195
10926562-5	2000	CCSP-beta(2)-AR mice were also less responsive to ozone (0.75 ppm for 4 h) because enhanced pause in NTG mice acutely increased to 77% over baseline (P < 0.05) but remained unchanged in the CCSP-beta(2)-AR mice.	Nitroglycerin	101-104	secretoglobin, family 1A, member 1 (uteroglobin)	Mus musculus	0-4
10926562-5	2000	CCSP-beta(2)-AR mice were also less responsive to ozone (0.75 ppm for 4 h) because enhanced pause in NTG mice acutely increased to 77% over baseline (P < 0.05) but remained unchanged in the CCSP-beta(2)-AR mice.	Nitroglycerin	101-104	adrenergic receptor, beta 2	Mus musculus	5-15
10930383-4	2000	METHODS & RESULTS: Both NTG and SNAP induced a dose-dependent decrease in PDGF-induced DNA synthesis and cell migration, which was associated with a decrease in PDGF-induced intracellular Ca(2+) increase and extracellular signal-regulated kinase (ERK) activity.	Nitroglycerin	28-31	mitogen-activated protein kinase 1	Homo sapiens	251-254
10866832-8	2000	Hepatic apoA-I mRNA decreased 30% in NTg and 180% in apoAI-Tg mice.	Nitroglycerin	37-40	apolipoprotein A-I	Mus musculus	8-14
10933381-7	2000	RESULTS: Continuous treatment with NTG caused tolerance to NTG, cross-tolerance to the endothelium-dependent vasodilator acetylcholine, increased vascular O2*-, reduced Cu/Zn SOD expression and increased sensitivity to vasoconstrictors such as phenylephrine, serotonin and angiotensin II.	Nitroglycerin	35-38	angiotensinogen	Homo sapiens	273-287
10953024-6	2000	In contrast, endothelium-dependent vasodilatation in response to acetylcholine was attenuated in vessels transduced with dn-Akt, although these vessels showed normal responses to nitroglycerin, an endothelium-independent vasodilator.	Nitroglycerin	179-192	thymoma viral proto-oncogene 1	Mus musculus	124-127
10903927-2	2000	In LLC-PK1 kidney epithelial cells, a 5-h pretreatment with glyceryl trinitrate (GTN, 0.1-1 microM) significantly attenuated the cyclic GMP response to a subsequent challenge with both NO-aspirin or GTN.	Nitroglycerin	60-79	5'-nucleotidase, cytosolic II	Homo sapiens	136-139
10903927-2	2000	In LLC-PK1 kidney epithelial cells, a 5-h pretreatment with glyceryl trinitrate (GTN, 0.1-1 microM) significantly attenuated the cyclic GMP response to a subsequent challenge with both NO-aspirin or GTN.	Nitroglycerin	81-84	5'-nucleotidase, cytosolic II	Homo sapiens	136-139
12212166-3	2000	Multiple linear stepwise regression analysis showed that FMD was positively related to high-density lipoprotein cholesterol and inversely related to baseline diameters of brachial arteries, age and low-density lipoprotein cholesterol, whereas GTN induced dilatation was positively related to FMD and inversely related to baseline diameters of brachial arteries.	Nitroglycerin	243-246	FSHMD1A	Homo sapiens	57-60
10884648-9	2000	Nitroglycerin infusion markedly reduced protein nitrotyrosine and tumor necrosis factor alpha levels in both groups.	Nitroglycerin	0-13	tumor necrosis factor	Homo sapiens	66-93
10884648-10	2000	In contrast, nitroglycerin infusion significantly increased C3a in patients without diabetes and increased elastase and interleukin 8 levels in patients with diabetes.	Nitroglycerin	13-26	complement C3	Homo sapiens	60-63
10884648-10	2000	In contrast, nitroglycerin infusion significantly increased C3a in patients without diabetes and increased elastase and interleukin 8 levels in patients with diabetes.	Nitroglycerin	13-26	C-X-C motif chemokine ligand 8	Homo sapiens	120-133
10841180-12	2000	However, a higher level of serum osteocalcin and bone-specific alkaline phosphatase levels were maintained only with once daily administration of NG.	Nitroglycerin	146-148	bone gamma-carboxyglutamate protein	Rattus norvegicus	33-44
10799659-4	2000	CGRP(8-37) (0.63 microM) induced rightward shifts in the vasodilatory concentration-response curves for nitroglycerin (NTG), Piloty"s acid (PA), and SIN-1 (linsidomine).	Nitroglycerin	104-117	calcitonin-related polypeptide alpha	Rattus norvegicus	0-4
10799659-4	2000	CGRP(8-37) (0.63 microM) induced rightward shifts in the vasodilatory concentration-response curves for nitroglycerin (NTG), Piloty"s acid (PA), and SIN-1 (linsidomine).	Nitroglycerin	119-122	calcitonin-related polypeptide alpha	Rattus norvegicus	0-4
10799659-6	2000	The release of CGRP from rat aorta in response to NTG and PA was measured specifically by radioimmunoassay.	Nitroglycerin	50-53	calcitonin-related polypeptide alpha	Rattus norvegicus	15-19
10799659-7	2000	Thirty-minute incubations of NTG or PA with rat aorta induced 189.5 and 214.6% increases, respectively, in CGRP release when compared with the control (P < 0.05).	Nitroglycerin	29-32	calcitonin-related polypeptide alpha	Rattus norvegicus	107-111
10799659-10	2000	These results indicate that only NTG and PA, and to a lesser extent SIN-1, stimulate the release of CGRP from the rat aorta, which subsequently contributes to the vasodilatory activity of these agents.	Nitroglycerin	33-36	calcitonin-related polypeptide alpha	Rattus norvegicus	100-104
10875718-7	2000	Nitroglycerine infusion was started at 10 mg x hr(-1) shortly after the initiation of DPD.	Nitroglycerin	0-14	dihydropyrimidine dehydrogenase	Homo sapiens	86-89
10790164-1	2000	Nitrovasodilators such as nitroglycerine, via production of nitric oxide and an increase in [cGMP], can induce arterial smooth muscle relaxation without proportional reduction in myosin light chain (MLC) phosphorylation or myoplasmic [Ca2+].	Nitroglycerin	26-40	myosin light chain 1	Sus scrofa	179-197
10790164-4	2000	Nitroglycerine-induced relaxation was associated with a reduction in O2 consumption, suggesting that the interaction between phosphorylated myosin and the thin filament was inhibited.	Nitroglycerin	0-14	myosin X	Sus scrofa	140-146
10790164-7	2000	When homogenates of nitroglycerine-relaxed tissues were centrifuged at 6000 g, phosphorylated HSP20 preferentially sedimented in the pellet, suggesting that phosphorylation of HSP20 may increase its affinity for the thin filament.	Nitroglycerin	20-34	HSPB6	Sus scrofa	94-99
10790164-7	2000	When homogenates of nitroglycerine-relaxed tissues were centrifuged at 6000 g, phosphorylated HSP20 preferentially sedimented in the pellet, suggesting that phosphorylation of HSP20 may increase its affinity for the thin filament.	Nitroglycerin	20-34	HSPB6	Sus scrofa	176-181
10699367-0	2000	Caldesmon and heat shock protein 20 phosphorylation in nitroglycerin- and magnesium-induced relaxation of swine carotid artery.	Nitroglycerin	55-68	HSPB6	Sus scrofa	14-35
11873750-3	2000	Therapies used to reduce PVR in the cardiac catheterization laboratory include high-flow oxygen; sublingual nitroglycerin; and intravenous inotropic agents, vasodilators, and selective pulmonary vasodilators.	Nitroglycerin	108-121	PVR cell adhesion molecule	Homo sapiens	25-28
10699367-7	2000	Addition of nitroglycerin induced a relaxation, significantly increased HSP20 phosphorylation to 0.18+/-0.02 mol P(i)/mol HSP20, did not significantly change caldesmon phosphorylation, and pH(i) returned to near unstimulated values.	Nitroglycerin	12-25	HSPB6	Sus scrofa	72-77
10699367-7	2000	Addition of nitroglycerin induced a relaxation, significantly increased HSP20 phosphorylation to 0.18+/-0.02 mol P(i)/mol HSP20, did not significantly change caldesmon phosphorylation, and pH(i) returned to near unstimulated values.	Nitroglycerin	12-25	HSPB6	Sus scrofa	122-127
10699367-10	2000	However, it is possible that HSP20 phosphorylation may be involved in nitroglycerin-induced relaxation without MRLC dephosphorylation.	Nitroglycerin	70-83	HSPB6	Sus scrofa	29-34
10604966-2	2000	The ability of XOR to act as an NADH oxidase is a less well recognized function of the enzyme, and it is this function that we used to explore the metabolism of glyceryl trinitrate.	Nitroglycerin	161-180	xanthine dehydrogenase	Homo sapiens	15-18
10766405-8	2000	Both basal and stimulated levels of t-PA antigen were significantly higher in HTG than in NTG.	Nitroglycerin	90-93	plasminogen activator, tissue type	Homo sapiens	36-40
10640313-7	2000	In the rat aorta, NTG appeared to exhibit its vasodilatory effect exclusively through activation of the heme site of sGC.	Nitroglycerin	18-21	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	117-120
10620000-0	2000	Effect of transdermal nitroglycerin on glucose-stimulated insulin release in healthy male volunteers.	Nitroglycerin	22-35	insulin	Homo sapiens	58-65
10620000-2	2000	We studied whether transdermal application of nitroglycerin, another NO donor widely used for angina prophylaxis, influenced glucose-stimulated insulin release in healthy, young, male volunteers.	Nitroglycerin	46-59	insulin	Homo sapiens	144-151
10620000-9	2000	CONCLUSION: We conclude that inhibition of glucose-stimulated insulin release by transdermal nitroglycerin without causing hyperglycaemia may serve as a novel component of the antianginal mechanism of action of nitrates.	Nitroglycerin	93-106	insulin	Homo sapiens	62-69
10625313-0	2000	Effects of long-term nitroglycerin treatment on endothelial nitric oxide synthase (NOS III) gene expression, NOS III-mediated superoxide production, and vascular NO bioavailability.	Nitroglycerin	21-34	nitric oxide synthase 3	Rattus norvegicus	83-90
10625313-3	2000	It remains to be elucidated, however, whether long-term treatment with NTG alters the activity and expression of the endothelial NO synthase (NOS III) and whether this enzyme can contribute to O(2)(.-) formation.	Nitroglycerin	71-74	nitric oxide synthase 3	Rattus norvegicus	142-149
10625313-4	2000	We studied the influence of long-term NTG treatment on the expression of NOS III as assessed by RNase protection assay and Western blot.	Nitroglycerin	38-41	nitric oxide synthase 3	Rattus norvegicus	73-80
10625313-14	2000	These findings suggest that NTG treatment increases the expression of a dysfunctional NOS III gene, leading to increased formation of O(2)(.-) and decreased vascular NO bioavailability.	Nitroglycerin	28-31	nitric oxide synthase 3	Rattus norvegicus	86-93
10604966-3	2000	The antiplatelet effect of nitric oxide (NO) on platelet aggregation was used as a bioassay to assess the bioconversion of glyceryl trinitrate to NO by XOR.	Nitroglycerin	123-142	xanthine dehydrogenase	Homo sapiens	152-155
10604966-6	2000	XOR produced a dose-dependent antiaggregant effect when incubated with glyceryl trinitrate (GTN), 220 microM.	Nitroglycerin	71-90	xanthine dehydrogenase	Homo sapiens	0-3
10604966-6	2000	XOR produced a dose-dependent antiaggregant effect when incubated with glyceryl trinitrate (GTN), 220 microM.	Nitroglycerin	92-95	xanthine dehydrogenase	Homo sapiens	0-3
10604966-12	2000	These findings suggest that GTN may be reduced to NO in vitro by the enzyme XOR in sufficient amounts to inhibit platelet aggregation.	Nitroglycerin	28-31	xanthine dehydrogenase	Homo sapiens	76-79
10490563-9	1999	The response to substance P is substantial and closely correlated with the response to glyceryl trinitrate in both "normal" patients and those with coronary disease.	Nitroglycerin	87-106	tachykinin precursor 1	Homo sapiens	16-27
10594029-5	2000	In MyoD, the myogenic BR residues establish specificity for particular CAN NTG sites indirectly, by influencing the conformation through which the BR helix binds DNA.	Nitroglycerin	75-78	myogenic differentiation 1	Homo sapiens	3-7
10594029-9	2000	Our findings indicate that E2A and its partner bHLH proteins bind to CAN NTG sites by adopting particular preferred BR-DNA conformations, from which they derive differences in sequence recognition that can be important for functional specificity.	Nitroglycerin	73-76	transcription factor 3	Homo sapiens	27-30
10630673-5	1999	The activities of microsomal cytochrome P-450, the hepatic level of glutathione, and the reduction rate of nitroxide radicals in the in vivo liver, measured using L-band ESR spectroscopy, were temporarily decreased following GTN administration.	Nitroglycerin	225-228	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	29-45
10423345-7	1999	Conversely, administration of the NO donor nitroglycerin induced an increase in iNOS mRNA levels similar to that induced by ischemic PC.	Nitroglycerin	43-56	nitric oxide synthase 2	Homo sapiens	80-84
10584234-8	1999	It should be noted, however, that sildenafil enhanced the hypotensive effect of glyceryl trinitrate, as a result of inhibition of PDE5 in vascular smooth muscle.	Nitroglycerin	80-99	phosphodiesterase 5A	Homo sapiens	130-134
10481072-5	1999	In addition, basal cardiac AC activities were normalized in the ACV/G alpha q mice (NTG=23+/-4.4, G alpha q=14+/-3.6, ACV/G alpha q=29+/-5.3 pmol/min/mg) as were maximal isoproterenol stimulated activities (59+/-8.9, 34+/-4.6, 52+/-6.7 pmol/min/mg respectively).	Nitroglycerin	84-87	guanine nucleotide binding protein, alpha q polypeptide	Mus musculus	68-77
10511130-10	1999	This effect on the cNOS pathway seems to attenuate the superoxide anion accumulation induced by nitroglycerin exposure (probably via a downregulation of oxidative enzyme).	Nitroglycerin	96-109	nitric oxide synthase 3	Rattus norvegicus	19-23
10526126-2	1999	Combined retrograde and anterograde tracers were injected into nuclei which consistently demonstrate robust Fos expression following our systemic nitroglycerin injection paradigm.	Nitroglycerin	146-159	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	108-111
10526126-4	1999	Dual Fos/tracer immunocytochemistry in treated animals documented the existence of a subset of autonomic nuclei which are activated by nitroglycerin injection and have reciprocal connections.	Nitroglycerin	135-148	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	5-8
10526126-6	1999	Nuclei which show strong Fos labeling following nitroglycerin administration, but not traced in this study, include the nucleus trigeminalis caudalis and the ventrolateral column of the periaqueductal gray, both of which mediate nociceptive modalities.	Nitroglycerin	48-61	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	25-28
10690349-3	1999	This study firstly investigates whether modulation of BKCa affects the vascular response to nitroglycerin (NTG)-derived NO in vivo and in the isolated heart and secondly examines the influence of endothelial BKCa on NTG-mediated vasodilation in vitro.	Nitroglycerin	92-105	potassium calcium-activated channel subfamily M alpha 1	Rattus norvegicus	54-58
10690349-3	1999	This study firstly investigates whether modulation of BKCa affects the vascular response to nitroglycerin (NTG)-derived NO in vivo and in the isolated heart and secondly examines the influence of endothelial BKCa on NTG-mediated vasodilation in vitro.	Nitroglycerin	107-110	potassium calcium-activated channel subfamily M alpha 1	Rattus norvegicus	54-58
10690349-11	1999	CONCLUSION: The results suggest, that modulation of endothelial BKCa significantly affects NTG-induced vasorelaxation in vitro, in the isolated perfused heart and in vivo.	Nitroglycerin	91-94	potassium calcium-activated channel subfamily M alpha 1	Rattus norvegicus	64-68
10371376-5	1999	Salt restriction significantly reduced maximal insulin-mediated vasodilation (normal sodium: 51% +/- 5% of maximum nitroglycerin-mediated response; low sodium: 28% +/- 6%, P < .01).	Nitroglycerin	115-128	insulin	Homo sapiens	47-54
10377083-1	1999	BACKGROUND: We have previously shown that nitroglycerin (NTG) therapy increases vascular expression of endothelin 1 (ET-1) and stimulates vascular superoxide (O2.-) production via activation of NADH/NADPH oxidases.	Nitroglycerin	42-55	endothelin-1	Oryctolagus cuniculus	103-115
10377083-1	1999	BACKGROUND: We have previously shown that nitroglycerin (NTG) therapy increases vascular expression of endothelin 1 (ET-1) and stimulates vascular superoxide (O2.-) production via activation of NADH/NADPH oxidases.	Nitroglycerin	42-55	endothelin-1	Oryctolagus cuniculus	117-121
10377083-1	1999	BACKGROUND: We have previously shown that nitroglycerin (NTG) therapy increases vascular expression of endothelin 1 (ET-1) and stimulates vascular superoxide (O2.-) production via activation of NADH/NADPH oxidases.	Nitroglycerin	57-60	endothelin-1	Oryctolagus cuniculus	103-115
10377083-1	1999	BACKGROUND: We have previously shown that nitroglycerin (NTG) therapy increases vascular expression of endothelin 1 (ET-1) and stimulates vascular superoxide (O2.-) production via activation of NADH/NADPH oxidases.	Nitroglycerin	57-60	endothelin-1	Oryctolagus cuniculus	117-121
10377083-4	1999	METHODS AND RESULTS: In New Zealand White rabbits, 3 days of treatment with NTG patches increased plasma renin activity for the entire treatment period.	Nitroglycerin	76-79	LOW QUALITY PROTEIN: renin	Oryctolagus cuniculus	105-110
10377083-5	1999	After 24 hours of NTG treatment, angiotensin II type 1 (AT1) receptor expression and vascular ACE activity were significantly decreased.	Nitroglycerin	18-21	type-1 angiotensin II receptor	Oryctolagus cuniculus	33-69
10377083-5	1999	After 24 hours of NTG treatment, angiotensin II type 1 (AT1) receptor expression and vascular ACE activity were significantly decreased.	Nitroglycerin	18-21	angiotensin-converting enzyme	Oryctolagus cuniculus	94-97
10455256-3	1999	Application to rats of a transdermal patch that releases doses of nitroglycerin comparable to those used in man (40, 80, 160 and 400 ng min(-1) rat(-1)) reduced gastric damage induced by indomethacin (25 mg kg(-1), p.o.	Nitroglycerin	66-79	CD59 molecule (CD59 blood group)	Homo sapiens	136-142
10455256-5	1999	The nitroglycerin patch (160 ng min(-1) rat(-1)) also diminished damage by oral administration (1 ml) of acidified bile salts (100 mg kg(-1) taurocholic acid in 150 mM HCl) or 50% ethanol.	Nitroglycerin	4-17	CD59 molecule (CD59 blood group)	Homo sapiens	32-38
10455256-6	1999	Transdermal nitroglycerin (160 ng min(-1) rat(-1)) did not influence basal gastric blood flow, as measured by lasser-doppler flowmetry, but prevented its reduction by indomethacin.	Nitroglycerin	12-25	CD59 molecule (CD59 blood group)	Homo sapiens	34-40
10455256-7	1999	Transdermal nitroglycerin (160 ng min(-1) rat(-1)) prevented in vivo leukocyte rolling and adherence in the rat mesentery microvessels superfused with indomethacin, as evaluated by intravital microscopy.	Nitroglycerin	12-25	CD59 molecule (CD59 blood group)	Homo sapiens	34-40
10367222-16	1999	Moreover, the ECG-dipyridamole test showed nitroglycerin tolerance because five patients with a negative acute test (Dip 1) became positive during chronic therapy (Dip 2).	Nitroglycerin	43-56	cyclin D1 binding protein 1	Homo sapiens	117-122
10464783-3	1999	METHODS AND RESULTS: Arterial functional properties, i.e. FAC(AUC) responses to glyceryl trinitrate (GTN-FAC(AUC)) and acetylcholine (ACh-FAC(AUC), four patients) and the effects on rest and peak forearm blood flow and vascular resistance were evaluated on the non-dominant arm using plethysmographic methods, that also allow the direct assessment of the non-linear "compliance-blood pressure" curve.	Nitroglycerin	80-99	FA complementation group C	Homo sapiens	58-61
10464783-3	1999	METHODS AND RESULTS: Arterial functional properties, i.e. FAC(AUC) responses to glyceryl trinitrate (GTN-FAC(AUC)) and acetylcholine (ACh-FAC(AUC), four patients) and the effects on rest and peak forearm blood flow and vascular resistance were evaluated on the non-dominant arm using plethysmographic methods, that also allow the direct assessment of the non-linear "compliance-blood pressure" curve.	Nitroglycerin	80-99	FA complementation group C	Homo sapiens	105-108
10464783-3	1999	METHODS AND RESULTS: Arterial functional properties, i.e. FAC(AUC) responses to glyceryl trinitrate (GTN-FAC(AUC)) and acetylcholine (ACh-FAC(AUC), four patients) and the effects on rest and peak forearm blood flow and vascular resistance were evaluated on the non-dominant arm using plethysmographic methods, that also allow the direct assessment of the non-linear "compliance-blood pressure" curve.	Nitroglycerin	80-99	FA complementation group C	Homo sapiens	105-108
10367222-16	1999	Moreover, the ECG-dipyridamole test showed nitroglycerin tolerance because five patients with a negative acute test (Dip 1) became positive during chronic therapy (Dip 2).	Nitroglycerin	43-56	disco interacting protein 2 homolog A	Homo sapiens	164-169
10090945-3	1999	NO donor glycerol trinitrate (at the concentration, which induces apoptotic cell death) caused (1) a significant decrease in the concentration of cardiolipin, a major mitochondrial lipid; (2) a downregulation in respiratory chain complex activities; (3) a release of the mitochondrial protein cytochrome c into the cytosol; and (4) an activation of caspase-9 and caspase-3.	Nitroglycerin	9-28	cytochrome c, somatic	Homo sapiens	293-305
10350003-1	1999	PURPOSE: Using an established cell culture model, the present study investigates whether linsidomine (SIN-1), a spontaneous donor of nitric oxide and active metabolite of the antianginal drug molsidomine, induces tolerance to its own cyclic GMP stimulatory action or shows a diminished response after tolerance induction with glyceryl trinitrate.	Nitroglycerin	326-345	MAPK associated protein 1	Homo sapiens	102-107
10350003-4	1999	RESULTS: A 5-h preincubation with glyceryl trinitrate (0.01-100 microM) led to complete inhibition of a subsequent cyclic GMP stimulation by glyceryl trinitrate but left the cyclic GMP response to SIN-1 unaltered.	Nitroglycerin	34-53	5'-nucleotidase, cytosolic II	Homo sapiens	122-125
10350003-4	1999	RESULTS: A 5-h preincubation with glyceryl trinitrate (0.01-100 microM) led to complete inhibition of a subsequent cyclic GMP stimulation by glyceryl trinitrate but left the cyclic GMP response to SIN-1 unaltered.	Nitroglycerin	34-53	5'-nucleotidase, cytosolic II	Homo sapiens	181-184
10350003-4	1999	RESULTS: A 5-h preincubation with glyceryl trinitrate (0.01-100 microM) led to complete inhibition of a subsequent cyclic GMP stimulation by glyceryl trinitrate but left the cyclic GMP response to SIN-1 unaltered.	Nitroglycerin	34-53	MAPK associated protein 1	Homo sapiens	197-202
10350003-4	1999	RESULTS: A 5-h preincubation with glyceryl trinitrate (0.01-100 microM) led to complete inhibition of a subsequent cyclic GMP stimulation by glyceryl trinitrate but left the cyclic GMP response to SIN-1 unaltered.	Nitroglycerin	141-160	5'-nucleotidase, cytosolic II	Homo sapiens	122-125
10090945-3	1999	NO donor glycerol trinitrate (at the concentration, which induces apoptotic cell death) caused (1) a significant decrease in the concentration of cardiolipin, a major mitochondrial lipid; (2) a downregulation in respiratory chain complex activities; (3) a release of the mitochondrial protein cytochrome c into the cytosol; and (4) an activation of caspase-9 and caspase-3.	Nitroglycerin	9-28	caspase 9	Homo sapiens	349-358
10090945-3	1999	NO donor glycerol trinitrate (at the concentration, which induces apoptotic cell death) caused (1) a significant decrease in the concentration of cardiolipin, a major mitochondrial lipid; (2) a downregulation in respiratory chain complex activities; (3) a release of the mitochondrial protein cytochrome c into the cytosol; and (4) an activation of caspase-9 and caspase-3.	Nitroglycerin	9-28	caspase 3	Homo sapiens	363-372
10206178-0	1999	The cardioprotective effects of nitroglycerin-induced preconditioning are mediated by calcitonin gene-related peptide.	Nitroglycerin	32-45	calcitonin-related polypeptide alpha	Rattus norvegicus	86-117
10206178-1	1999	Previous investigations have shown that endogenous calcitonin gene-related peptide (CGRP) may play an important role in the mediation of ischemic preconditioning and that nitroglycerin evokes the release of CGRP.	Nitroglycerin	171-184	calcitonin-related polypeptide alpha	Rattus norvegicus	207-211
10206178-5	1999	The content of CGRP-like immunoreactivity in coronary effluent was increased during nitroglycerin perfusion.	Nitroglycerin	84-97	calcitonin-related polypeptide alpha	Rattus norvegicus	15-19
10206178-6	1999	However, the cardioprotection afforded by nitroglycerin was abolished by CGRP-(8-37) (10(-7) M), a selective CGRP receptor antagonist.	Nitroglycerin	42-55	calcitonin-related polypeptide alpha	Rattus norvegicus	73-77
10206178-6	1999	However, the cardioprotection afforded by nitroglycerin was abolished by CGRP-(8-37) (10(-7) M), a selective CGRP receptor antagonist.	Nitroglycerin	42-55	calcitonin-related polypeptide alpha	Rattus norvegicus	109-113
10206178-7	1999	Pretreatment with capsaicin (50 mg/kg, s.c.), which specifically depletes the transmitter content of sensory nerves, also abolished the protective effects of nitroglycerin and markedly reduced the release of CGRP from the heart during nitroglycerin perfusion.	Nitroglycerin	235-248	calcitonin-related polypeptide alpha	Rattus norvegicus	208-212
10022397-6	1999	Compared with controls (IL-6, 1.1 +/- 0.3 ng/L; IL-8, 3.2 +/- 0.8 ng/L), untreated patients with GD and TNG had elevated IL-6 (GD, 7.11 +/- 0.88 ng/L; TNG, 7.30 +/- 0.77 ng/L; P < 0.001) and IL-8 (GD, 10.3 +/- 1.23 ng/L; TNG, 9.81 +/- 1.27 ng/L; P < 0.001).	Nitroglycerin	104-107	C-X-C motif chemokine ligand 8	Homo sapiens	48-52
10070091-5	1999	Intracoronary BNP induced dose-dependent increases in CSA, APV, and CBF similar in magnitude to those induced by nitroglycerin (NTG).	Nitroglycerin	128-131	natriuretic peptides B	Sus scrofa	14-17
10226173-10	1999	Administration of GTN (20 microg kg-1 min-1) significantly reduced the indomethacin-induced mucosal dysfunction.	Nitroglycerin	18-21	CD59 molecule (CD59 blood group)	Homo sapiens	38-43
10226173-11	1999	By contrast, higher doses of GTN (80 microg kg-1 min-1) exacerbated epithelial dysfunction induced by indomethacin.	Nitroglycerin	29-32	CD59 molecule (CD59 blood group)	Homo sapiens	49-54
10226173-12	1999	Elevated levels of carbonyls and myeloperoxidase (MPO) observed after indomethacin administration were significantly reduced, to the control values, when GTN (20 microg kg-1 min-1) was administered along with indomethacin.	Nitroglycerin	154-157	myeloperoxidase	Rattus norvegicus	33-48
10226173-12	1999	Elevated levels of carbonyls and myeloperoxidase (MPO) observed after indomethacin administration were significantly reduced, to the control values, when GTN (20 microg kg-1 min-1) was administered along with indomethacin.	Nitroglycerin	154-157	myeloperoxidase	Rattus norvegicus	50-53
10226173-12	1999	Elevated levels of carbonyls and myeloperoxidase (MPO) observed after indomethacin administration were significantly reduced, to the control values, when GTN (20 microg kg-1 min-1) was administered along with indomethacin.	Nitroglycerin	154-157	CD59 molecule (CD59 blood group)	Homo sapiens	174-179
10022397-6	1999	Compared with controls (IL-6, 1.1 +/- 0.3 ng/L; IL-8, 3.2 +/- 0.8 ng/L), untreated patients with GD and TNG had elevated IL-6 (GD, 7.11 +/- 0.88 ng/L; TNG, 7.30 +/- 0.77 ng/L; P < 0.001) and IL-8 (GD, 10.3 +/- 1.23 ng/L; TNG, 9.81 +/- 1.27 ng/L; P < 0.001).	Nitroglycerin	104-107	interleukin 6	Homo sapiens	24-28
9832382-5	1998	Finally, glyceryl trinitrate on its own (3-300 microM) significantly increased the naloxone-induced contraction after exposure to mu- and kappa-opioid receptor agonist and it was also able to reverse the inhibition of opioid withdrawal caused by L-N(G)-nitro arginine methyl ester.	Nitroglycerin	9-28	mu-type opioid receptor	Cavia porcellus	130-159
9890402-10	1999	Increased plasma ANP levels, an index of cardiac filling pressure after induction of acute ischemic heart failure, were decreased significantly by cromakalim and tended to decrease by nicorandil or nitroglycerin.	Nitroglycerin	198-211	natriuretic peptide A	Canis lupus familiaris	17-20
10426492-7	1999	Compared to vehicle, glyceryl trinitrate-induced hypotension caused a marked induction of Fos protein in the caudal one-third of the nucleus tractus solitarius (bregma -14 to -13.3 mm), which tailed off rapidly in more rostral sections.	Nitroglycerin	21-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-93
9813175-2	1998	A 5-h pretreatment with glyceryl trinitrate (GTN, 0.01-100 microM) resulted in desensitization of the intracellular cyclic GMP response to a subsequent 10-min challenge with GTN (1 microM).	Nitroglycerin	24-43	5'-nucleotidase, cytosolic II	Homo sapiens	123-126
9813175-2	1998	A 5-h pretreatment with glyceryl trinitrate (GTN, 0.01-100 microM) resulted in desensitization of the intracellular cyclic GMP response to a subsequent 10-min challenge with GTN (1 microM).	Nitroglycerin	45-48	5'-nucleotidase, cytosolic II	Homo sapiens	123-126
9813175-2	1998	A 5-h pretreatment with glyceryl trinitrate (GTN, 0.01-100 microM) resulted in desensitization of the intracellular cyclic GMP response to a subsequent 10-min challenge with GTN (1 microM).	Nitroglycerin	174-177	5'-nucleotidase, cytosolic II	Homo sapiens	123-126
10464004-1	1999	The objective of the present study is to compare the effectiveness of transdermal glyceryl-trinitrate versus oral nifedipine in lowering blood pressure in patients affected by pregnancy-induced hypertension (PIH).	Nitroglycerin	82-101	pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included)	Homo sapiens	208-211
10772065-7	1999	Subsequent administration of GTN resulted in dose-dependent amelioration of GSH content and GR activity with concomitant inhibition of lipid peroxidation, and BUN and creatinine levels.	Nitroglycerin	29-32	glutathione-disulfide reductase	Homo sapiens	92-94
10772065-8	1999	In addition, GTN administration to KBrO3-intoxicated rats resulted in significant dose-dependent down regulation of enhanced ODC activity and rate of [3H]-thymidine incorporation in renal DNA, providing support for the protective role of NO in attenuation of KBrO3-induced oxidative stress and cell proliferation.	Nitroglycerin	13-16	ornithine decarboxylase 1	Rattus norvegicus	125-128
9930486-13	1998	Myeloperoxidase activity (U/g) was markedly lower in glycerol trinitrate-treated LDMs, mainly in the distal part of the graft (glycerol trinitrate versus control, 20.5+/-2.1 versus 40.9+/-3.1 U/g, p<0.001).	Nitroglycerin	53-72	myeloperoxidase	Homo sapiens	0-15
9930486-13	1998	Myeloperoxidase activity (U/g) was markedly lower in glycerol trinitrate-treated LDMs, mainly in the distal part of the graft (glycerol trinitrate versus control, 20.5+/-2.1 versus 40.9+/-3.1 U/g, p<0.001).	Nitroglycerin	127-146	myeloperoxidase	Homo sapiens	0-15
9774150-1	1998	We reported previously that the flavoprotein inhibitor diphenyleneiodonium sulfate (DPI) irreversibly inhibited the metabolic activation of glyceryl trinitrate (GTN) in isolated aorta, possibly through inhibition of vascular NADPH-cytochrome P450 reductase (CPR).	Nitroglycerin	140-159	cytochrome p450 oxidoreductase	Rattus norvegicus	258-261
9774150-1	1998	We reported previously that the flavoprotein inhibitor diphenyleneiodonium sulfate (DPI) irreversibly inhibited the metabolic activation of glyceryl trinitrate (GTN) in isolated aorta, possibly through inhibition of vascular NADPH-cytochrome P450 reductase (CPR).	Nitroglycerin	161-164	cytochrome p450 oxidoreductase	Rattus norvegicus	225-256
9774150-1	1998	We reported previously that the flavoprotein inhibitor diphenyleneiodonium sulfate (DPI) irreversibly inhibited the metabolic activation of glyceryl trinitrate (GTN) in isolated aorta, possibly through inhibition of vascular NADPH-cytochrome P450 reductase (CPR).	Nitroglycerin	161-164	cytochrome p450 oxidoreductase	Rattus norvegicus	258-261
9774150-3	1998	Purified CPR incubated with NADPH and GTN under anaerobic, but not aerobic conditions formed the GTN metabolites glyceryl-1,3-dinitrate (1,3-GDN) and glyceryl-1,2-dinitrate (1,2-GDN).	Nitroglycerin	38-41	cytochrome p450 oxidoreductase	Rattus norvegicus	9-12
9774150-3	1998	Purified CPR incubated with NADPH and GTN under anaerobic, but not aerobic conditions formed the GTN metabolites glyceryl-1,3-dinitrate (1,3-GDN) and glyceryl-1,2-dinitrate (1,2-GDN).	Nitroglycerin	97-100	cytochrome p450 oxidoreductase	Rattus norvegicus	9-12
9774150-4	1998	GTN biotransformation by purified CPR and by aortic and hepatic microsomes was inhibited > 90% after treatment with DPI and NADPH.	Nitroglycerin	0-3	cytochrome p450 oxidoreductase	Rattus norvegicus	34-37
9774150-9	1998	We conclude that vascular CPR is a site of action for the inhibition by DPI of the metabolic activation of GTN, and that vascular CPR is a novel site of GTN biotransformation that should be considered when investigating the mechanism of GTN action in vascular tissue.	Nitroglycerin	107-110	cytochrome p450 oxidoreductase	Rattus norvegicus	26-29
9774150-9	1998	We conclude that vascular CPR is a site of action for the inhibition by DPI of the metabolic activation of GTN, and that vascular CPR is a novel site of GTN biotransformation that should be considered when investigating the mechanism of GTN action in vascular tissue.	Nitroglycerin	153-156	cytochrome p450 oxidoreductase	Rattus norvegicus	130-133
9774150-9	1998	We conclude that vascular CPR is a site of action for the inhibition by DPI of the metabolic activation of GTN, and that vascular CPR is a novel site of GTN biotransformation that should be considered when investigating the mechanism of GTN action in vascular tissue.	Nitroglycerin	153-156	cytochrome p450 oxidoreductase	Rattus norvegicus	130-133
9645484-1	1998	In LLC-PK1 kidney epithelial cells, a 5-h pretreatment with glyceryl trinitrate (GTN) resulted in substantial desensitization of the intracellular cyclic GMP response to a subsequent 10-min challenge with GTN (1 microM).	Nitroglycerin	60-79	5'-nucleotidase, cytosolic II	Homo sapiens	154-157
9649558-7	1998	However, coadministration of Vit-C and GTN fully maintained the GTN-induced changes in the orthostatic blood pressure, and the rise of a/b ratio was augmented by 310% for the duration of the test period.	Nitroglycerin	64-67	vitrin	Homo sapiens	29-32
9649558-8	1998	Changes in vascular tolerance in GTN-treated subjects were paralleled by upregulation of the activity of isolated platelets, which was also reversed by Vit-C administration.	Nitroglycerin	33-36	vitrin	Homo sapiens	152-155
9649558-9	1998	These findings demonstrate that dietary supplementation with Vit-C eliminates vascular tolerance and concomitant upregulation of ex vivo-washed platelet activity during long-term nonintermittent administration of GTN in humans.	Nitroglycerin	213-216	vitrin	Homo sapiens	61-64
9690407-4	1998	METHODS: We used positron emission tomography (PET) to assess the changes in rCBF, as an index of synaptic activity, during nitroglycerin-induced cluster headache attacks in nine patients who had chronic cluster headache.	Nitroglycerin	124-137	CCAAT/enhancer binding protein zeta	Rattus norvegicus	77-81
9676716-4	1998	In contrast, NAC potentiated both nitroglycerin- and nicorandil-induced vasodilation.	Nitroglycerin	34-47	synuclein alpha	Homo sapiens	13-16
9676716-6	1998	NAC augmented the nitroglycerin- and nicorandil-induced vasodilation in the small epicardial coronary artery, but not in the large epicardial segments.	Nitroglycerin	18-31	synuclein alpha	Homo sapiens	0-3
9676716-7	1998	In both groups, NAC potentiated the increase in CBF in response to nitroglycerin.	Nitroglycerin	67-80	synuclein alpha	Homo sapiens	16-19
9596680-2	1998	In the present report the NO donor glycerol trinitrate was found to induce apoptosis in Jurkat cells that are sensitive to CD95-mediated kill.	Nitroglycerin	35-54	Fas cell surface death receptor	Homo sapiens	123-127
9645484-1	1998	In LLC-PK1 kidney epithelial cells, a 5-h pretreatment with glyceryl trinitrate (GTN) resulted in substantial desensitization of the intracellular cyclic GMP response to a subsequent 10-min challenge with GTN (1 microM).	Nitroglycerin	81-84	5'-nucleotidase, cytosolic II	Homo sapiens	154-157
9645484-3	1998	Cyclic GMP stimulation by GTN was up to 3.1-fold higher when vitamin C (1-10 mM) was present during the pretreatment period.	Nitroglycerin	26-29	5'-nucleotidase, cytosolic II	Homo sapiens	7-10
9607316-1	1998	Xanthine oxidoreductase (XOR) catalyses the reduction of the therapeutic organic nitrate, nitroglycerin (glyceryl trinitrate, GTN), as well as inorganic nitrate and nitrite, to nitric oxide (NO) under hypoxic conditions in the presence of NADH.	Nitroglycerin	90-103	xanthine dehydrogenase	Homo sapiens	0-23
9607316-1	1998	Xanthine oxidoreductase (XOR) catalyses the reduction of the therapeutic organic nitrate, nitroglycerin (glyceryl trinitrate, GTN), as well as inorganic nitrate and nitrite, to nitric oxide (NO) under hypoxic conditions in the presence of NADH.	Nitroglycerin	90-103	xanthine dehydrogenase	Homo sapiens	25-28
9607316-1	1998	Xanthine oxidoreductase (XOR) catalyses the reduction of the therapeutic organic nitrate, nitroglycerin (glyceryl trinitrate, GTN), as well as inorganic nitrate and nitrite, to nitric oxide (NO) under hypoxic conditions in the presence of NADH.	Nitroglycerin	105-124	xanthine dehydrogenase	Homo sapiens	0-23
9607316-1	1998	Xanthine oxidoreductase (XOR) catalyses the reduction of the therapeutic organic nitrate, nitroglycerin (glyceryl trinitrate, GTN), as well as inorganic nitrate and nitrite, to nitric oxide (NO) under hypoxic conditions in the presence of NADH.	Nitroglycerin	105-124	xanthine dehydrogenase	Homo sapiens	25-28
9607316-1	1998	Xanthine oxidoreductase (XOR) catalyses the reduction of the therapeutic organic nitrate, nitroglycerin (glyceryl trinitrate, GTN), as well as inorganic nitrate and nitrite, to nitric oxide (NO) under hypoxic conditions in the presence of NADH.	Nitroglycerin	126-129	xanthine dehydrogenase	Homo sapiens	0-23
9607316-1	1998	Xanthine oxidoreductase (XOR) catalyses the reduction of the therapeutic organic nitrate, nitroglycerin (glyceryl trinitrate, GTN), as well as inorganic nitrate and nitrite, to nitric oxide (NO) under hypoxic conditions in the presence of NADH.	Nitroglycerin	126-129	xanthine dehydrogenase	Homo sapiens	25-28
9663721-8	1998	RESULTS: In the in vitro study, GTN and SNP significantly reduced the tension of CCK-stimulated muscle contraction whilst Kreb"s solution had no effect.	Nitroglycerin	32-35	cholecystokinin	Homo sapiens	81-84
9626903-0	1998	Preventive effects of angiotensin-converting enzyme inhibitors on nitrate tolerance during continuous transdermal application of nitroglycerin in patients with chronic heart failure.	Nitroglycerin	129-142	angiotensin I converting enzyme	Homo sapiens	22-51
9626903-1	1998	This study was designed to investigate the effect of angiotensin-converting enzyme (ACE) inhibitors with and without a sulfhydryl group on intracellular production of cGMP, forearm blood flow, and neurohormonal factors during continuous transdermal application of nitroglycerin in patients with chronic heart failure.	Nitroglycerin	264-277	angiotensin I converting enzyme	Homo sapiens	53-82
9626903-6	1998	These results indicate that concomitant therapy with ACE inhibitors may be helpful in preventing the attenuation of intracellular cGMP production in patients with chronic heart failure during continuous transdermal application of NTG.	Nitroglycerin	230-233	angiotensin I converting enzyme	Homo sapiens	53-56
9527094-1	1998	In 10 patients with uncomplicated anterior acute myocardial infarction, within 24 hours after onset, heart rate, plasma renin activity, and the low- to high-frequency power ratio increased and high-frequency power decreased during nitroglycerin infusion; however, both heart rate and plasma renin activity did not change, the low- to high-frequency power ratio decreased, and high-frequency power increased during atrial natriuretic peptide infusion.	Nitroglycerin	231-244	renin	Homo sapiens	120-125
9527094-1	1998	In 10 patients with uncomplicated anterior acute myocardial infarction, within 24 hours after onset, heart rate, plasma renin activity, and the low- to high-frequency power ratio increased and high-frequency power decreased during nitroglycerin infusion; however, both heart rate and plasma renin activity did not change, the low- to high-frequency power ratio decreased, and high-frequency power increased during atrial natriuretic peptide infusion.	Nitroglycerin	231-244	renin	Homo sapiens	291-296
9523665-11	1998	The infusion of the nitric oxide synthase inhibitor N(omega)-nitro-L-arginine methyl ester increased the tone of the HCC tissues and significantly reduced (P < 0.01) the relaxation induced by BK (74%), Lys-BK (90%), Met-Lys-BK (87%) and acetylcholine (89%) without affecting those induced by GTN.	Nitroglycerin	295-298	kininogen 1	Homo sapiens	195-197
9435622-2	1997	Ceruloplasmin at physiological, i.e., micromolar, concentrations inhibited relaxation of rabbit aorta induced by endothelium-dependent agonists like acetylcholine or ADP, whereas it was ineffective toward vasodilation due to direct stimulation of smooth muscle cells by nitroglycerin.	Nitroglycerin	270-283	ceruloplasmin	Oryctolagus cuniculus	0-13
9489619-16	1998	The nitroglycerin-induced relaxation of guinea-pig trachea preconstricted by histamine was fully inhibited by NS 2028 (1 microM), whereas the relaxations to terbutaline, theophylline and vasoactive intestinal polypeptide (VIP) were not affected.	Nitroglycerin	4-17	VIP peptides	Cavia porcellus	187-220
9489619-16	1998	The nitroglycerin-induced relaxation of guinea-pig trachea preconstricted by histamine was fully inhibited by NS 2028 (1 microM), whereas the relaxations to terbutaline, theophylline and vasoactive intestinal polypeptide (VIP) were not affected.	Nitroglycerin	4-17	VIP peptides	Cavia porcellus	222-225
9426022-8	1998	RESULTS: In patients treated with NTG alone, the maximal reductions in forearm blood flow in response to angiotensin II and phenylephrine were markedly greater (-64 +/- 3% and -53 +/- 4%, respectively) than those in patients receiving placebo (-41 +/- 2% and -42 +/- 2%, respectively).	Nitroglycerin	34-37	angiotensinogen	Homo sapiens	105-119
9426022-9	1998	Captopril treatment completely prevented the NTG-induced hypersensitivity to angiotensin II and phenylephrine (-33 +/- 3% and -35 +/- 3%, respectively) but had no significant effect on blood flow responses in patients without NTG treatment (-34 +/- 2% and -37 +/- 3%, respectively).	Nitroglycerin	45-48	angiotensinogen	Homo sapiens	77-129
9426022-10	1998	CONCLUSIONS: We conclude that continuous administration of NTG is associated with an increased sensitivity to phenylephrine and angiotensin II that is prevented by concomitant treatment with captopril.	Nitroglycerin	59-62	angiotensinogen	Homo sapiens	128-142
9426022-11	1998	The prevention of NTG-induced hypersensitivity to vasoconstrictors by ACE inhibition indicates an involvement of the renin-angiotensin system in mediating this phenomenon.	Nitroglycerin	18-21	angiotensin I converting enzyme	Homo sapiens	70-73
9426022-11	1998	The prevention of NTG-induced hypersensitivity to vasoconstrictors by ACE inhibition indicates an involvement of the renin-angiotensin system in mediating this phenomenon.	Nitroglycerin	18-21	renin	Homo sapiens	117-122
10684481-6	1998	Spin-trap 1-hydroxy-3-carboxy-pyrrolidine (CP-H) was used to estimate the rate of ROS formation in platelets incubated for 15 minutes with 0.5 mM GTN; the rate amounted to 14.6 +/- 1.1 nM/min/mg protein compared with 4.0 +/- 0.4 nM/min/mg protein in controls.	Nitroglycerin	146-149	carboxypeptidase E	Homo sapiens	43-47
9495841-10	1998	These results suggest that NTG, in the therapeutic concentration range, produces coronary relaxation primarily via two cellular mechanisms: plasmalemmal BK channel activation and stimulation of SR Ca(++)-ATPase to produce increased SR Ca++ accumulation.	Nitroglycerin	27-30	potassium calcium-activated channel subfamily M alpha 1	Canis lupus familiaris	153-163
9475264-1	1998	S-Nitrosocaptopril (S-NO-Cap), a nitrate and an angiotensin-converting enzyme (ACE) inhibitor, may be produced after coadministration of nitroglycerin (NTG) and captopril (CAP).	Nitroglycerin	137-150	angiotensin I converting enzyme	Canis lupus familiaris	48-77
9475264-1	1998	S-Nitrosocaptopril (S-NO-Cap), a nitrate and an angiotensin-converting enzyme (ACE) inhibitor, may be produced after coadministration of nitroglycerin (NTG) and captopril (CAP).	Nitroglycerin	137-150	angiotensin I converting enzyme	Canis lupus familiaris	79-82
9475264-1	1998	S-Nitrosocaptopril (S-NO-Cap), a nitrate and an angiotensin-converting enzyme (ACE) inhibitor, may be produced after coadministration of nitroglycerin (NTG) and captopril (CAP).	Nitroglycerin	152-155	angiotensin I converting enzyme	Canis lupus familiaris	48-77
9475264-1	1998	S-Nitrosocaptopril (S-NO-Cap), a nitrate and an angiotensin-converting enzyme (ACE) inhibitor, may be produced after coadministration of nitroglycerin (NTG) and captopril (CAP).	Nitroglycerin	152-155	angiotensin I converting enzyme	Canis lupus familiaris	79-82
9475264-21	1998	The in vivo coronary vascular response to S-NO-Cap may, therefore, be partially reduced by activation of the adrenergic or renin-angiotensin-aldosterone systems or both induced by NTG, because S-NO-Cap showed no cross-tolerance with NTG in our earlier in vitro study.	Nitroglycerin	180-183	renin	Canis lupus familiaris	123-128
9538627-5	1998	2) After NTG, the P-Tc and P/T increased, but the T and FVI decreased significantly in both groups of subjects.	Nitroglycerin	9-12	coagulation factor IX	Homo sapiens	18-22
10651168-1	1998	We investigated the effects of the sulfhydryl-donor, N-acetylcysteine (NAC), on nitroglycerin (NTG)-induced relaxation of the vascular smooth muscle.	Nitroglycerin	80-93	synuclein alpha	Homo sapiens	71-74
10651168-1	1998	We investigated the effects of the sulfhydryl-donor, N-acetylcysteine (NAC), on nitroglycerin (NTG)-induced relaxation of the vascular smooth muscle.	Nitroglycerin	95-98	synuclein alpha	Homo sapiens	71-74
10651168-5	1998	Application of NAC (NTG-NAC) enhanced the relaxing effects of NTG on the histamine-induced tonic contraction rather than the acute contraction.	Nitroglycerin	20-23	synuclein alpha	Homo sapiens	15-18
10651168-6	1998	In phosphorylation studies, changes in the phosphorylation of an intermediate filament, desmin, were parallel with changes in contraction in NTG-treated and NTG-NAC samples at 48 min.	Nitroglycerin	141-144	desmin	Homo sapiens	88-94
10651168-8	1998	These results suggest that treatment with the sulfhydryl donor, NAC, inhibited the phosphorylation of desmin associated with the enhancement of NTG-induced relaxation, which might be related to the mechanisms of recovery from NTG tolerance by sulfhydryl groups.	Nitroglycerin	144-147	synuclein alpha	Homo sapiens	64-67
10651168-8	1998	These results suggest that treatment with the sulfhydryl donor, NAC, inhibited the phosphorylation of desmin associated with the enhancement of NTG-induced relaxation, which might be related to the mechanisms of recovery from NTG tolerance by sulfhydryl groups.	Nitroglycerin	144-147	desmin	Homo sapiens	102-108
10651168-8	1998	These results suggest that treatment with the sulfhydryl donor, NAC, inhibited the phosphorylation of desmin associated with the enhancement of NTG-induced relaxation, which might be related to the mechanisms of recovery from NTG tolerance by sulfhydryl groups.	Nitroglycerin	226-229	synuclein alpha	Homo sapiens	64-67
10651168-8	1998	These results suggest that treatment with the sulfhydryl donor, NAC, inhibited the phosphorylation of desmin associated with the enhancement of NTG-induced relaxation, which might be related to the mechanisms of recovery from NTG tolerance by sulfhydryl groups.	Nitroglycerin	226-229	desmin	Homo sapiens	102-108
9428622-3	1997	As a vasodilator, nitroglycerin activates compensatory neurohumoral mechanisms such as the renin-angiotensin system and increases catecholamine and vasopressin levels, all of which may attenuate its vasodilator potency.	Nitroglycerin	18-31	renin	Homo sapiens	91-96
10453541-4	1997	In addition, nitroglycerine (2.2 x 10(-3) mol/L) remarkably reduced medium ET-1 levels in cultured endothelial cells, which suggested that nitric oxide might inhibit the secretion of ET-1.	Nitroglycerin	13-27	endothelin 1	Homo sapiens	75-79
10453541-4	1997	In addition, nitroglycerine (2.2 x 10(-3) mol/L) remarkably reduced medium ET-1 levels in cultured endothelial cells, which suggested that nitric oxide might inhibit the secretion of ET-1.	Nitroglycerin	13-27	endothelin 1	Homo sapiens	183-187
9422847-6	1997	The activity of this enzyme system is regulated by angiotensin II and is elevated following prolonged exposure to nitroglycerin.	Nitroglycerin	114-127	angiotensinogen	Homo sapiens	51-65
9428622-3	1997	As a vasodilator, nitroglycerin activates compensatory neurohumoral mechanisms such as the renin-angiotensin system and increases catecholamine and vasopressin levels, all of which may attenuate its vasodilator potency.	Nitroglycerin	18-31	arginine vasopressin	Homo sapiens	148-159
9428622-8	1997	Interestingly, these vascular consequences of in vivo NTG treatment such as superoxide production and PKC activation can be mimicked in vitro by incubating cultured endothelial and smooth muscle cells with angiotensin II.	Nitroglycerin	54-57	angiotensinogen	Homo sapiens	206-220
9351518-0	1997	Nitroglycerin-inhibited whole blood aggregation is partially mediated by calcitonin gene-related peptide -- a neurogenic mechanism.	Nitroglycerin	0-13	calcitonin-related polypeptide alpha	Rattus norvegicus	73-104
9351518-2	1997	The role of the vasculature and calcitonin gene-related peptide (CGRP) in nitroglycerin (NTG)-mediated platelet inhibition was studied.	Nitroglycerin	74-87	calcitonin-related polypeptide alpha	Rattus norvegicus	65-69
9354311-0	1997	Comparison of nitroprusside and nitroglycerin in inhibition of angiotensin II and other vasoconstrictor-mediated contraction in human coronary bypass conduits.	Nitroglycerin	32-45	angiotensinogen	Homo sapiens	63-77
9351518-14	1997	Furthermore, NTG apparently evokes the release of CGRP from vascular tissue and this neuropeptide contributes to the antiplatelet actions of NTG.	Nitroglycerin	13-16	calcitonin-related polypeptide alpha	Rattus norvegicus	50-54
9354311-1	1997	AIMS: To compare the effect of nitroprusside (SNP) and nitroglycerin (NTG) on angiotensin II (ANGII), endothelin-1 (ET-1), and alpha1-adrenoceptor (phenylephrine, PE)-mediated contraction in internal mammary artery (IMA).	Nitroglycerin	70-73	angiotensinogen	Homo sapiens	78-92
9389267-6	1997	infusion of NTG 4-8 micrograms kg-1 min-1 significantly inhibited platelet aggregation and the increase in intracellular Ca2+ concentration (first phase, mean 439.9 (SEM 68.7) vs 210.6 (38.7) nmol litre-1; second phase, 154.4 (19.8) vs 106.7 (18.0) nmol litre-1).	Nitroglycerin	12-15	CD59 molecule (CD59 blood group)	Homo sapiens	36-41
9351518-14	1997	Furthermore, NTG apparently evokes the release of CGRP from vascular tissue and this neuropeptide contributes to the antiplatelet actions of NTG.	Nitroglycerin	141-144	calcitonin-related polypeptide alpha	Rattus norvegicus	50-54
9423929-1	1997	Nitroglycerin is a nitric oxide donor which induces sustained expression of Fos protein, a marker of neuronal activation, in specific neuronal groups in the central nervous system.	Nitroglycerin	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	76-79
9423929-6	1997	All the pharmacological treatments administered before injecting nitroglycerin selectively influenced Fos expression in the different brain nuclei.	Nitroglycerin	65-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-105
9190888-0	1997	Investigation of aortic CYP3A bioactivation of nitroglycerin in vivo.	Nitroglycerin	47-60	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	24-29
9260860-1	1997	Nitric oxide (NO), a gaseous molecule synthesized in the arteriolar endothelium from the amino acid L-arginine (L-arg), has been identified as the previously described Endothelium-Derived Relaxing Factor (EDRF): nitroderivatives such as nitroglycerin are known to induce vasodilation via NO release.	Nitroglycerin	237-250	alpha hemoglobin stabilizing protein	Homo sapiens	168-203
9260860-1	1997	Nitric oxide (NO), a gaseous molecule synthesized in the arteriolar endothelium from the amino acid L-arginine (L-arg), has been identified as the previously described Endothelium-Derived Relaxing Factor (EDRF): nitroderivatives such as nitroglycerin are known to induce vasodilation via NO release.	Nitroglycerin	237-250	alpha hemoglobin stabilizing protein	Homo sapiens	205-209
9262367-4	1997	The NO-donor drugs molsidomine, 3-morpholinosydnone-imine (SIN-1), sodium nitroprusside (SNP) and glyceryl-trinitrate reduced the pulmonary hypertension in a dose-dependent fashion, whether admixed to the perfusate or inhaled as alveolar-accessible aerosol particles (aerosolization time 3-6 min), with an efficiency ranking of SNP > SIN-1 >> molsidomine and glyceryl-trinitrate.	Nitroglycerin	98-117	MAPK associated protein 1	Homo sapiens	337-342
9262367-4	1997	The NO-donor drugs molsidomine, 3-morpholinosydnone-imine (SIN-1), sodium nitroprusside (SNP) and glyceryl-trinitrate reduced the pulmonary hypertension in a dose-dependent fashion, whether admixed to the perfusate or inhaled as alveolar-accessible aerosol particles (aerosolization time 3-6 min), with an efficiency ranking of SNP > SIN-1 >> molsidomine and glyceryl-trinitrate.	Nitroglycerin	368-387	MAPK associated protein 1	Homo sapiens	59-64
9321821-7	1997	In summary, VEGF stimulates nitric oxide (NO)-dependent dilation of coronary microvessels, and repeat administrations of VEGF resulted in rapid development of tachyphylaxis to VEGF as well as serotonin, but not to nitroglycerin or adenosine, which appeared to be secondary to impaired NO production.	Nitroglycerin	214-227	vascular endothelial growth factor A	Sus scrofa	121-125
9321821-7	1997	In summary, VEGF stimulates nitric oxide (NO)-dependent dilation of coronary microvessels, and repeat administrations of VEGF resulted in rapid development of tachyphylaxis to VEGF as well as serotonin, but not to nitroglycerin or adenosine, which appeared to be secondary to impaired NO production.	Nitroglycerin	214-227	vascular endothelial growth factor A	Sus scrofa	121-125
9270062-12	1997	Thus, administration of an NO donor (nitroglycerin or nitroprusside) and, to a lesser extent L-arginine, reversed aspirin"s antagonism of t-PA thrombolysis.	Nitroglycerin	37-50	plasminogen activator, tissue type	Homo sapiens	138-142
9441903-4	1997	The nitric oxide donor glyceryl trinitrate was also found to induce transcriptional and translational expression of ferritin heavy chain.	Nitroglycerin	23-42	ferritin heavy chain 1	Homo sapiens	116-136
9190888-3	1997	Recent studies, using hepatic microsomes, have suggested the involvement of cytochrome P450 3A (CYP3A) in GTN biotransformation.	Nitroglycerin	106-109	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	76-94
9190888-3	1997	Recent studies, using hepatic microsomes, have suggested the involvement of cytochrome P450 3A (CYP3A) in GTN biotransformation.	Nitroglycerin	106-109	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	96-101
9190888-4	1997	Here, we used an animal model to test the hypothesis that aortic CYP3A plays a role in the bioactivation of GTN in vivo.	Nitroglycerin	108-111	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	65-70
9190888-9	1997	), a strong CYP3A inducer, they exhibited a significant (approximately 50%) higher cGMP response to GTN than the control group.	Nitroglycerin	100-103	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	12-17
9190888-15	1997	In conclusion, our results demonstrate that CYP3A activity in aorta is correlated with GTN bioactivation in vivo, but the contribution of this enzyme to overall GTN bioactivation is limited.	Nitroglycerin	87-90	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	44-49
9113368-5	1997	In contrast, pretreatment with the intracellular sulphydryl donor, N-acetyl-L-cysteine (NAC, 1 mM), significantly attenuated GTN-induced tolerance.	Nitroglycerin	125-128	X-linked Kx blood group	Homo sapiens	88-91
9112397-4	1997	We found that liver-specific GH binding is significantly higher in both bGH- and bGHA-Tg mice compared to that in their NTg controls.	Nitroglycerin	120-123	growth hormone	Mus musculus	29-31
9112397-5	1997	In contrast, kidney GH binding is significantly lower in bGH-Tg mice compared to that in NTg littermates.	Nitroglycerin	89-92	growth hormone	Mus musculus	20-22
9112397-7	1997	STZ-induced diabetes decreased GH-specific binding in both liver and kidney of NTg and GHA-Tg mice, but not in bGH-Tg mice.	Nitroglycerin	79-82	growth hormone	Mus musculus	31-33
9112397-8	1997	The lowered GHR binding in diabetic NTg and GHA-Tg mice suggests the involvement of insulin in the regulation of GHR expression.	Nitroglycerin	36-39	growth hormone receptor	Mus musculus	12-15
9112397-8	1997	The lowered GHR binding in diabetic NTg and GHA-Tg mice suggests the involvement of insulin in the regulation of GHR expression.	Nitroglycerin	36-39	growth hormone receptor	Mus musculus	113-116
9179898-1	1997	OBJECTIVE: To determine the capability of donors of nitric oxide (NO) (sodium nitroprusside, nitroglycerine) to reverse endothelin-1 (ET-1)-induced cerebral vasoconstriction in vivo, when administered through the cerebrospinal fluid (CSF) to the adventitial side of the constricted blood vessel.	Nitroglycerin	93-107	endothelin 1	Homo sapiens	120-132
9179898-1	1997	OBJECTIVE: To determine the capability of donors of nitric oxide (NO) (sodium nitroprusside, nitroglycerine) to reverse endothelin-1 (ET-1)-induced cerebral vasoconstriction in vivo, when administered through the cerebrospinal fluid (CSF) to the adventitial side of the constricted blood vessel.	Nitroglycerin	93-107	endothelin 1	Homo sapiens	134-138
9179898-6	1997	RESULTS: Sodium nitroprusside and nitroglycerine, both donors of NO, rapidly and completely reversed ET-1-induced vasoconstriction without causing hypotension.	Nitroglycerin	34-48	endothelin 1	Homo sapiens	101-105
9162750-6	1997	Large and small VLDL isolated from the NTG group were enriched with apoE and C-I, and cholesterol, but depleted of apoC-II in the postprandial state, whereas the apoC-III, triglyceride, and phospholipid contents were essentially unchanged.	Nitroglycerin	39-42	apolipoprotein E	Homo sapiens	68-72
9061003-5	1997	Subsequent addition of 100 microM nitroglycerin (NTG) or 100 microM sodium nitroprusside (NP) to histamine-stimulated tissues increased [cGMP], decreased both MLC phosphorylation and force, but did not significantly alter [cAMP], [Ca2+]i, or MLCK site A phosphorylation.	Nitroglycerin	34-47	myosin light chain kinase	Sus scrofa	242-246
9061003-5	1997	Subsequent addition of 100 microM nitroglycerin (NTG) or 100 microM sodium nitroprusside (NP) to histamine-stimulated tissues increased [cGMP], decreased both MLC phosphorylation and force, but did not significantly alter [cAMP], [Ca2+]i, or MLCK site A phosphorylation.	Nitroglycerin	49-52	myosin light chain kinase	Sus scrofa	242-246
9061003-6	1997	Addition of NTG and NP alone to unstimulated tissues increased MLCK site A phosphorylation, but did not alter [Ca2+]i.	Nitroglycerin	12-15	myosin light chain kinase	Sus scrofa	63-67
9054864-7	1997	Platelet aggregation induced by thrombin also decreased at 3 (12.4 +/- 1.3), 24 (12.6 +/- 1.7), and 48 hours (10.8 +/- 1.6) of nitroglycerin treatment compared with baseline (16.3 +/- 1.4) but remained unchanged in the control group.	Nitroglycerin	127-140	coagulation factor II, thrombin	Sus scrofa	32-40
9051308-16	1997	A concentration of YC-1 (3 microM), which elicited only minor effects on relaxation and cyclic GMP, increased the vasodilator potency of SNP and nitroglycerin (NTG) by 10 fold and markedly enhanced SNP- and NTG-induced cyclic GMP formation.	Nitroglycerin	145-158	glutathione S-transferase alpha 1	Rattus norvegicus	19-23
9051308-16	1997	A concentration of YC-1 (3 microM), which elicited only minor effects on relaxation and cyclic GMP, increased the vasodilator potency of SNP and nitroglycerin (NTG) by 10 fold and markedly enhanced SNP- and NTG-induced cyclic GMP formation.	Nitroglycerin	160-163	glutathione S-transferase alpha 1	Rattus norvegicus	19-23
9051308-16	1997	A concentration of YC-1 (3 microM), which elicited only minor effects on relaxation and cyclic GMP, increased the vasodilator potency of SNP and nitroglycerin (NTG) by 10 fold and markedly enhanced SNP- and NTG-induced cyclic GMP formation.	Nitroglycerin	207-210	glutathione S-transferase alpha 1	Rattus norvegicus	19-23
9084577-0	1997	Downregulation of nitric oxide synthase activity in human platelets by nitroglycerin and authentic nitric oxide.	Nitroglycerin	71-84	nitric oxide synthase 2	Homo sapiens	18-39
9162750-6	1997	Large and small VLDL isolated from the NTG group were enriched with apoE and C-I, and cholesterol, but depleted of apoC-II in the postprandial state, whereas the apoC-III, triglyceride, and phospholipid contents were essentially unchanged.	Nitroglycerin	39-42	apolipoprotein C2	Homo sapiens	115-122
8994427-8	1997	GTN inhibited platelet fibrinogen binding and expression of P-selectin at rest and in response to agonist stimulation, whereas amlodipine enhanced P-selectin expression and atenolol increased fibrinogen binding in response to agonists.	Nitroglycerin	0-3	fibrinogen beta chain	Homo sapiens	23-33
8994427-8	1997	GTN inhibited platelet fibrinogen binding and expression of P-selectin at rest and in response to agonist stimulation, whereas amlodipine enhanced P-selectin expression and atenolol increased fibrinogen binding in response to agonists.	Nitroglycerin	0-3	selectin P	Homo sapiens	60-70
9008257-0	1997	Isosorbide nitrates, nitroglycerin, and sodium nitroprusside induce vasodilation concomitantly with inhibition of carbonic anhydrase I in erythrocytes.	Nitroglycerin	21-34	carbonic anhydrase 1	Homo sapiens	114-134
8968066-9	1996	Preneoplastic foci, mainly of clear cell and mixed cell type (identified as positive for glutathione S-transferase placental form) were found from 14 weeks of age in rats receiving GTN in the diet.	Nitroglycerin	181-184	hematopoietic prostaglandin D synthase	Rattus norvegicus	89-114
9035610-5	1996	NTG also enhanced nitrite levels in PRP and stimulated cyclic GMP accumulation in platelets.	Nitroglycerin	0-3	5'-nucleotidase, cytosolic II	Homo sapiens	62-65
8968379-5	1996	Purified GST Yc and Yb2/Yp mediated GTN biotransformation with similar rates.	Nitroglycerin	36-39	Y box binding protein 3	Rattus norvegicus	20-23
8968379-7	1996	Removal of GST Yb2 from rat aortic cytosol by immunoprecipitation resulted in marked inhibition of GST activity and GTN biotransformation.	Nitroglycerin	116-119	glutathione S-transferase mu 2	Rattus norvegicus	11-18
9455782-8	1997	Postoperative PVR and mPAP were accurately estimated by preoperative NTG infusion (NTG vs 24 h posttranspl: PVR 2.2 +/- 0.2 vs 1.9 +/- 0.2 Wood units, p > 0.05; mPAP 30 +/- 2 vs 26 +/- 1 mmHg, p > 0.05).	Nitroglycerin	69-72	phospholipid phosphatase 1	Mus musculus	22-26
9455782-8	1997	Postoperative PVR and mPAP were accurately estimated by preoperative NTG infusion (NTG vs 24 h posttranspl: PVR 2.2 +/- 0.2 vs 1.9 +/- 0.2 Wood units, p > 0.05; mPAP 30 +/- 2 vs 26 +/- 1 mmHg, p > 0.05).	Nitroglycerin	83-86	phospholipid phosphatase 1	Mus musculus	22-26
8959734-9	1996	Pretreatment with (4-Cl-D-Phe6, Leu17) VIP blocked the inhibitory action of glyceryl trinitrate and preserved MMC pattern (P < 0.05).	Nitroglycerin	76-95	vasoactive intestinal peptide	Rattus norvegicus	39-42
8874825-2	1996	It has been shown that some glutathione S-transferases (GSTs) catalyze the metabolic conversion from GTN to glyceryl dinitrates (GDNs).	Nitroglycerin	101-104	glutathione S-transferase kappa 1	Homo sapiens	56-60
8841348-11	1996	After the administration of nitroglycerin for 3 hours, the cerebral vessels were significantly dilated on both sides (P < .05), and rCBF was significantly increased on the right side (P < .05) but not on the left side.	Nitroglycerin	28-41	CCAAT/enhancer binding protein zeta	Rattus norvegicus	135-139
8841348-16	1996	Given the increase in rCBF, nitroglycerin may be therapeutic for the treatment of vasospasm.	Nitroglycerin	28-41	CCAAT/enhancer binding protein zeta	Rattus norvegicus	22-26
8877589-9	1996	In both ET-1- and L-NMMA-contracted rings, vascular relaxation in response to NTG was preserved (80 +/- 6 and 88 +/- 8% relaxation, respectively).	Nitroglycerin	78-81	endothelin 1	Rattus norvegicus	8-13
8877589-11	1996	Rings contracted with L-NMMA or ET-1, but not NE, accumulated cyclic GMP when exposed to NTG (280 +/- 20 fmol/mg).	Nitroglycerin	89-92	endothelin 1	Rattus norvegicus	32-36
8877589-13	1996	Contraction of NTG-tolerant rings with ET-1 or L-NMMA restores NTG-mediated relaxation.	Nitroglycerin	15-18	endothelin 1	Rattus norvegicus	39-43
8877589-13	1996	Contraction of NTG-tolerant rings with ET-1 or L-NMMA restores NTG-mediated relaxation.	Nitroglycerin	63-66	endothelin 1	Rattus norvegicus	39-43
8877591-5	1996	During NTG infusion, platelet-rich plasma (PRP) cyclic GMP was increased by 41.4 +/- 13.6% as compared with control and remained increased throughout the infusion (p < 0.05).	Nitroglycerin	7-10	proline rich protein 2-like 1	Rattus norvegicus	43-46
8877591-8	1996	NTG also decreased the PRP platelet concentration by 30% in 8 h, whereas D5W had no effect.	Nitroglycerin	0-3	proline rich protein 2-like 1	Rattus norvegicus	23-26
8874825-3	1996	In this study, we examined the substrate specificity of GSTs for GTN.	Nitroglycerin	65-68	glutathione S-transferase kappa 1	Homo sapiens	56-60
8640982-2	1996	Long-term nitroglycerin infusion is associated with increases in plasma renin activity and catecholamine release rates, both of which may lead to excess angiotensin II and alpha-adrenergic-mediated vasoconstriction, particularly on withdrawal of nitroglycerin.	Nitroglycerin	10-23	renin	Homo sapiens	72-77
8869312-6	1996	The significant increase in MPO activity produced by IR to a level of 7.99 units g-1 was prevented by GTN which reduced the level to 4.73 units g-1.	Nitroglycerin	102-105	myeloperoxidase	Rattus norvegicus	28-31
8698782-8	1996	TnT values above the critical border of 1.0 microgram/l in the early period after CPB were less often seen in the nitroglycerine and nifedipine group.	Nitroglycerin	114-128	troponin T1, slow skeletal type	Homo sapiens	0-3
8844236-15	1996	The mean NTG infusion rate while MAP was within 5 mmHg of target MAP was 1.14 (0.84 SD) micrograms kg-1 min-1.	Nitroglycerin	9-12	CD59 molecule (CD59 blood group)	Homo sapiens	104-109
8640982-2	1996	Long-term nitroglycerin infusion is associated with increases in plasma renin activity and catecholamine release rates, both of which may lead to excess angiotensin II and alpha-adrenergic-mediated vasoconstriction, particularly on withdrawal of nitroglycerin.	Nitroglycerin	10-23	angiotensinogen	Homo sapiens	153-167
8640982-6	1996	Nitroglycerin infusion also was accompanied by a transient increase in plasma renin activity.	Nitroglycerin	0-13	renin	Homo sapiens	78-83
8640982-10	1996	CONCLUSIONS: Long-term ACE inhibition with high-dose enalapril reduces nitroglycerin tolerance and prevents rebound vasoconstriction in coronary arteries.	Nitroglycerin	71-84	angiotensin I converting enzyme	Homo sapiens	23-26
8640982-12	1996	This observation suggests that during long-term nitroglycerin treatment, intrinsic abnormalities of the vascular smooth muscle may have developed that are suppressed by concomitant ACE inhibitor therapy.	Nitroglycerin	48-61	angiotensin I converting enzyme	Homo sapiens	181-184
8640982-13	1996	The present study also favors a combination of nitroglycerin and ACE inhibitors to maintain nitrate sensitivity of the vasculature during long-term nitroglycerin treatment.	Nitroglycerin	148-161	angiotensin I converting enzyme	Homo sapiens	65-68
8761850-7	1996	In both nitrate-tolerant and nontolerant coronary arteries, glibenclamide (GLI 10(-6) M), a selective KATP channel blocker, caused a parallel rightward shift in the concentration-response curve to cromakalim, but had no effect on responses to NTG or SNP.	Nitroglycerin	243-246	GLI family zinc finger 1	Homo sapiens	75-78
8557897-2	1996	BACKGROUND: Nitroglycerin therapy is associated with increased plasma renin activity and aldosterone levels and a decrease in hematocrit.	Nitroglycerin	12-25	renin	Homo sapiens	70-75
8638523-5	1996	Interestingly, these vascular consequences of in vivo nitroglycerin treatment can be mimicked by incubating cultured endothelial and smooth muscle cells with angiotensin II.	Nitroglycerin	54-67	angiotensinogen	Homo sapiens	158-172
8638523-7	1996	These data strongly suggest that increased circulating levels of angiotensin II, which are encountered during in vivo nitroglycerin treatment, initiate cellular events that ultimately attenuate the nitroglycerin vasodilator effects during prolonged treatment periods.	Nitroglycerin	118-131	angiotensinogen	Homo sapiens	65-79
8638523-7	1996	These data strongly suggest that increased circulating levels of angiotensin II, which are encountered during in vivo nitroglycerin treatment, initiate cellular events that ultimately attenuate the nitroglycerin vasodilator effects during prolonged treatment periods.	Nitroglycerin	198-211	angiotensinogen	Homo sapiens	65-79
8621776-6	1996	Angiotensin II-, but not NE-, induced hypertension was associated with impaired relaxations to acetylcholine, the calcium ionophore A23187, and nitroglycerin.	Nitroglycerin	144-157	angiotensinogen	Rattus norvegicus	0-14
9367942-12	1996	In the case of GTN, the decrease of PAI-1 concentration was delayed.	Nitroglycerin	15-18	serpin family E member 1	Homo sapiens	36-41
8682599-3	1996	In internal mammary and gastroepiploic arteries, the nitrovasodilators, sodium nitroprusside and glyceryl trinitrate, effectively reversed the spasms induced either with noradrenaline (for sodium nitroprusside; internal mammary artery: 101.07% +/- 1.63%; gastroepiploic artery: 94.10% +/- 2.07%) or endothelin-1 (for sodium nitroprusside; internal mammary artery: 97.67% +/- 4.94%; gastroepiploic artery: 90.69% +/- 2.61%).	Nitroglycerin	97-116	endothelin 1	Homo sapiens	299-311
8803519-7	1996	Heart rate increased from 67.4 to 70.9 beats.min-1 after nitroglycerin and from 58.9 to 69.4 beats.min-1 after nifedipine.	Nitroglycerin	57-70	CD59 molecule (CD59 blood group)	Homo sapiens	45-50
8769841-11	1996	In the presence of 10(-9) M ADH, NTG also decreased Pf(P < 0.04).	Nitroglycerin	33-36	arginine vasopressin	Homo sapiens	28-31
8649654-9	1996	ApoC-peptides and apo E were also elevated in VLDL of NTG and HTG, but their increase was only significant in HTG (P < 0.01).	Nitroglycerin	54-57	apolipoprotein E	Homo sapiens	18-23
8603131-6	1996	This NTG tolerance significantly attenuated vasorelaxation to either ISDN, SNP or EDRF stimulated by bradykinin.	Nitroglycerin	5-8	alpha hemoglobin stabilizing protein	Homo sapiens	82-86
8603131-6	1996	This NTG tolerance significantly attenuated vasorelaxation to either ISDN, SNP or EDRF stimulated by bradykinin.	Nitroglycerin	5-8	kininogen 1	Homo sapiens	101-111
8809212-5	1996	Nitroglycerine increased basal PTH levels (< 0.02), but had no significant effect on basal LH, FSH, TSH, cortisol, calcium, or prolactin levels.	Nitroglycerin	0-14	parathyroid hormone	Homo sapiens	31-34
8735971-1	1996	In this study, we carried out an immunohistochemical evaluation of the neurochemical characteristics of neurons that are activated (i.e., express Fos protein) in response to systemic administration of nitroglycerin.	Nitroglycerin	201-214	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	146-149
8719811-2	1995	In this study we investigated the role of catalase in relaxation induced by hydroxylamine, sodium azide, glyceryl trinitrate and hydrogen peroxide in isolated rings of rat aorta.	Nitroglycerin	105-124	catalase	Rattus norvegicus	42-50
8719811-14	1995	Pretreatment of endothelium-denuded rings with AT (1-50 mM, 90 min) to inhibit endogenous catalase blocked relaxation induced by sodium azide (1-300 nM) and hydroxylamine (1-300 nM) but had no effect on relaxation induced by hydrogen peroxide (10 microM-1 mM) or glyceryl trinitrate (1-100 nM).	Nitroglycerin	263-282	catalase	Rattus norvegicus	90-98
7572574-0	1995	Concurrent nitroglycerin administration reduces the efficacy of recombinant tissue-type plasminogen activator in patients with acute anterior wall myocardial infarction.	Nitroglycerin	11-24	plasminogen activator, tissue type	Homo sapiens	76-109
8728945-0	1995	Effect of angiotensin converting enzyme inhibitors on tolerance of nitroglycerin.	Nitroglycerin	67-80	angiotensin I converting enzyme	Homo sapiens	10-39
8574645-0	1995	NADPH-diaphorase activity and Fos expression in brain nuclei following nitroglycerin administration.	Nitroglycerin	71-84	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	30-33
8574645-3	1995	Previous reports have shown that systemic nitroglycerin is able to induce Fos expression in brain nuclei which are known to contain nitric oxide synthesizing enzyme.	Nitroglycerin	42-55	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	74-77
8529333-4	1995	Venoconstrictor effects of human neuropeptide Y lasted several hours and were unchanged by simultaneous administration of alpha-adrenergic antagonists but were readily reversed by nitroglycerin or bradykinin.	Nitroglycerin	180-193	neuropeptide Y	Homo sapiens	33-47
8750888-3	1995	The degree of hsp70 induction was somewhat greater in nTg than Tg mice at 4 and 24 h after TBI.	Nitroglycerin	54-57	heat shock protein 1B	Mus musculus	14-19
8750888-6	1995	There was a time-dependent difference in cortical c-fos expression between nTg and Tg mice.	Nitroglycerin	75-78	FBJ osteosarcoma oncogene	Mus musculus	50-55
8750888-7	1995	The induction of c-fos mRNA in the striatum was greater in nTg at 24 h and decreased in both animals by 48 h. Edema of the injured cortex was significantly attenuated in Tg mice at all time points (1-48 h).	Nitroglycerin	59-62	FBJ osteosarcoma oncogene	Mus musculus	17-22
8747803-11	1995	Exogenous thiol compounds (e.g. NAC) augments the hypotensive effect of NTG by a tolerance nonspecific mechanism.	Nitroglycerin	72-75	synuclein alpha	Homo sapiens	32-35
7572574-1	1995	The aim of this study was to evaluate the impact of concurrent nitroglycerin administration on the thrombolytic efficacy of recombinant tissue-type plasminogen activator (rTPA) in patients with acute anterior myocardial infarction (AMI).	Nitroglycerin	63-76	plasminogen activator, tissue type	Homo sapiens	136-169
7572574-1	1995	The aim of this study was to evaluate the impact of concurrent nitroglycerin administration on the thrombolytic efficacy of recombinant tissue-type plasminogen activator (rTPA) in patients with acute anterior myocardial infarction (AMI).	Nitroglycerin	63-76	plasminogen activator, tissue type	Rattus norvegicus	171-175
7572574-9	1995	In conclusion, concurrent nitroglycerin administration reduces the thrombolytic efficacy of rTPA in patients with AMI probably by lowering the plasma levels of rTPA antigen.	Nitroglycerin	26-39	plasminogen activator, tissue type	Rattus norvegicus	92-96
7572574-9	1995	In conclusion, concurrent nitroglycerin administration reduces the thrombolytic efficacy of rTPA in patients with AMI probably by lowering the plasma levels of rTPA antigen.	Nitroglycerin	26-39	plasminogen activator, tissue type	Rattus norvegicus	160-164
7671372-1	1995	BACKGROUND: The objectives of this study were (1) to assess glyceryl trinitrate (GTN)-derived nitric oxide (NO) formation in vascular tissues and organs of anesthetized rabbits in vivo, (2) to establish a correlation between tissue NO levels and a biological response, and (3) to verify biotransformation of GTN to NO by cytochrome P-450.	Nitroglycerin	60-79	cytochrome P-450	Oryctolagus cuniculus	321-337
7488446-6	1995	RESULTS: Of the 201Tl protocols, the redistribution scan 1 h after treatment with glyceryl trinitrate best demonstrated myocardial viability.	Nitroglycerin	82-101	calcium activated nucleotidase 1	Homo sapiens	52-58
7671372-9	1995	Purified cytochrome P-450 catalyzed NO formation from GTN in a P-450-NADPH reductase- and NADPH-dependent fashion.	Nitroglycerin	54-57	cytochrome P-450	Oryctolagus cuniculus	9-25
7671372-12	1995	High NO formation in cytochrome P-450-rich organs in vivo and efficient NO formation from GTN by cytochrome P-450 in vitro highlights the importance of this pathway for NO formation from GTN in the intact organism.	Nitroglycerin	90-93	cytochrome P-450	Oryctolagus cuniculus	97-113
7671372-12	1995	High NO formation in cytochrome P-450-rich organs in vivo and efficient NO formation from GTN by cytochrome P-450 in vitro highlights the importance of this pathway for NO formation from GTN in the intact organism.	Nitroglycerin	187-190	cytochrome P-450	Oryctolagus cuniculus	97-113
8573727-3	1995	We elucidated the possible involvement of EDRF in early non-insulin-dependent diabetes mellitus (NIDDM) and glomerular hyperfiltration (GHF) by DDAVP and GTN infusions.	Nitroglycerin	154-157	alpha hemoglobin stabilizing protein	Homo sapiens	42-46
8557064-3	1995	The (mean +/- SD) insulin sensitivity index, as assessed by the Minimal Model method, was significantly lower in the HTG compared with the NTG group (3.69 +/- 2.96 vs. 6.29 +/- 3.38 x 10(-4) min-1 per mUL-1; P < 0.001).	Nitroglycerin	139-142	insulin	Homo sapiens	18-25
7556582-6	1995	Application of nitroglycerin (1 microM) 48 min after histamine stimulation inhibited the phosphorylation of desmin, synemin, and the three cytosolic proteins.	Nitroglycerin	15-28	desmin	Homo sapiens	108-114
7556582-6	1995	Application of nitroglycerin (1 microM) 48 min after histamine stimulation inhibited the phosphorylation of desmin, synemin, and the three cytosolic proteins.	Nitroglycerin	15-28	synemin	Homo sapiens	116-123
7556582-1	1995	The smooth muscle relaxation induced by nitroglycerin is hypothesized to be mediated by an increase in the cytoplasmic concentration of guanosine 3",5"-monophosphate (cGMP) and subsequent dephosphorylation of the 20-kilodalton myosin light chain (MLC).	Nitroglycerin	40-53	modulator of VRAC current 1	Homo sapiens	227-245
7556582-1	1995	The smooth muscle relaxation induced by nitroglycerin is hypothesized to be mediated by an increase in the cytoplasmic concentration of guanosine 3",5"-monophosphate (cGMP) and subsequent dephosphorylation of the 20-kilodalton myosin light chain (MLC).	Nitroglycerin	40-53	modulator of VRAC current 1	Homo sapiens	247-250
7556582-9	1995	Intermediate filament proteins, rather than MLC, may also be the target for the relaxant action of nitroglycerin during histamine-induced sustained contraction.	Nitroglycerin	99-112	modulator of VRAC current 1	Homo sapiens	44-47
7540279-0	1995	Increase in plasma calcitonin gene-related peptide from the extracerebral circulation during nitroglycerin-induced cluster headache attack.	Nitroglycerin	93-106	calcitonin related polypeptide alpha	Homo sapiens	19-50
8729740-12	1995	Our observations suggest that individual reactions to transdermal glyceryl trinitrate (GTN) with its active component nitric oxide (NO) depends on physiological conditions, related to endogenous vasoactive substances, mainly the interaction with EDRF (the endogenous NO) and the activity of the Renin-Angiotensin System.	Nitroglycerin	66-85	alpha hemoglobin stabilizing protein	Homo sapiens	246-250
8729740-12	1995	Our observations suggest that individual reactions to transdermal glyceryl trinitrate (GTN) with its active component nitric oxide (NO) depends on physiological conditions, related to endogenous vasoactive substances, mainly the interaction with EDRF (the endogenous NO) and the activity of the Renin-Angiotensin System.	Nitroglycerin	87-90	alpha hemoglobin stabilizing protein	Homo sapiens	246-250
7488328-1	1995	We have carried out a pilot study to examine the influence on postprandial lipid and lipoprotein metabolism of common genetic variation in the gene coding for apolipoprotein (apo) B, in a previously described group of 30 individuals who had survived a myocardial infarction (MI) before the age of 45 (normo (NTG)- and hypertriglyceridaemic (HTG) patients) and 11 age-matched healthy individuals.	Nitroglycerin	308-311	apolipoprotein B	Homo sapiens	159-181
7769833-8	1995	Glyceryl trinitrate alone increased HMPS activity and G6PD mRNA levels and also reduced cell proliferation.	Nitroglycerin	0-19	glucose-6-phosphate dehydrogenase	Homo sapiens	54-58
7835300-8	1995	GHR-binding assays revealed that liver GHR-binding sites were significantly reduced in diabetic NTG mice and transgenic dwarf mice when compared with their nondiabetic controls.	Nitroglycerin	96-99	growth hormone receptor	Mus musculus	0-3
7835300-8	1995	GHR-binding assays revealed that liver GHR-binding sites were significantly reduced in diabetic NTG mice and transgenic dwarf mice when compared with their nondiabetic controls.	Nitroglycerin	96-99	growth hormone receptor	Mus musculus	39-42
7835300-9	1995	Conversely, liver GHR-binding ability was significantly increased in bGH transgenic mice as compared with their NTG littermates and remained high during diabetes.	Nitroglycerin	112-115	growth hormone receptor	Mus musculus	18-21
7572010-3	1995	Therefore, we compared the acute effects of nitroglycerin (0.5 micrograms kg-1 min-1) and isosorbide dinitrate (0.5 or 2.5 micrograms kg-1 min-1) with those of placebo on platelet function both before and after cardiopulmonary bypass in 40 patients undergoing coronary artery bypass grafting (CABG).	Nitroglycerin	44-57	CD59 molecule (CD59 blood group)	Homo sapiens	79-84
7552308-0	1995	Systemic nitroglycerin induces Fos immunoreactivity in brainstem and forebrain structures of the rat.	Nitroglycerin	9-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
7552308-3	1995	In this study, we evaluated the distribution and intensity of Fos immunoreactivity in rat brain nuclei following the systemic administration of nitroglycerin.	Nitroglycerin	144-157	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-65
7539147-0	1995	Evidence for a role of endothelin 1 and protein kinase C in nitroglycerin tolerance.	Nitroglycerin	60-73	endothelin-1	Oryctolagus cuniculus	23-35
7539147-6	1995	Immunocytochemical analysis revealed intense endothelin 1-like and big endothelin 1-like immunoreactivity in the media of nitroglycerin-tolerant but not of control aortas.	Nitroglycerin	122-135	endothelin-1	Oryctolagus cuniculus	71-83
8820253-0	1995	Additive effect of nitroglycerine inhalation on beta2-agonist-induced bronchodilatation in asthmatics.	Nitroglycerin	19-33	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	48-53
8820253-4	1995	We wondered whether an additive effect of nitroglycerin (NTG) on beta2-agonist-induced bronchodilatation was present in asthmatic patients.	Nitroglycerin	42-55	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	65-70
8820253-4	1995	We wondered whether an additive effect of nitroglycerin (NTG) on beta2-agonist-induced bronchodilatation was present in asthmatic patients.	Nitroglycerin	57-60	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	65-70
7605366-6	1995	32-33 split proinsulin (SPI) was the major insulin-like molecule present in HTG and was present in significantly higher amounts in these patients (P < 0.05) than either NTG or control subjects and correlated significantly with the presence of small dense LDL particles.	Nitroglycerin	172-175	insulin	Homo sapiens	12-22
7605366-6	1995	32-33 split proinsulin (SPI) was the major insulin-like molecule present in HTG and was present in significantly higher amounts in these patients (P < 0.05) than either NTG or control subjects and correlated significantly with the presence of small dense LDL particles.	Nitroglycerin	172-175	insulin	Homo sapiens	15-22
7875768-7	1995	Nitroglycerin (10(-7) to 10(-3) mol/L) dose-dependently increased NO production; however, only the highest dose (10(-3) mol/L) reduced basal and phenylephrine-stimulated total protein content and BNP secretion.	Nitroglycerin	0-13	natriuretic peptide B	Homo sapiens	196-199
7540279-1	1995	In this study, changes in plasma levels of calcitonin gene-related peptide (CGRP) and substance P (SP) during a spontaneous-like cluster headache attack provoked by nitroglycerin were evaluated.	Nitroglycerin	165-178	calcitonin related polypeptide alpha	Homo sapiens	43-74
7540279-1	1995	In this study, changes in plasma levels of calcitonin gene-related peptide (CGRP) and substance P (SP) during a spontaneous-like cluster headache attack provoked by nitroglycerin were evaluated.	Nitroglycerin	165-178	calcitonin related polypeptide alpha	Homo sapiens	76-80
7540279-1	1995	In this study, changes in plasma levels of calcitonin gene-related peptide (CGRP) and substance P (SP) during a spontaneous-like cluster headache attack provoked by nitroglycerin were evaluated.	Nitroglycerin	165-178	tachykinin precursor 1	Homo sapiens	99-101
7540279-8	1995	The augmented levels of CGRP-LI measured before and after nitroglycerin administration, when the provoked attack reached the maximum intensity, suggest an activation of the trigeminovascular system during the active period of cluster headache.	Nitroglycerin	58-71	calcitonin related polypeptide alpha	Homo sapiens	24-28
7753760-1	1995	We have investigated the effects of the novel phospholipid drug glyceryl-phosphoryl-O-serine (GPS) on pituitary ACTH and hypothalamic corticotropin releasing hormone secretion in vitro in cultures from both 2- and 24 month-old Sprague-Dawley rats.	Nitroglycerin	64-72	corticotropin releasing hormone	Rattus norvegicus	134-165
7815811-8	1995	Nitroglycerin reversed vasoconstriction produced by endothelin-1 and endothelin-1 plus norepinephrine both before and after ischemia-reperfusion.	Nitroglycerin	0-13	endothelin 1	Homo sapiens	52-64
7815811-8	1995	Nitroglycerin reversed vasoconstriction produced by endothelin-1 and endothelin-1 plus norepinephrine both before and after ischemia-reperfusion.	Nitroglycerin	0-13	endothelin 1	Homo sapiens	69-81
7815811-11	1995	Nitroglycerin reverses coronary vasoconstriction induced by endothelin-1 and may therefore be beneficial in the postoperative management of neonates after cardiac operations.	Nitroglycerin	0-13	endothelin 1	Homo sapiens	60-72
8532597-3	1995	Pretreatment with 10(-9) M endothelin-1 significantly reduced endothelium-dependent relaxation elicited by substance P and endothelium-independent relaxations by nitroglycerin, prostaglandin I2, and KCl.	Nitroglycerin	162-175	endothelin 1	Canis lupus familiaris	27-39
8839227-6	1995	In all blood vessels except for the basilar artery, nitroglycerin caused larger relaxations than ITF 296: The ED50 for nitroglycerin was comparable in all blood vessels studied except for the mesenteric artery, where it was less.	Nitroglycerin	119-132	trefoil factor 3	Canis lupus familiaris	97-100
7534182-15	1994	Desensitization to the relaxant effect of VIP partially reduced relaxations induced by vagal stimulation, glyceryl trinitrate or sodium nitroprusside but not noradrenaline.	Nitroglycerin	106-125	VIP peptides	Cavia porcellus	42-45
7888288-5	1994	This study was designed to investigate the effect of glyceryl trinitrate (GTN) and calcium antagonists on ET-1 contraction in the human IMA.	Nitroglycerin	53-72	endothelin 1	Homo sapiens	106-110
7888288-5	1994	This study was designed to investigate the effect of glyceryl trinitrate (GTN) and calcium antagonists on ET-1 contraction in the human IMA.	Nitroglycerin	74-77	endothelin 1	Homo sapiens	106-110
7888288-10	1994	In separate experiments, the concentration-relaxation curves to GTN or nifedipine were established in the IMA rings precontracted with ET-1 (10 nM).	Nitroglycerin	64-67	endothelin 1	Homo sapiens	135-139
7880995-0	1994	Methemoglobin levels during prolonged combined nitroglycerin and sodium nitroprusside infusions in infants after cardiac surgery.	Nitroglycerin	47-60	hemoglobin subunit gamma 2	Homo sapiens	0-13
7888288-15	1994	On the other hand, GTN caused 76.44 +/- 6.35% relaxation in ET-1-precontracted IMA.	Nitroglycerin	19-22	endothelin 1	Homo sapiens	60-64
7736342-7	1994	Furthermore, GTN-induced guanylyl cyclase activation mediated by microsomes from DEX-treated male and female rats was markedly inhibited by a polyclonal antibody raised to rat CYP3A1.	Nitroglycerin	13-16	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	176-182
7736342-8	1994	Since CYP3A2 is absent or very low in hepatic microsomes from DEX-treated adult female rats, this identifies CYP3A1 as an isoform capable of biotransforming GTN to an activator of guanylyl cyclase.	Nitroglycerin	157-160	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	6-12
7736342-8	1994	Since CYP3A2 is absent or very low in hepatic microsomes from DEX-treated adult female rats, this identifies CYP3A1 as an isoform capable of biotransforming GTN to an activator of guanylyl cyclase.	Nitroglycerin	157-160	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	109-115
7736342-9	1994	Similarly, CYP2C11 was identified as an isoform capable of biotransforming GTN to an activator of guanylyl cyclase, since monoclonal antibody to CYP2C11 inhibited GTN-induced activation of guanylyl cyclase mediated by microsomes from control male rats.	Nitroglycerin	75-78	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	11-18
7736342-9	1994	Similarly, CYP2C11 was identified as an isoform capable of biotransforming GTN to an activator of guanylyl cyclase, since monoclonal antibody to CYP2C11 inhibited GTN-induced activation of guanylyl cyclase mediated by microsomes from control male rats.	Nitroglycerin	75-78	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	145-152
7736342-9	1994	Similarly, CYP2C11 was identified as an isoform capable of biotransforming GTN to an activator of guanylyl cyclase, since monoclonal antibody to CYP2C11 inhibited GTN-induced activation of guanylyl cyclase mediated by microsomes from control male rats.	Nitroglycerin	163-166	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	11-18
7736342-9	1994	Similarly, CYP2C11 was identified as an isoform capable of biotransforming GTN to an activator of guanylyl cyclase, since monoclonal antibody to CYP2C11 inhibited GTN-induced activation of guanylyl cyclase mediated by microsomes from control male rats.	Nitroglycerin	163-166	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	145-152
7880995-6	1994	The median MetHb was 0.6% (range 0.0 to 1.5) after infusions of NTG, 1.8 micrograms/kg/min (range 0.5 to 4), and SNP, 1.3 micrograms/kg/min (range 0.3 to 8.4) (N = 69 measurements).	Nitroglycerin	64-67	hemoglobin subunit gamma 2	Homo sapiens	11-16
7527856-11	1994	To clarify the mechanism of the saturable clearance of NTG, the in vitro metabolic activities in rat bone marrow, spleen cells and peripheral leukocytes, which possess the G-CSF receptor, were determined.	Nitroglycerin	55-58	colony stimulating factor 3	Homo sapiens	172-177
7965786-1	1994	Recent studies suggest a role for the vascular cytochrome P450-NADPH cytochrome P450 reductase system in mediating the biotransformation of glyceryl trinitrate (GTN) to nitric oxide (or some closely related species), resulting in increased cyclic GMP accumulation and vasodilation.	Nitroglycerin	140-159	cytochrome p450 oxidoreductase	Rattus norvegicus	63-94
7526102-6	1994	In 7 control patients, PTCA caused a rise in platelet surface expression of P-selectin and glycoprotein IIb/IIIa, which was maximal 5 minutes after PTCA, indicating increased platelet activation despite treatment with aspirin, glyceryl trinitrate, and heparin.	Nitroglycerin	227-246	selectin P	Homo sapiens	76-86
7965786-1	1994	Recent studies suggest a role for the vascular cytochrome P450-NADPH cytochrome P450 reductase system in mediating the biotransformation of glyceryl trinitrate (GTN) to nitric oxide (or some closely related species), resulting in increased cyclic GMP accumulation and vasodilation.	Nitroglycerin	161-164	cytochrome p450 oxidoreductase	Rattus norvegicus	63-94
7965786-8	1994	Together, these data provide evidence for the involvement of a flavoprotein (e.g., NADPH cytochrome P450 reductase) in the metabolic activation of GTN required for expression of its vasodilator activity.	Nitroglycerin	147-150	cytochrome p450 oxidoreductase	Rattus norvegicus	83-114
7942523-0	1994	Concurrent nitroglycerin therapy impairs tissue-type plasminogen activator-induced thrombolysis in patients with acute myocardial infarction.	Nitroglycerin	11-24	plasminogen activator, tissue type	Homo sapiens	41-74
7942523-1	1994	Nitroglycerin given with tissue-type plasminogen activator (t-PA) has been shown to decrease the thrombolytic effect of t-PA in animal models of coronary artery thrombosis.	Nitroglycerin	0-13	plasminogen activator, tissue type	Homo sapiens	25-58
7942523-1	1994	Nitroglycerin given with tissue-type plasminogen activator (t-PA) has been shown to decrease the thrombolytic effect of t-PA in animal models of coronary artery thrombosis.	Nitroglycerin	0-13	plasminogen activator, tissue type	Homo sapiens	60-64
7942523-1	1994	Nitroglycerin given with tissue-type plasminogen activator (t-PA) has been shown to decrease the thrombolytic effect of t-PA in animal models of coronary artery thrombosis.	Nitroglycerin	0-13	plasminogen activator, tissue type	Homo sapiens	120-124
7942523-2	1994	The present study was conducted to determine whether such an interaction between nitroglycerin and t-PA occurs in patients with acute myocardial infarction undergoing thrombolytic treatment.	Nitroglycerin	81-94	plasminogen activator, tissue type	Homo sapiens	99-103
7942523-7	1994	These observations indicate that nitroglycerin given with t-PA significantly decreases the plasma t-PA antigen concentrations and impairs the thrombolytic effect of t-PA in patients with acute myocardial infarction.	Nitroglycerin	33-46	plasminogen activator, tissue type	Homo sapiens	58-62
7942523-7	1994	These observations indicate that nitroglycerin given with t-PA significantly decreases the plasma t-PA antigen concentrations and impairs the thrombolytic effect of t-PA in patients with acute myocardial infarction.	Nitroglycerin	33-46	plasminogen activator, tissue type	Homo sapiens	98-102
7942523-7	1994	These observations indicate that nitroglycerin given with t-PA significantly decreases the plasma t-PA antigen concentrations and impairs the thrombolytic effect of t-PA in patients with acute myocardial infarction.	Nitroglycerin	33-46	plasminogen activator, tissue type	Homo sapiens	98-102
7834179-7	1994	The measurement of platelet cyclic GMP may represent a simple approach for monitoring the degree of venous tolerance to NTG in animals or patients, facilitating further mechanistic investigations.	Nitroglycerin	120-123	5'-nucleotidase, cytosolic II	Homo sapiens	35-38
7810336-10	1994	Intravenously infused GTN (4-512 micrograms kg body wt-1 min-1) and SNP (4-64 micrograms kg body wt-1 min-1) decreased arterial pressure and elicited, via reflex sympathetic activation, a dose-dependent vasoconstriction in skeletal muscle, a decrease in Pc,v, and net transcapillary fluid absorption.	Nitroglycerin	22-25	CD59 molecule (CD59 blood group)	Homo sapiens	57-62
7833219-10	1994	Bradykinin (10 and 100 pmol min-1; 3 min each dose) and GTN (2 and 5 nmol min-1; 3 min each dose) increased forearm blood flow in a dose-dependent manner (percentage changes 171 +/- 17% and 398 +/- 35%, and 176 +/- 21% and 268 +/- 42%, respectively; n = 6).	Nitroglycerin	56-59	CD59 molecule (CD59 blood group)	Homo sapiens	74-79
7834179-1	1994	The effects of acute intravenous nitroglycerin (NTG) administration on platelet cyclic GMP in relation to changes in indices of preload (end-diastolic volume) and afterload (effective arterial elastance) were evaluated in the anaesthetized mini-pig, using pressure-volume analysis.	Nitroglycerin	33-46	5'-nucleotidase, cytosolic II	Homo sapiens	87-90
7834179-1	1994	The effects of acute intravenous nitroglycerin (NTG) administration on platelet cyclic GMP in relation to changes in indices of preload (end-diastolic volume) and afterload (effective arterial elastance) were evaluated in the anaesthetized mini-pig, using pressure-volume analysis.	Nitroglycerin	48-51	5'-nucleotidase, cytosolic II	Homo sapiens	87-90
7834179-6	1994	Therefore, platelet cyclic GMP appears to reflect NTG-induced venous tolerance, rather than arterial responsiveness.	Nitroglycerin	50-53	5'-nucleotidase, cytosolic II	Homo sapiens	27-30
7875541-7	1994	Cromakalim at 10(-5) M and nitroglycerin at 10(-7) M completely eliminated 3,4-DAP-induced rythmic contractions in all preparations.	Nitroglycerin	27-40	death associated protein	Homo sapiens	79-82
8025986-7	1994	Forearm blood flow responses to acetylcholine and nitroglycerin were significantly greater in these 10 patients than in the 7 patients without detectable serum TNF alpha and were closely correlated with TNF alpha serum concentrations (r > or = .81, P < .01 and r > or = .65, P < .05 respectively).	Nitroglycerin	50-63	tumor necrosis factor	Homo sapiens	160-169
8025986-13	1994	The significant correlation between serum concentrations of TNF alpha and forearm blood flow responses to acetylcholine and nitroglycerin suggests that both the inducible and the constitutive forms of nitric oxide synthase are involved in the regulation of peripheral vasomotor tone in patients with CHF.	Nitroglycerin	124-137	tumor necrosis factor	Homo sapiens	60-69
7835640-12	1994	These relaxant effects of KRN2391 and nitroglycerin on endothelin-1-induced contraction of porcine coronary artery were greater than those of cromakalim and nifedipine.	Nitroglycerin	38-51	endothelin-1	Sus scrofa	55-67
7835641-7	1994	Despite producing submaximal relaxation at KRN2391 (10(-6) M) and nitroglycerin (10(-6) M), the increase in cyclic GMP caused by KRN2391 was lower than that caused by nitroglycerin.	Nitroglycerin	66-79	5'-nucleotidase, cytosolic II	Homo sapiens	115-118
7982287-9	1994	CER by concomitant infusion of a subpressor dose of angiotensin II (AII) attenuated the progressive reduction of GLU release (87 +/- 4%, P < 0.05 compared with NTG group), whereas GLY release was not affected (106 +/- 5%, NS compared with NTG group).	Nitroglycerin	163-166	angiotensinogen	Rattus norvegicus	52-66
7982287-9	1994	CER by concomitant infusion of a subpressor dose of angiotensin II (AII) attenuated the progressive reduction of GLU release (87 +/- 4%, P < 0.05 compared with NTG group), whereas GLY release was not affected (106 +/- 5%, NS compared with NTG group).	Nitroglycerin	163-166	angiotensinogen	Rattus norvegicus	68-71
7982287-9	1994	CER by concomitant infusion of a subpressor dose of angiotensin II (AII) attenuated the progressive reduction of GLU release (87 +/- 4%, P < 0.05 compared with NTG group), whereas GLY release was not affected (106 +/- 5%, NS compared with NTG group).	Nitroglycerin	242-245	angiotensinogen	Rattus norvegicus	52-66
7982287-9	1994	CER by concomitant infusion of a subpressor dose of angiotensin II (AII) attenuated the progressive reduction of GLU release (87 +/- 4%, P < 0.05 compared with NTG group), whereas GLY release was not affected (106 +/- 5%, NS compared with NTG group).	Nitroglycerin	242-245	angiotensinogen	Rattus norvegicus	68-71
8025986-7	1994	Forearm blood flow responses to acetylcholine and nitroglycerin were significantly greater in these 10 patients than in the 7 patients without detectable serum TNF alpha and were closely correlated with TNF alpha serum concentrations (r > or = .81, P < .01 and r > or = .65, P < .05 respectively).	Nitroglycerin	50-63	tumor necrosis factor	Homo sapiens	203-212
8025986-12	1994	CONCLUSIONS: Increased TNF alpha concentrations are closely correlated with forearm blood flow responses to regional administration of acetylcholine and nitroglycerin.	Nitroglycerin	153-166	tumor necrosis factor	Homo sapiens	23-32
8163590-2	1994	In the ischemic cortex of nTg mice, hsp70 mRNA was detected 1 h after reperfusion and was observed for up to 6 h. In Tg mice, however, it was still detectable within the cortex even at 24 h. In the caudate putamen, hsp70 mRNA appeared at 1 h and was present for up to 6 h in both nTg and Tg mice.	Nitroglycerin	26-29	heat shock protein 1B	Mus musculus	36-41
8163590-2	1994	In the ischemic cortex of nTg mice, hsp70 mRNA was detected 1 h after reperfusion and was observed for up to 6 h. In Tg mice, however, it was still detectable within the cortex even at 24 h. In the caudate putamen, hsp70 mRNA appeared at 1 h and was present for up to 6 h in both nTg and Tg mice.	Nitroglycerin	280-283	heat shock protein 1B	Mus musculus	36-41
8163590-3	1994	Although hsp70 mRNA was detected in the thalamus only at 1 h in nTg mice, it was observed for up to 6 h in Tg mice.	Nitroglycerin	64-67	heat shock protein 1B	Mus musculus	9-14
7911801-16	1994	Bolus infusion of nitroglycerin (15 micrograms) induced an immediate decrease in Ppa and PVR during ALI.	Nitroglycerin	18-31	PVR cell adhesion molecule	Canis lupus familiaris	89-92
8199279-19	1994	As compared to Gr.I the administration of TNG resulted in significant decreases of APS, APD, TPR, ESV and LVEDP close to control values.	Nitroglycerin	42-45	translocated promoter region, nuclear basket protein	Canis lupus familiaris	93-96
8170522-7	1994	Nitroglycerin also potentiated rCGRP-induced vasorelaxations in endothelium-denuded rings, thus uncovering a direct (endothelium-independent) relaxant effect of rCGRP in rat aorta.	Nitroglycerin	0-13	calcitonin-related polypeptide alpha	Rattus norvegicus	31-36
8170522-9	1994	This nitroglycerin-induced potentiation of CGRP effects likely involves inhibition of cyclic-GMP-inhibited-phosphodiesterase in smooth muscle cells, thus allowing cyclic AMP to accumulate and mediate the direct vasodilator effects of rCGRP.	Nitroglycerin	5-18	calcitonin-related polypeptide alpha	Rattus norvegicus	43-47
8170522-0	1994	Nitroglycerin (exogenous nitric oxide) substitutes for endothelium-derived nitric oxide in potentiating vasorelaxations and cyclic AMP elevations induced by calcitonin gene-related peptide (CGRP) in rat aorta.	Nitroglycerin	0-13	calcitonin-related polypeptide alpha	Rattus norvegicus	157-188
8170522-0	1994	Nitroglycerin (exogenous nitric oxide) substitutes for endothelium-derived nitric oxide in potentiating vasorelaxations and cyclic AMP elevations induced by calcitonin gene-related peptide (CGRP) in rat aorta.	Nitroglycerin	0-13	calcitonin-related polypeptide alpha	Rattus norvegicus	190-194
8170522-9	1994	This nitroglycerin-induced potentiation of CGRP effects likely involves inhibition of cyclic-GMP-inhibited-phosphodiesterase in smooth muscle cells, thus allowing cyclic AMP to accumulate and mediate the direct vasodilator effects of rCGRP.	Nitroglycerin	5-18	calcitonin-related polypeptide alpha	Rattus norvegicus	234-239
8026713-0	1994	Reduced endothelium-dependent vasodilation by acetylcholine and bradykinin in isolated nitroglycerin-tolerant blood vessels.	Nitroglycerin	87-100	kininogen 1	Homo sapiens	64-74
8304511-3	1994	Under control conditions, nitroglycerin caused potent dilations of large (> 200 microns diam) coronary microvessels while having minimal effects on small (< 100 microns diam) coronary microvessels [peak relaxations 85 +/- 4 vs. 23 +/- 3% (mean +/- SE) of endothelin-1-constricted vessels, respectively].	Nitroglycerin	26-39	endothelin 1	Homo sapiens	261-273
7870346-9	1994	In NTG patients the increase of apoC-III was found in VLDL-LDL and in HDL.	Nitroglycerin	3-6	apolipoprotein C3	Homo sapiens	32-40
8131770-1	1993	We have previously shown that transdermal nitroglycerin may induce an increase in the activity of the adrenergic and the renin-angiotensin-aldosterone systems (SRAA) in patients with chronic stable angina pectoris (SA); when the activation of these systems is more pronounced, the antianginal effect of this drug seems to be reduced.	Nitroglycerin	42-55	renin	Homo sapiens	121-126
8185413-2	1993	KRN2391, nitroglycerin and cromakalim concentration-dependently inhibited the 10(-8) M endothelin-1-induced contraction, but less potently inhibited the 40 mM KCl-induced contraction.	Nitroglycerin	9-22	endothelin 1	Homo sapiens	87-99
8185413-7	1993	The combination of cromakalim and nitroglycerin relaxed the 10(-8) M endothelin-1- and 40 mM KCl-induced contractions in a concentration-dependent manner.	Nitroglycerin	34-47	endothelin 1	Homo sapiens	69-81
8185413-9	1993	The maximum relaxation of the combination of cromakalim (3 x 10(-5) M) and nitroglycerin (3 x 10(-6) M) was complete for the endothelin-1-induced contraction but a relaxation of 77.8% was obtained for the 40 mM KCl-induced contraction, i.e. the relaxant effects using this combination were greater than those by cromakalim (3 x 10(-5) M) alone.	Nitroglycerin	75-88	endothelin 1	Homo sapiens	125-137
8185413-4	1993	KRN2391 and nitroglycerin produced a complete relaxation of arteries contracted by endothelin-1 at its maximum effect.	Nitroglycerin	12-25	endothelin 1	Homo sapiens	83-95
8391401-2	1993	BACKGROUND: The present study was designed to investigate the intracellular production of cyclic GMP (cGMP) in platelets in response to nitroglycerin and to determine the potential clinical value of platelet cGMP as an indicator of the effects of nitroglycerin and nitrate tolerance.	Nitroglycerin	136-149	5'-nucleotidase, cytosolic II	Homo sapiens	97-100
8335833-3	1993	METHODS: In patients with angina pectoris, the effects of 10 days of treatment with the sulfhydryl-containing angiotensin-converting enzyme inhibitor captopril on the coronary vasodilator responses to intracoronary nitroglycerin (1- to 20-micrograms doses) were examined utilizing a double-blind, placebo-controlled, randomized design.	Nitroglycerin	215-228	angiotensin I converting enzyme	Homo sapiens	110-139
7688473-9	1993	Exogenous NO either as a gaseous solution or released by a NO donor, sodium nitroprusside or glyceryl trinitrate, increased COX activity in the interleukin 1 beta-stimulated fibroblasts by 5-fold; these effects were abolished by coincubation with hemoglobin (10 microM), which binds and inactivates NO, but not by methylene blue, an inhibitor of the soluble guanylate cyclase.	Nitroglycerin	93-112	cytochrome c oxidase II, mitochondrial	Mus musculus	124-127
7688473-9	1993	Exogenous NO either as a gaseous solution or released by a NO donor, sodium nitroprusside or glyceryl trinitrate, increased COX activity in the interleukin 1 beta-stimulated fibroblasts by 5-fold; these effects were abolished by coincubation with hemoglobin (10 microM), which binds and inactivates NO, but not by methylene blue, an inhibitor of the soluble guanylate cyclase.	Nitroglycerin	93-112	interleukin 1 beta	Homo sapiens	144-162
8391401-2	1993	BACKGROUND: The present study was designed to investigate the intracellular production of cyclic GMP (cGMP) in platelets in response to nitroglycerin and to determine the potential clinical value of platelet cGMP as an indicator of the effects of nitroglycerin and nitrate tolerance.	Nitroglycerin	247-260	5'-nucleotidase, cytosolic II	Homo sapiens	97-100
8461525-7	1993	By increasing EDRF production or inhibiting its breakdown, EDRF precursors such as L-arginine, the superoxide radical scavenger superoxide dismutase, nitroglycerin, and nitroprusside all cause vasodilation by increasing NO levels in the setting of myocardial ischemia.	Nitroglycerin	150-163	alpha hemoglobin stabilizing protein	Homo sapiens	14-18
7690081-7	1993	Incubation of isolated porcine coronary artery rings with GTN or SPM 3672 resulted in a similar increase in vascular cyclic GMP levels.	Nitroglycerin	58-61	5'-nucleotidase, cytosolic II	Homo sapiens	124-127
8101080-4	1993	These results may have significant implications for the design of heart-regulating drugs (e.g. those used in angina), such as glyceryl trinitrate, which act via guanylate cyclase.	Nitroglycerin	126-145	guanylate cyclase	Bos taurus	161-178
8364671-3	1993	This is due to the ability of nitroglycerin to reduce the detrimental effects of vasopressin while preserving its beneficial effects.	Nitroglycerin	30-43	arginine vasopressin	Homo sapiens	81-92
8477563-2	1993	Recently vascular glutathione S-transferase (EC 2.5.1.18) of the mu-class (GST mu), a polymorphic group of enzymes present in only about 60% of the population, have been identified and shown in vitro to possess high metabolic activity toward nitroglycerin.	Nitroglycerin	242-255	glutathione S-transferase kappa 1	Homo sapiens	18-43
7681498-8	1993	Platelets from patients with angina pectoris were 100-fold less responsive to the cyclic GMP-increasing and disaggregating effects of NTG in vitro, which, together with increased aggregability, could imply reduced platelet sensitivity to endogenous sources of nitric oxide (NO) in vivo.	Nitroglycerin	134-137	5'-nucleotidase, cytosolic II	Homo sapiens	89-92
8481559-3	1993	The final goal was to examine the effects of the glutathione S-transferase (GST) inhibitor Basilen Blue (BB) on glyceryl trinitrate biotransformation in porcine kidney epithelial (PK1) cells after intracellular delivery.	Nitroglycerin	112-131	microsomal glutathione S-transferase 1	Sus scrofa	76-79
8450477-1	1993	The present study was conducted to test the hypothesis that glyceryl trinitrate (GTN) metabolic activation in blood vessels is mediated by cytochrome P-450 or some other hemoprotein.	Nitroglycerin	60-79	cytochrome P-450	Oryctolagus cuniculus	139-155
8450477-1	1993	The present study was conducted to test the hypothesis that glyceryl trinitrate (GTN) metabolic activation in blood vessels is mediated by cytochrome P-450 or some other hemoprotein.	Nitroglycerin	81-84	cytochrome P-450	Oryctolagus cuniculus	139-155
8450477-2	1993	The effects of cytochrome P-450 inhibitor [2-dimethylaminoethyl-2,2-diphenyl-n-pentanoate (SKF-525A) and metyrapone] on the response of rabbit aortic rings to GTN was determined by recording cumulative GTN dose-response curves in the presence of either or both inhibitors.	Nitroglycerin	159-162	cytochrome P-450	Oryctolagus cuniculus	15-31
8385958-6	1993	Further, nitroglycerin effectively blocked endothelin-1-mediated coronary flow reductions, but only partially antagonized reductions in renal blood flow.	Nitroglycerin	9-22	endothelin 1	Canis lupus familiaris	43-55
8448809-0	1993	Particular ability of cytochrome P-450 CYP3A to reduce glyceryl trinitrate in rat liver microsomes: subsequent formation of nitric oxide.	Nitroglycerin	55-74	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	22-38
8448809-6	1993	In the hepatic 9000 x g supernatant containing both NADPH and cytochrome P-450 and glutathione and glutathione transferase, the cytochrome P-450-dependent reaction accounts for 30-40% of the total denitration activity observed under anaerobic conditions, using 100 microM GTN.	Nitroglycerin	272-275	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	62-78
8448809-6	1993	In the hepatic 9000 x g supernatant containing both NADPH and cytochrome P-450 and glutathione and glutathione transferase, the cytochrome P-450-dependent reaction accounts for 30-40% of the total denitration activity observed under anaerobic conditions, using 100 microM GTN.	Nitroglycerin	272-275	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	128-144
8381319-12	1993	Exposure of non-tolerant SMC or EC (10(5) cells) to GTN (200 microM) for 3 min increased (3-4 fold) the levels of guanosine 3":5"-cyclic monophosphate (cyclic GMP).	Nitroglycerin	52-55	5'-nucleotidase, cytosolic II	Homo sapiens	159-162
8381319-15	1993	Sodium nitroprusside (80 JAM) or atrial natriuretic factor (ANF, I0- M) increased the levels of cyclic GMP in normal or tolerant SMC or EC to the same extent.5 The anti-platelet effects of GTN (44 JM) were potentiated by the sulphydryl donor N-acetylcysteine(NAC, 0.5mM).	Nitroglycerin	189-192	natriuretic peptide A	Homo sapiens	60-63
8381319-16	1993	Incubation of GTN (150-1200fJM) for 30min with NAC (0.1-1mM) led to aconcentration-dependent increase in N02- formation.	Nitroglycerin	14-17	synuclein alpha	Homo sapiens	47-50
8381319-17	1993	The reduced ability of tolerant SMC or EC to potentiate the anti-platelet activity of GTN was restored by NAC (0.5 mM).	Nitroglycerin	86-89	synuclein alpha	Homo sapiens	106-109
8381319-19	1993	Furthermore, when compared to normal cells, tolerant SMC or EC metabolize GTN to NO less effectively as assessed by the reduced capacity to potentiate the antiplatelet effects of GTN, to release NO2- and to increase the level of cyclic GMP.	Nitroglycerin	74-77	5'-nucleotidase, cytosolic II	Homo sapiens	236-239
8381319-21	1993	NAC, by directly forming NO from GTN, compensates for this failing mechanism.	Nitroglycerin	33-36	synuclein alpha	Homo sapiens	0-3
1529924-7	1992	In the presence of inadequate EDRF production and/or release, it appears that nitroglycerin may partially replenish EDRF-like activity.	Nitroglycerin	78-91	alpha hemoglobin stabilizing protein	Homo sapiens	116-120
8432288-5	1993	After 6 h of nitroglycerin infusion, mean arterial pressure was decreased, but circulating neurohumoral levels remained unchanged and NPY-Li levels decreased (653 +/- 37 to 517 +/- 26 pg.ml-1, P < 0.01).	Nitroglycerin	13-26	neuropeptide Y	Homo sapiens	134-137
8436154-2	1993	NTG 0.5 microgram.kg-1 x min-1 or saline were infused i.v.	Nitroglycerin	0-3	CD59 molecule (CD59 blood group)	Homo sapiens	25-30
7509975-5	1993	Although GTN partially prevented ET-1-induced constriction (maximum 33 +/- 5%, p = 0.004 versus ET-1), inhibition of NOS did not affect ET-1-induced venoconstriction (maximum 55 +/- 4%).	Nitroglycerin	9-12	endothelin 1	Homo sapiens	33-37
1490968-8	1992	The increase mediated by angiotensin II was blocked by glycerol trinitrate (2.2 microM), which had no effect on lactate release by isoproterenol.	Nitroglycerin	55-74	angiotensinogen	Rattus norvegicus	25-39
1388322-0	1992	Atrial natriuretic peptide in severe heart failure: response to controlled changes in atrial pressures during intravenous nitroglycerin therapy.	Nitroglycerin	122-135	natriuretic peptide A	Homo sapiens	0-26
1388322-4	1992	In patients with hemodynamic tolerance to constant-dose nitroglycerin infusion, the resulting increase in atrial pressures was accompanied by an appropriate secondary increase in the plasma ANP level.	Nitroglycerin	56-69	natriuretic peptide A	Homo sapiens	190-193
1382082-9	1992	It decreased to 0.2 +/- 0.3 mm during acetylcholine-induced spasm (p less than 0.001) and increased to 2.3 +/- 0.8 mm after nitroglycerin administration (p less than 0.001 vs. baseline and p = NS vs. after substance P infusion).	Nitroglycerin	124-137	tachykinin precursor 1	Homo sapiens	206-217
1623866-4	1992	Overall, the decrease in PVR ranged from 9 +/- 12% (nitroglycerin) to 38 +/- 23% (prostacyclin).	Nitroglycerin	52-65	PVR cell adhesion molecule	Homo sapiens	25-28
1362924-8	1992	Our data provide further evidence for the role of the cytochrome P-450--cytochrome P-450 reductase system in the biotransformation of GTN to an activator (presumably nitric oxide) of guanylyl cyclase.	Nitroglycerin	134-137	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	54-70
1362924-8	1992	Our data provide further evidence for the role of the cytochrome P-450--cytochrome P-450 reductase system in the biotransformation of GTN to an activator (presumably nitric oxide) of guanylyl cyclase.	Nitroglycerin	134-137	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	72-88
1352550-2	1992	In cultured rat lung fibroblasts (RFL-6 cells), the inhibitor of cytochrome P-450 proadifen (0.1 mM) decreased cyclic GMP stimulation by glyceryl trinitrate (GTN, 1-100 microM) by up to 81%.	Nitroglycerin	137-156	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	65-81
1352550-2	1992	In cultured rat lung fibroblasts (RFL-6 cells), the inhibitor of cytochrome P-450 proadifen (0.1 mM) decreased cyclic GMP stimulation by glyceryl trinitrate (GTN, 1-100 microM) by up to 81%.	Nitroglycerin	158-161	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	65-81
1352550-6	1992	In the same cell type, a 24-hr pretreatment with the inducer of cytochrome P-450 3-methylcholanthrene (10 microM) augmented cyclic GMP stimulation by GTN or isoidide dinitrate by up to 102%.	Nitroglycerin	150-153	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	64-80
1377922-4	1992	Substance P (10(-9) to 10(-6) mol/l) induced relaxation with a maximum response (mean (SEM)) 23.0 (6.6)% of the total relaxation induced by glyceryl trinitrate 1 microgram/ml and a 50% maximal effective concentration of 6.8 x 10(-9) mol/l.	Nitroglycerin	140-159	tachykinin precursor 1	Homo sapiens	0-11
1371193-4	1992	NG-substituted L-arginine analogs inhibited the release of both insulin and NO.	Nitroglycerin	0-2	insulin	Homo sapiens	64-78
1359526-5	1992	In the presence of GTP and GTP gamma S, nitroglycerin, but not sodium nitrite, was able to increase lymphocyte cyclic GMP.	Nitroglycerin	40-53	5'-nucleotidase, cytosolic II	Homo sapiens	118-121
1359526-6	1992	Cysteine (1 mM) enhanced cyclic GMP formation induced by sodium nitroprusside and nitroglycerin.	Nitroglycerin	82-95	5'-nucleotidase, cytosolic II	Homo sapiens	32-35
1349646-0	1992	Hepatic cytochrome P-450-mediated activation of rat aortic guanylyl cyclase by glyceryl trinitrate.	Nitroglycerin	79-98	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	8-24
1384972-7	1992	Glyceryl trinitrate and sodium nitroprusside elicited significant further increases in cyclic GMP in native vein and internal mammary artery.	Nitroglycerin	0-19	5'-nucleotidase, cytosolic II	Homo sapiens	94-97
1733199-6	1992	Nitric oxide generated by addition of glyceryl trinitrate (10(-6) mol/L) attenuated the vasoconstrictor effects of U46619 (p less than 0.026) or endothelin-1 (p less than 0.01).	Nitroglycerin	38-57	endothelin 1	Homo sapiens	145-157
1540213-8	1992	Indocyanine green, a non-substrate inhibitor of glutathione S-transferase, inhibited GTN metabolism by smooth muscle cells.	Nitroglycerin	85-88	glutathione S-transferase kappa 1	Homo sapiens	48-73
1540213-10	1992	Pretreatment with phorone, a glutathione S-transferase substrate, depleted cellular glutathione and decreased nitrite production from GTN.	Nitroglycerin	134-137	glutathione S-transferase kappa 1	Homo sapiens	29-54
1540213-13	1992	This study shows that glutathione S-transferase and glutathione are involved in GTN metabolism by cultured smooth muscle cells.	Nitroglycerin	80-83	glutathione S-transferase kappa 1	Homo sapiens	22-47
1553339-3	1992	In the first set of experiments, GTN was incubated with the 9000g supernatant of fresh, homogenized tissue in the presence and absence of glutathione (GSH), a cofactor for glutathione-S-transferase.	Nitroglycerin	33-36	hematopoietic prostaglandin D synthase	Mus musculus	172-197
1725563-3	1991	Thrombin or collagen-induced aggregation of human washed platelets was inhibited in a concentration-dependent fashion by a 3 min incubation with GTN (40-200 microM).	Nitroglycerin	145-148	coagulation factor II, thrombin	Homo sapiens	0-8
1577025-0	1992	Transdermal nitroglycerin efficacy in patients with chronic stable angina pectoris as related to sympathetic and renin-angiotensin-aldosterone activity.	Nitroglycerin	12-25	renin	Homo sapiens	113-118
1577025-1	1992	The aim of this study was to evaluate the acute effects of transdermal nitroglycerin on the sympathetic and renin-angiotensin-aldosterone systems activity, in a group of patients with stable exercise induced angina pectoris.	Nitroglycerin	71-84	renin	Homo sapiens	108-113
1577025-8	1992	Plasma epinephrine and aldosterone concentrations and plasma renin activity were also increased after nitroglycerin administration.	Nitroglycerin	102-115	renin	Homo sapiens	61-66
1436316-2	1992	PAI activity rose within 1 h of the injection of nephrotoxic globulin (NTG), peaked at 2 h and returned to the normal range within 24 h. PAI activity was dependent on the dose of NTG and increased significantly during passage through the kidney.	Nitroglycerin	71-74	serpin family E member 1	Rattus norvegicus	0-3
1436316-2	1992	PAI activity rose within 1 h of the injection of nephrotoxic globulin (NTG), peaked at 2 h and returned to the normal range within 24 h. PAI activity was dependent on the dose of NTG and increased significantly during passage through the kidney.	Nitroglycerin	71-74	serpin family E member 1	Rattus norvegicus	137-140
1436316-2	1992	PAI activity rose within 1 h of the injection of nephrotoxic globulin (NTG), peaked at 2 h and returned to the normal range within 24 h. PAI activity was dependent on the dose of NTG and increased significantly during passage through the kidney.	Nitroglycerin	179-182	serpin family E member 1	Rattus norvegicus	0-3
1436316-2	1992	PAI activity rose within 1 h of the injection of nephrotoxic globulin (NTG), peaked at 2 h and returned to the normal range within 24 h. PAI activity was dependent on the dose of NTG and increased significantly during passage through the kidney.	Nitroglycerin	179-182	serpin family E member 1	Rattus norvegicus	137-140
1436316-5	1992	The injection of TNF to rats with NTG synergistically accelerated both the increase in PAI activity and the prevalence of fibrin deposits.	Nitroglycerin	34-37	tumor necrosis factor-like	Rattus norvegicus	17-20
1436316-5	1992	The injection of TNF to rats with NTG synergistically accelerated both the increase in PAI activity and the prevalence of fibrin deposits.	Nitroglycerin	34-37	serpin family E member 1	Rattus norvegicus	87-90
1684947-3	1991	Complications caused by vasopressin treatment can be avoided by concomitant application of nitroglycerin or by alternative treatment with somatostatin.	Nitroglycerin	91-104	arginine vasopressin	Homo sapiens	24-35
1809623-5	1991	Our results showed that NTG caused a significant reduction of right atrial pressure (RAP, 4 +/- 3.5 vs -1 +/- 4 mmHg, p less than 0.001), systolic pulmonary artery pressure (36 +/- 8 vs 21 +/- 11 mmHg, p less than 0.001) and PCWP (16 +/- 5 vs 7 +/- 3 mmHg, p less than 0.001).	Nitroglycerin	24-27	LDL receptor related protein associated protein 1	Homo sapiens	85-88
1813669-3	1991	Nitroglycerin, a vasorelaxant, completely reverses the ET-induced phosphorylation of MLC, but not that of caldesmon.	Nitroglycerin	0-13	endothelin 1	Homo sapiens	55-57
1813669-3	1991	Nitroglycerin, a vasorelaxant, completely reverses the ET-induced phosphorylation of MLC, but not that of caldesmon.	Nitroglycerin	0-13	modulator of VRAC current 1	Homo sapiens	85-88
1815874-7	1991	Sublingual administration of Nitrostat and intramuscular injection of Vit K3 could reduce SO PP markedly, SO BP didn"t change statistically.	Nitroglycerin	29-38	sine oculis binding protein homolog	Homo sapiens	106-111
1682478-2	1991	In endothelium-denuded rat aortic rings, the sustained contractile effects produced by endothelin-1 (ET-1; 3.2 nM) were concentration-dependently overcome by nicorandil, aprikalim (RP 52891), a specific K+ channel opener, and nitroglycerin, a stimulant of guanylate cyclase (EC50: 2.55 +/- 0.06, 0.37 +/- 0.05 and 0.3 +/- 0.008 microM respectively, n = 13-16/group).	Nitroglycerin	226-239	endothelin 1	Rattus norvegicus	87-99
1682478-2	1991	In endothelium-denuded rat aortic rings, the sustained contractile effects produced by endothelin-1 (ET-1; 3.2 nM) were concentration-dependently overcome by nicorandil, aprikalim (RP 52891), a specific K+ channel opener, and nitroglycerin, a stimulant of guanylate cyclase (EC50: 2.55 +/- 0.06, 0.37 +/- 0.05 and 0.3 +/- 0.008 microM respectively, n = 13-16/group).	Nitroglycerin	226-239	endothelin 1	Rattus norvegicus	101-105
1909702-3	1991	s-IL-2R levels were significantly higher in all patients with hyperthyroidism (mean +/- SD, 3276 +/- 1273 U/mL for GD, 4183 +/- 1832 for TNG, and 1671 +/- 648 for TA) compared to normal control values (P less than 0.001 for GD and TNG and P less than 0.01 for TA), while in the euthyroid state they were within the normal range (535 +/- 240 U/mL).	Nitroglycerin	137-140	interleukin 2 receptor subunit alpha	Homo sapiens	2-7
1909702-3	1991	s-IL-2R levels were significantly higher in all patients with hyperthyroidism (mean +/- SD, 3276 +/- 1273 U/mL for GD, 4183 +/- 1832 for TNG, and 1671 +/- 648 for TA) compared to normal control values (P less than 0.001 for GD and TNG and P less than 0.01 for TA), while in the euthyroid state they were within the normal range (535 +/- 240 U/mL).	Nitroglycerin	231-234	interleukin 2 receptor subunit alpha	Homo sapiens	2-7
1905490-2	1991	Stress-strain relationships values calculated at control and during bolus administration of angiotensin and nitroglycerin enabled quantification of angiotensin and nitroglycerin enabled quantification of elastic moduli of elastin (EE = 4.868 +/- 1.753 x 10(6) dyn/cm2; means +/- SD) and collagen (EC = 1,306 +/- 637 x 10(6) dyn/cm2) according to a biphasic model of elastin and collagen parallel arrangement.	Nitroglycerin	108-121	elastin	Canis lupus familiaris	222-229
1786509-9	1991	GTN elicited significant hypotension and increases in renal blood flow and vascular conductance, indicating that activation of the renin-angiotension system opposed the dilator effects of GTN in this vascular bed.	Nitroglycerin	0-3	renin	Rattus norvegicus	131-136
1786509-9	1991	GTN elicited significant hypotension and increases in renal blood flow and vascular conductance, indicating that activation of the renin-angiotension system opposed the dilator effects of GTN in this vascular bed.	Nitroglycerin	188-191	renin	Rattus norvegicus	131-136
1714727-12	1991	In summary, NO synthesis by cytokine-activated MBE is THB-dependent, calmodulin-independent and inhibited by NG-substituted arginine analogs with a rank-order profile distinct from that for untreated endothelial cells but identical to that for cytokine-activated macrophages.	Nitroglycerin	109-111	calmodulin 2	Mus musculus	69-79
1909561-4	1991	In coronary arteries preincubated with 0.44 mM GTN or SIN-1 to study tolerance development, there was a significant loss of efficacy to the relaxant effect of GTN, whereas the effect SIN-1 was essentially maintained.	Nitroglycerin	47-50	target of rapamycin complex 2 subunit MAPKAP1	Ovis aries	183-188
1909561-4	1991	In coronary arteries preincubated with 0.44 mM GTN or SIN-1 to study tolerance development, there was a significant loss of efficacy to the relaxant effect of GTN, whereas the effect SIN-1 was essentially maintained.	Nitroglycerin	159-162	target of rapamycin complex 2 subunit MAPKAP1	Ovis aries	54-59
1905490-2	1991	Stress-strain relationships values calculated at control and during bolus administration of angiotensin and nitroglycerin enabled quantification of angiotensin and nitroglycerin enabled quantification of elastic moduli of elastin (EE = 4.868 +/- 1.753 x 10(6) dyn/cm2; means +/- SD) and collagen (EC = 1,306 +/- 637 x 10(6) dyn/cm2) according to a biphasic model of elastin and collagen parallel arrangement.	Nitroglycerin	164-177	elastin	Canis lupus familiaris	222-229
1769029-6	1991	Hemodynamic parameters were significantly changed after the first nitroglycerin patch application: particularly, mean systemic arterial (MAP), right atrial (RAP) and pulmonary wedge pressures (PWP) declined from 96 +/- 10, 8.9 +/- 1.8 and 20.1 +/- 5 to 81 +/- 6, 4.7 +/- 1.5 and 12.2 +/- 3 mmHg (-15.6, -47.2 and -59.3%, respectively); systemic vascular resistance (SVR) and heart rate (HR) were reduced from 1645 +/- 121 to 1288 +/- 89 dyne.s.cm-5 and from 85 +/- 7 to 81 +/- 7 b/min; lastly, cardiac index (CI), stroke volume (SVI) and stroke work index (SWI) increased from 2.3 +/- 0.3, 28.2 +/- 5 and 28.7 +/- 9 to 2.7 +/- 0.3 l/min/m2, 33.3 +/- 5 ml/min/m2 and 31.5 +/- 8 g.m/m2 (+17.4, 18.1 and 9.7%).	Nitroglycerin	66-79	LDL receptor related protein associated protein 1	Homo sapiens	157-160
1901528-2	1991	In an attempt to prevent nitrate tolerance, this study evaluated the interaction of nitroglycerin with angiotensin converting enzyme (ACE) inhibitors with and without a sulfhydryl group.	Nitroglycerin	84-97	angiotensin I converting enzyme	Homo sapiens	134-137
1903680-2	1991	Experiments were designed to examine the effect of hirudin (which inactivates thrombin) and the nitrovasodilators nitroglycerin and 3-morpholinosydnonimine on the spontaneous and thrombin-stimulated release of endothelin in intact blood vessels.	Nitroglycerin	114-127	coagulation factor II, thrombin	Homo sapiens	179-187
1903680-7	1991	The inhibitory effects of both 3-morpholinosydnonimine and nitroglycerin on the thrombin-stimulated release of endothelin were abolished in the presence of an inhibitor of soluble guanylate cyclase, methylene blue (10(-5) M).	Nitroglycerin	59-72	coagulation factor II, thrombin	Homo sapiens	80-88
1651871-3	1991	The antagonism was reversible and specific for BK since responses to glyceryl trinitrate were not affected.	Nitroglycerin	69-88	kininogen 1	Homo sapiens	47-49
1906734-6	1991	Dipyridamole, a phosphodiesterase (PDe) inhibitor, significantly potentiated the responses to SIN1 on control rings (EC50 = 57.1 +/- 1.8 nM), and on NTG-tolerant rings it reversed the responsiveness to SIN1 (EC50 = 88.9 +/- 9.2 nM), which suggests that nitrate tolerance may be partially due to an increase in PDe activity.	Nitroglycerin	149-152	MAPK associated protein 1	Homo sapiens	202-206
1906734-3	1991	Vessels precontracted by serotonin (0.25 microM) and made tolerant to NTG exhibited a slight but significant shift (p less than 0.01) to the right of the dose-response curve to SIN1 (EC50 increased from 1.12 +/- 0.21 microM to 2.74 +/- 0.32 microM).	Nitroglycerin	70-73	MAPK associated protein 1	Homo sapiens	177-181
1906734-8	1991	Nevertheless, after induction of in vitro NTG tolerance, the attenuation of responses to SIN1 is much less pronounced that the alteration of NTG relaxations.	Nitroglycerin	42-45	MAPK associated protein 1	Homo sapiens	89-93
1909212-0	1991	Pathological basis of failure of concurrent glyceryl trinitrate therapy to improve efficacy of tissue type plasminogen activator in coronary thrombosis.	Nitroglycerin	44-63	tissue-type plasminogen activator	Canis lupus familiaris	95-128
1909212-13	1991	Whole blood platelet aggregation decreased significantly with t-PA alone, but less so with t-PA + GTN [magnitude of platelet aggregation 0.23(0.57) and 5.67(6.23) ohms, respectively, p less than 0.02], suggesting lower plasma concentrations of t-PA when given with glyceryl trinitrate.	Nitroglycerin	265-284	tissue-type plasminogen activator	Canis lupus familiaris	91-95
1909212-14	1991	Glyceryl trinitrate given after thrombolysis induced by t-PA failed to sustain reperfusion.	Nitroglycerin	0-19	tissue-type plasminogen activator	Canis lupus familiaris	56-60
1909212-18	1991	The potentially "detrimental" effects of glyceryl trinitrate may be due to increase in hepatic blood flow and subsequent enhanced catabolism of t-PA.	Nitroglycerin	41-60	tissue-type plasminogen activator	Canis lupus familiaris	144-148
1909212-1	1991	STUDY OBJECTIVE: The aim was to examine the effect of glyceryl trinitrate, a potent coronary vasodilator, on the thrombolytic effects of tissue type plasminogen inhibitor (t-PA) in dogs with coronary thrombosis.	Nitroglycerin	54-73	tissue-type plasminogen activator	Canis lupus familiaris	144-170
1909212-1	1991	STUDY OBJECTIVE: The aim was to examine the effect of glyceryl trinitrate, a potent coronary vasodilator, on the thrombolytic effects of tissue type plasminogen inhibitor (t-PA) in dogs with coronary thrombosis.	Nitroglycerin	54-73	tissue-type plasminogen activator	Canis lupus familiaris	172-176
1909212-13	1991	Whole blood platelet aggregation decreased significantly with t-PA alone, but less so with t-PA + GTN [magnitude of platelet aggregation 0.23(0.57) and 5.67(6.23) ohms, respectively, p less than 0.02], suggesting lower plasma concentrations of t-PA when given with glyceryl trinitrate.	Nitroglycerin	265-284	tissue-type plasminogen activator	Canis lupus familiaris	91-95
1848694-4	1991	Moreover, the potency of glyceryl trinitrate (n3Gro) and sodium nitroprusside (SNP) as relaxing agents and the ability of SNP to induce increases in cGMP in aortic rings were significantly enhanced in those rings denuded of endothelium or treated with the inhibitors.	Nitroglycerin	25-44	C-X-C motif chemokine ligand 1	Rattus norvegicus	48-51
2175599-1	1990	Atrial natriuretic peptide (ANP) and the nitrovasodilator drugs nitroglycerine and nitroprusside were shown here to decrease both basal and thrombin stimulated production of endothelin-1 (ET-1) from cultured human endothelial cells as measured by radioimmunoassay.	Nitroglycerin	64-78	endothelin 1	Homo sapiens	188-192
1711602-1	1991	The angiotensin-converting enzyme (ACE) inhibitor captopril has been shown to reverse vascular tolerance to nitroglycerin (NTG).	Nitroglycerin	108-121	angiotensin I converting enzyme	Rattus norvegicus	4-33
1711602-1	1991	The angiotensin-converting enzyme (ACE) inhibitor captopril has been shown to reverse vascular tolerance to nitroglycerin (NTG).	Nitroglycerin	108-121	angiotensin I converting enzyme	Rattus norvegicus	35-38
1711602-1	1991	The angiotensin-converting enzyme (ACE) inhibitor captopril has been shown to reverse vascular tolerance to nitroglycerin (NTG).	Nitroglycerin	123-126	angiotensin I converting enzyme	Rattus norvegicus	4-33
1711602-1	1991	The angiotensin-converting enzyme (ACE) inhibitor captopril has been shown to reverse vascular tolerance to nitroglycerin (NTG).	Nitroglycerin	123-126	angiotensin I converting enzyme	Rattus norvegicus	35-38
1992693-5	1991	In fact, in umbilical vessels collected from normal parturients, bradykinin at a dose of 20 pmol produces a release of endothelial-derived relaxing factor equivalent to a relaxation induced by 59.9 +/- 11.0 and 30.8 +/- 11.4 pmol of glyceryl trinitrate for the artery and vein, respectively.	Nitroglycerin	233-252	kininogen 1	Homo sapiens	65-75
1992693-6	1991	The same dose of bradykinin in umbilical vessels, collected from pregnancy-induced hypertensive parturients, produces a release equivalent to 6.6 +/- 2.2 and 5.7 +/- 3.5 pmol of glyceryl trinitrate equivalent for the artery and vein, respectively.	Nitroglycerin	178-197	kininogen 1	Homo sapiens	17-27
1899681-0	1991	Concurrent nitroglycerin administration decreases thrombolytic potential of tissue-type plasminogen activator.	Nitroglycerin	11-24	tissue-type plasminogen activator	Canis lupus familiaris	76-109
2175599-1	1990	Atrial natriuretic peptide (ANP) and the nitrovasodilator drugs nitroglycerine and nitroprusside were shown here to decrease both basal and thrombin stimulated production of endothelin-1 (ET-1) from cultured human endothelial cells as measured by radioimmunoassay.	Nitroglycerin	64-78	endothelin 1	Homo sapiens	174-186
2175599-4	1990	Part of the vasodilatory action of ANP, nitroprusside and nitroglycerine may be due to suppression of endothelial ET-1 production.	Nitroglycerin	58-72	endothelin 1	Homo sapiens	114-118
1705189-8	1990	The experiment was repeated in the same patients when the clinical status worsened and the levels of vWF:Ag were noted to rise: the endothelium dependent vasodilatory response to SP was still deficient as before and a decrease in vasodilatory response to GT was noted.	Nitroglycerin	255-257	von Willebrand factor	Homo sapiens	101-104
2128204-2	1990	In the current study, we assessed the involvement of cytochrome P-450 in the denitration of glyceryl trinitrate and the enantiomers of isoidide dinitrate.	Nitroglycerin	92-111	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	53-69
1704357-6	1990	The maximum response of substance P was equivalent to 89 +/- 8.5% of the maximum effect induced by 1 microgram/ml glyceryl trinitrate.	Nitroglycerin	114-133	tachykinin precursor 1	Homo sapiens	24-35
1704357-8	1990	L-NG-monomethyl-arginine (10(-4) M), a specific inhibitor of formation of nitric oxide from L-arginine, antagonised the relaxations induced by substance P, decreasing the maximum response of substance P to 34 +/- 10.5% of the response to glyceryl trinitrate.	Nitroglycerin	238-257	tachykinin precursor 1	Homo sapiens	143-154
1704357-8	1990	L-NG-monomethyl-arginine (10(-4) M), a specific inhibitor of formation of nitric oxide from L-arginine, antagonised the relaxations induced by substance P, decreasing the maximum response of substance P to 34 +/- 10.5% of the response to glyceryl trinitrate.	Nitroglycerin	238-257	tachykinin precursor 1	Homo sapiens	191-202
2127552-7	1990	However, comparing the differences between the response to glyceryl trinitrate and that to any other agonist in the absence and presence of L-NAME showed that there were relative attenuations of the hypotensive responses to bradykinin and endothelin-1, but not to acetylcholine, in the presence of L-NAME.	Nitroglycerin	59-78	endothelin 1	Rattus norvegicus	239-251
1965331-0	1990	Inhibitors of cytochrome P-450 reduce cyclic GMP stimulation by glyceryl trinitrate in LLC-PK1 kidney epithelial cells.	Nitroglycerin	64-83	cytochrome P450 family 2 subfamily D member 6	Sus scrofa	14-30
1965331-1	1990	The inhibitor of cytochrome P-450 cimetidine was used to assess the role of cytochrome P-450-dependent enzymes for cyclic GMP stimulation by glyceryl trinitrate in a kidney epithelial cell line (LLC-PK1).	Nitroglycerin	141-160	cytochrome P450 family 2 subfamily D member 6	Sus scrofa	76-92
1965331-4	1990	Glyceryl trinitrate-induced cyclic GMP stimulation remained unaltered by ranitidine (0.1 mmol/l), which has a much lower affinity for the cytochrome P-450 enzyme system.	Nitroglycerin	0-19	cytochrome P450 family 2 subfamily D member 6	Sus scrofa	138-154
1965331-5	1990	Another inhibitor of cytochrome P-450, miconazole (0.1 mmol/l), also attenuated glyceryl trinitrate-induced cyclic GMP stimulation.	Nitroglycerin	80-99	cytochrome P450 family 2 subfamily D member 6	Sus scrofa	21-37
1965331-7	1990	These results suggest that in intact cells, glyceryl trinitrate-induced cyclic GMP stimulation is dependent on cytochrome P-450 enzymes which may be relevant for nitric oxide formation from organic nitrates.	Nitroglycerin	44-63	cytochrome P450 family 2 subfamily D member 6	Sus scrofa	111-127
2127557-1	1990	In order to estimate the pharmaceutical usefulness of 1,3-glyceryl dinitrate (1,3-GDN), an active metabolite of nitroglycerin, a trial transdermal delivery system designed to sustain a suitable plasma concentration of 1,3-GDN was produced using a porous membrane (Hipore 2100 or 4500) and it was a gel base or ethylhexyl acrylate-based adhesive (adhesive) and it was applied to rats.	Nitroglycerin	112-125	serpin family E member 2	Rattus norvegicus	82-85
2121114-2	1990	The purpose of this randomized crossover study was to determine whether nitroglycerin interacts with heparin in terms of its anticoagulative properties as determined by activated partial thromboplastin time and thrombin time.	Nitroglycerin	72-85	coagulation factor II, thrombin	Homo sapiens	211-219
2121325-3	1990	It has been proposed that the sulfhydryl group-containing angiotensin converting enzyme (ACE) inhibitor captopril may be useful in preventing tolerance to nitroglycerin by repleting sulfhydryl groups and by decreasing reflex neurohumoral activation.	Nitroglycerin	155-168	angiotensin I converting enzyme	Homo sapiens	89-92
2119139-5	1990	Nitroglycerin decreased the area under the aggregation curve induced by ADP from 43 +/- 3.6 to 30 +/- 6.3 cm2 (p = 0.007) and by thrombin from 8.9 +/- 1.7 to 4.1 +/- 0.9 cm2 (p = 0.003).	Nitroglycerin	0-13	coagulation factor II, thrombin	Homo sapiens	129-137
2112878-0	1990	Intravenous nitroglycerin-induced heparin resistance: a qualitative antithrombin III abnormality.	Nitroglycerin	12-25	serpin family C member 1	Homo sapiens	68-84
2112878-10	1990	A nitroglycerin-induced qualitative ATIII abnormality may be the underlying mechanism.	Nitroglycerin	2-15	serpin family C member 1	Homo sapiens	36-41
2112998-0	1990	Nitroglycerin-resistant coronary spasm treated with intracoronary linsidomine chlorhydrate (SIN-1).	Nitroglycerin	0-13	MAPK associated protein 1	Homo sapiens	92-97
2112348-6	1990	The increase in mean Rp after a single dose of NTG (250 micrograms) was sustained for at least 20 min and transiently reversed by vasopressin (0.2 units, p less than 0.05) but not by isoproterenol (100 micrograms).	Nitroglycerin	47-50	arginine vasopressin	Homo sapiens	130-141
2114437-10	1990	The addition of nitroglycerin improved the detrimental systemic haemodynamic effects produced by triglycyllysine vasopressin without further reducing the hepatic venous pressure gradient.	Nitroglycerin	16-29	arginine vasopressin	Homo sapiens	113-124
2178911-7	1990	The combination of vasopressin with either sodium nitroprusside or nitroglycerin (glyceryl trinitrate) has resulted in a further decline of portal pressure, along with amelioration of most of the adverse haemodynamic effects of vasopressin.	Nitroglycerin	67-80	arginine vasopressin	Homo sapiens	228-239
1980046-5	1990	The addition of nitroglycerin to a vasopressin regime has recently been shown to reduce such complications and to improve overall efficacy.	Nitroglycerin	16-29	arginine vasopressin	Homo sapiens	35-46
1972575-6	1990	NPY (10(-6) mol.l-1) also produced a rightward shift in the concentration-response curves for the vasodilators forskolin and glyceryl trinitrate, but did not reduce the maximum relaxations to these compounds.	Nitroglycerin	125-144	pro-neuropeptide Y	Cavia porcellus	0-3
2333409-3	1990	Coincident with the development of irreversible injury, myocytes evidenced a rapid, net production of PAF which was sustained for some 3-6 h and reached, maximally, low-ng levels within approximately 0.5 h of injury.	Nitroglycerin	169-171	PCNA clamp associated factor	Rattus norvegicus	102-105
2155798-1	1990	The effects of nitroglycerin tolerance on relaxation and cyclic GMP accumulation by nitroglycerin, nitric oxide and S-nitroso-N-acetylpenicillamine were examined in isolated rate aortic rings.	Nitroglycerin	84-97	5'-nucleotidase, cytosolic II	Homo sapiens	64-67
2155798-2	1990	Cyclic GMP accumulation by nitroglycerin, S-nitroso-N-acetylpenicillamine and nitric oxide was diminished in nitroglycerin-tolerant aorta.	Nitroglycerin	27-40	5'-nucleotidase, cytosolic II	Homo sapiens	7-10
2155798-2	1990	Cyclic GMP accumulation by nitroglycerin, S-nitroso-N-acetylpenicillamine and nitric oxide was diminished in nitroglycerin-tolerant aorta.	Nitroglycerin	109-122	5'-nucleotidase, cytosolic II	Homo sapiens	7-10
2178911-7	1990	The combination of vasopressin with either sodium nitroprusside or nitroglycerin (glyceryl trinitrate) has resulted in a further decline of portal pressure, along with amelioration of most of the adverse haemodynamic effects of vasopressin.	Nitroglycerin	82-101	arginine vasopressin	Homo sapiens	19-30
2178911-7	1990	The combination of vasopressin with either sodium nitroprusside or nitroglycerin (glyceryl trinitrate) has resulted in a further decline of portal pressure, along with amelioration of most of the adverse haemodynamic effects of vasopressin.	Nitroglycerin	82-101	arginine vasopressin	Homo sapiens	228-239
34816764-9	2022	The Kir6.1 smooth muscle knockout mouse was protected from both GTN and levcromakalim induced hypersensitivity, and their arteries had impaired dilatory response to the latter.	Nitroglycerin	64-67	potassium inwardly-rectifying channel, subfamily J, member 8	Mus musculus	4-10
2087623-15	1990	The administration of Nitroglycerin Spofa was followed by a significant decrease in RAP, PAP, AOP, RVEDP as well as in CO. No significant changes in blood gases were observed.	Nitroglycerin	22-35	LDL receptor related protein associated protein 1	Homo sapiens	84-87
33774949-6	2021	OCT procedure was performed following intracoronary injection of 100-150 ug of nitroglycerine.	Nitroglycerin	79-93	plexin A2	Homo sapiens	0-3
34926239-12	2021	Targeting DPP4/DHCR24 signaling might help to sensitize MTX-resistant GTN to MTX treatment.	Nitroglycerin	70-73	dipeptidyl peptidase 4	Homo sapiens	10-14
34893074-0	2021	MicroRNA-155-5p promotes neuroinflammation and central sensitization via inhibiting SIRT1 in a nitroglycerin-induced chronic migraine mouse model.	Nitroglycerin	95-108	sirtuin 1	Mus musculus	84-89
34893074-11	2021	RESULTS: After the NTG-induced mouse model of CM was established, the expression of miR-155-5p was increased.	Nitroglycerin	19-22	microRNA 155	Mus musculus	84-91
34872933-5	2021	Consumption of atorvastatin, aspirin, and glyceryl trinitrate was found to be higher in the CAD groups compared with the control group.	Nitroglycerin	42-61	aconitate decarboxylase 1	Homo sapiens	92-95
34926239-12	2021	Targeting DPP4/DHCR24 signaling might help to sensitize MTX-resistant GTN to MTX treatment.	Nitroglycerin	70-73	24-dehydrocholesterol reductase	Homo sapiens	15-21
34926239-5	2021	Manipulation of DPP4 expression remarkably affected the level of cellular cholesterol in GTN cells.	Nitroglycerin	89-92	dipeptidyl peptidase 4	Homo sapiens	16-20
34363208-5	2021	KEY RESULTS: NTG induced sensory hypersensitivity of C57BL/6 wild-type (P2ry12+/+ ) mice, accompanied by an increase in c-fos and CGRP expression in the upper cervical spinal cord (C1-C2) and trigeminal nucleus caudalis (TNC).	Nitroglycerin	13-16	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	72-78
34926239-7	2021	Manipulation of DHCR24 expression affected cellular cholesterol level, reactive oxygen species (ROS) accumulation, and chemosensitivity to MTX in GTN cell models.	Nitroglycerin	146-149	24-dehydrocholesterol reductase	Homo sapiens	16-22
34926239-8	2021	In addition, over-expression of DHCR24 could markedly restore cellular cholesterol level and rescue cell survival in DPP4-depleted MTX-resistant GTN cells.	Nitroglycerin	145-148	24-dehydrocholesterol reductase	Homo sapiens	32-38
34926239-8	2021	In addition, over-expression of DHCR24 could markedly restore cellular cholesterol level and rescue cell survival in DPP4-depleted MTX-resistant GTN cells.	Nitroglycerin	145-148	dipeptidyl peptidase 4	Homo sapiens	117-121
34926239-9	2021	Highly correlated expression of DPP4 and DHCR24 was observed in clinical GTN specimens.	Nitroglycerin	73-76	dipeptidyl peptidase 4	Homo sapiens	32-36
34926239-9	2021	Highly correlated expression of DPP4 and DHCR24 was observed in clinical GTN specimens.	Nitroglycerin	73-76	24-dehydrocholesterol reductase	Homo sapiens	41-47
34363208-5	2021	KEY RESULTS: NTG induced sensory hypersensitivity of C57BL/6 wild-type (P2ry12+/+ ) mice, accompanied by an increase in c-fos and CGRP expression in the upper cervical spinal cord (C1-C2) and trigeminal nucleus caudalis (TNC).	Nitroglycerin	13-16	FBJ osteosarcoma oncogene	Mus musculus	120-125
34363208-5	2021	KEY RESULTS: NTG induced sensory hypersensitivity of C57BL/6 wild-type (P2ry12+/+ ) mice, accompanied by an increase in c-fos and CGRP expression in the upper cervical spinal cord (C1-C2) and trigeminal nucleus caudalis (TNC).	Nitroglycerin	13-16	calcitonin/calcitonin-related polypeptide, alpha	Mus musculus	130-134
34363208-10	2021	Platelet depletion by anti-mouse CD41 antibody and clopidogrel attenuated NTG-induced thermal hypersensitivity and head grooming time in mice.	Nitroglycerin	74-77	integrin alpha 2b	Mus musculus	33-37
34880623-8	2021	Becaplermin, a medication that targets MMP-9, glyceryl trinitrate, which inhibits the bacterial quorum sensing system, probiotic therapy, and nano technological solutions are just a few of the novel pharmaceuticals being developed for diabetic foot ulcers treatment.	Nitroglycerin	46-65	platelet derived growth factor subunit B	Homo sapiens	0-11
34407650-0	2021	CGRP-dependent signalling pathways involved in mouse models of GTN- cilostazol- and levcromakalim-induced migraine.	Nitroglycerin	63-66	calcitonin/calcitonin-related polypeptide, alpha	Mus musculus	0-4
34407650-7	2021	RESULTS: Glyceryl trinitrate-induced hypersensitivity was dependent on both prostaglandins and transient receptor potential cation channel, subfamily A, member 1, whereas cilostazol- and levcromakalim-induced hypersensitivity were independent of both.	Nitroglycerin	9-28	transient receptor potential cation channel, subfamily A, member 1	Mus musculus	95-161
34560171-8	2021	NTG-related anxiety and social conflicts were attenuated by orexin-A (25, 50 pM).	Nitroglycerin	0-3	hypocretin neuropeptide precursor	Rattus norvegicus	60-68
34560171-10	2021	The orexin-A-mediated suppression of NTG-induced anxiety and social conflicts were prevented by either SB334867 (20 nM) or AM251 (2 microg).	Nitroglycerin	37-40	hypocretin neuropeptide precursor	Rattus norvegicus	4-12
34790097-5	2021	Second, we demonstrated that the small-molecule inhibitor ML204, a specific TRPC4 antagonist, significantly reduced episodic and chronic migraine-like behaviors in male and female mice after injection of nitroglycerin (NTG), a well-known migraine inducer in rodents and humans.	Nitroglycerin	204-217	transient receptor potential cation channel, subfamily C, member 4	Mus musculus	76-81
34803150-10	2022	GLIPR2 overexpression in normal concentration of glucose (NG)-induced SV40 MES13 cells partly simulated HG-induced effects.	Nitroglycerin	58-60	GLI pathogenesis-related 2	Mus musculus	0-6
34790097-5	2021	Second, we demonstrated that the small-molecule inhibitor ML204, a specific TRPC4 antagonist, significantly reduced episodic and chronic migraine-like behaviors in male and female mice after injection of nitroglycerin (NTG), a well-known migraine inducer in rodents and humans.	Nitroglycerin	219-222	transient receptor potential cation channel, subfamily C, member 4	Mus musculus	76-81
34790097-8	2021	Collectively, our findings identify TRPC4 in peripheral sensory neurons as a mediator of CGRP release and NTG-evoked migraine.	Nitroglycerin	106-109	transient receptor potential cation channel, subfamily C, member 4	Mus musculus	36-41
34373588-3	2021	A total of 1111 phosphosites on 713 proteins were significantly changed, with highly elevated Ribosomal S6 Kinase 2 (RSK2) phosphorylation (pS227) observed in MTX-resistant GTN cells.	Nitroglycerin	173-176	ribosomal protein S6 kinase A3	Homo sapiens	94-115
34373588-3	2021	A total of 1111 phosphosites on 713 proteins were significantly changed, with highly elevated Ribosomal S6 Kinase 2 (RSK2) phosphorylation (pS227) observed in MTX-resistant GTN cells.	Nitroglycerin	173-176	ribosomal protein S6 kinase A3	Homo sapiens	117-121
34373588-7	2021	Highly activated RSK2/SOX8 signaling was observed in MTX-resistant GTN specimens.	Nitroglycerin	67-70	ribosomal protein S6 kinase A3	Homo sapiens	17-21
34129219-9	2021	Notably, there was lower protein expression of DIO3 in pre-GTN cases (5-fold, p < 0.03).	Nitroglycerin	59-62	iodothyronine deiodinase 3	Homo sapiens	47-51
34373588-7	2021	Highly activated RSK2/SOX8 signaling was observed in MTX-resistant GTN specimens.	Nitroglycerin	67-70	SRY-box transcription factor 8	Homo sapiens	22-26
34373588-9	2021	Collectively, our findings suggested that RSK2 activation could promote MTX resistance via upregulating SOX8 and attenuating MTX-induced ROS in GTN cells, which may help to develop experimental therapeutics to treat MTX-resistant GTN.	Nitroglycerin	144-147	ribosomal protein S6 kinase A3	Homo sapiens	42-46
34373588-9	2021	Collectively, our findings suggested that RSK2 activation could promote MTX resistance via upregulating SOX8 and attenuating MTX-induced ROS in GTN cells, which may help to develop experimental therapeutics to treat MTX-resistant GTN.	Nitroglycerin	230-233	ribosomal protein S6 kinase A3	Homo sapiens	42-46
34370177-3	2021	However, the cellular and molecular effects of TRPM2 in the TG of migraine model (glyceryl trinitrate, GTN) on the induction of pain, OS, apoptosis, and inflammation remain elusive.	Nitroglycerin	82-101	transient receptor potential cation channel, subfamily M, member 2	Mus musculus	47-52
34370177-3	2021	However, the cellular and molecular effects of TRPM2 in the TG of migraine model (glyceryl trinitrate, GTN) on the induction of pain, OS, apoptosis, and inflammation remain elusive.	Nitroglycerin	103-106	transient receptor potential cation channel, subfamily M, member 2	Mus musculus	47-52
34370177-6	2021	The current data indicate that the maintaining activation of TRPM2 is not only important for the quenching OS, inflammation, and neurotoxicity in the TG neurons of mice with experimental migraine but also equally critical to the modulation of GTN-induced pain.	Nitroglycerin	243-246	transient receptor potential cation channel, subfamily M, member 2	Mus musculus	61-66
34456674-4	2021	CM models were established here by repeated intraperitoneal injection of nitroglycerin (NTG) every other day for 9 days to early growth response gene 1 (Egr1)-enhanced green fluorescent protein (EGFP) transgenic mice, which allowed monitoring of neuronal activities in the whole brain.	Nitroglycerin	73-86	early growth response 1	Mus musculus	123-151
34644194-5	2022	RESULTS: In specific pathogen-free mice, a decreased mechanical threshold in the hind paw, increased grooming time, increased c-Fos expression level and decreased calcitonin gene-related peptide expression level as well as increased tumor necrosis factor-alpha concentration in the trigeminal nucleus caudalis were observed after nitroglycerin administration compared with saline treatment.	Nitroglycerin	330-343	FBJ osteosarcoma oncogene	Mus musculus	126-131
34644194-5	2022	RESULTS: In specific pathogen-free mice, a decreased mechanical threshold in the hind paw, increased grooming time, increased c-Fos expression level and decreased calcitonin gene-related peptide expression level as well as increased tumor necrosis factor-alpha concentration in the trigeminal nucleus caudalis were observed after nitroglycerin administration compared with saline treatment.	Nitroglycerin	330-343	tumor necrosis factor	Mus musculus	233-260
34644194-6	2022	However, increased basal sensitivity and higher basal concentrations of TNF-alpha in the trigeminal nucleus caudalis were observed in germ-free and ABX mice, while no significant difference in hyperalgesia was observed between the nitroglycerin group and saline group in germ-free and ABX mice.	Nitroglycerin	231-244	tumor necrosis factor	Mus musculus	72-81
34469702-0	2021	Exogenous HSP70 attenuates nitroglycerin-induced migraine-like symptoms in mice.	Nitroglycerin	27-40	heat shock protein 1B	Mus musculus	10-15
34469702-2	2021	This study aimed to investigate the potential of exogenous HSP70 for treating migraine-like symptoms in a mouse model of nitroglycerin (NTG) induced migraine.	Nitroglycerin	121-134	heat shock protein 1B	Mus musculus	59-64
34469702-2	2021	This study aimed to investigate the potential of exogenous HSP70 for treating migraine-like symptoms in a mouse model of nitroglycerin (NTG) induced migraine.	Nitroglycerin	136-139	heat shock protein 1B	Mus musculus	59-64
34469702-4	2021	Migraine was induced in mice by NTG and HSP70 expression was examined in the trigeminal nucleus caudalis (TNC) tissue of mice treated with NTG and NTG together with exogenous HSP70.	Nitroglycerin	139-142	heat shock protein 1B	Mus musculus	40-45
34469702-4	2021	Migraine was induced in mice by NTG and HSP70 expression was examined in the trigeminal nucleus caudalis (TNC) tissue of mice treated with NTG and NTG together with exogenous HSP70.	Nitroglycerin	147-150	heat shock protein 1B	Mus musculus	40-45
34469702-8	2021	NTG administration significantly suppressed HSP70 expression in mouse TNC tissue which were reversed by exogenous HSP70.	Nitroglycerin	0-3	heat shock protein 1B	Mus musculus	44-49
34469702-8	2021	NTG administration significantly suppressed HSP70 expression in mouse TNC tissue which were reversed by exogenous HSP70.	Nitroglycerin	0-3	heat shock protein 1B	Mus musculus	114-119
34469702-9	2021	HSP70 alleviated NTG-induced mechanical hypersensitivity, light aversion and anxiety-like behavior.	Nitroglycerin	17-20	heat shock protein 1B	Mus musculus	0-5
34469702-10	2021	Finally, exogenous HSP70 suppressed NTG-induced oxidative stress and NF-kappaB signaling.	Nitroglycerin	36-39	heat shock protein 1B	Mus musculus	19-24
34108435-0	2021	Protein kinase C delta as a neuronal mechanism for headache in a chronic intermittent nitroglycerin model of migraine in mice.	Nitroglycerin	86-99	protein kinase C, delta	Mus musculus	0-22
34108435-5	2021	The peptide antagonist of calcitonin gene related peptide (CGRP) alpha-CGRP (8-37), but not topiramate nor sumatriptan, effectively blocked ongoing pain and elicited pain relief-induced CPP in NTG-treated mice.	Nitroglycerin	193-196	calcitonin/calcitonin-related polypeptide, alpha	Mus musculus	26-57
34108435-5	2021	The peptide antagonist of calcitonin gene related peptide (CGRP) alpha-CGRP (8-37), but not topiramate nor sumatriptan, effectively blocked ongoing pain and elicited pain relief-induced CPP in NTG-treated mice.	Nitroglycerin	193-196	calcitonin/calcitonin-related polypeptide, alpha	Mus musculus	59-63
34108435-6	2021	Prominent activation of PKCdelta was observed in chronic NTG-treated mice.	Nitroglycerin	57-60	protein kinase C, delta	Mus musculus	24-32
34722383-7	2021	Real-time PCRs were performed to evaluate the alterations in the regulation of ERG11 and CDR1 genes under nitroglycerin derivatives-treated and untreated conditions.	Nitroglycerin	106-119	cerebellar degeneration related antigen 1	Mus musculus	89-93
34722383-10	2021	The nitroglycerin derivatives were able to reduce the transcription level of CDR1 and ERG11 genes in all susceptible and resistant C. albicans isolates.	Nitroglycerin	4-17	cerebellar degeneration related antigen 1	Mus musculus	77-81
34456674-4	2021	CM models were established here by repeated intraperitoneal injection of nitroglycerin (NTG) every other day for 9 days to early growth response gene 1 (Egr1)-enhanced green fluorescent protein (EGFP) transgenic mice, which allowed monitoring of neuronal activities in the whole brain.	Nitroglycerin	73-86	early growth response 1	Mus musculus	153-157
34456674-6	2021	Elevation of Egr1 expression signals was detected in trigeminal nucleus caudalis (TNC), primary somatosensory cortex (SSp), lateral amygdala nucleus (LA), primary visual area (VISp), and temporal association areas (TEa) 2 h after the last injection of NTG by immunofluorescence and digital slice scanning technology.	Nitroglycerin	252-255	early growth response 1	Mus musculus	13-17
34456674-10	2021	Meanwhile, NTG-induced increase in Egr1 expression was completely reversed in TNC, SSp, and VISp and partially reduced in LA and TEa by topiramate at the same time point mentioned above.	Nitroglycerin	11-14	early growth response 1	Mus musculus	35-39
35144528-0	2022	Sphingosine-1 phosphate receptor 1 contributes to central sensitization in recurrent nitroglycerin-induced chronic migraine model.	Nitroglycerin	85-98	sphingosine-1-phosphate receptor 1	Mus musculus	0-34
34445170-0	2021	Nitric Oxide-Releasing Drug Glyceryl Trinitrate Targets JAK2/STAT3 Signaling, Migration and Invasion of Triple-Negative Breast Cancer Cells.	Nitroglycerin	28-47	signal transducer and activator of transcription 3	Homo sapiens	61-66
34445170-4	2021	In the present study we examined the impact of the NO-donor glyceryl trinitrate (GTN) on the activation of the JAK2/STAT3 signaling pathway and subsequent migration, invasion and metastasis ability of TNBC cells through in vitro and in vivo experiments.	Nitroglycerin	60-79	Janus kinase 2	Homo sapiens	111-115
34445170-4	2021	In the present study we examined the impact of the NO-donor glyceryl trinitrate (GTN) on the activation of the JAK2/STAT3 signaling pathway and subsequent migration, invasion and metastasis ability of TNBC cells through in vitro and in vivo experiments.	Nitroglycerin	60-79	signal transducer and activator of transcription 3	Homo sapiens	116-121
34445170-4	2021	In the present study we examined the impact of the NO-donor glyceryl trinitrate (GTN) on the activation of the JAK2/STAT3 signaling pathway and subsequent migration, invasion and metastasis ability of TNBC cells through in vitro and in vivo experiments.	Nitroglycerin	81-84	Janus kinase 2	Homo sapiens	111-115
34445170-4	2021	In the present study we examined the impact of the NO-donor glyceryl trinitrate (GTN) on the activation of the JAK2/STAT3 signaling pathway and subsequent migration, invasion and metastasis ability of TNBC cells through in vitro and in vivo experiments.	Nitroglycerin	81-84	signal transducer and activator of transcription 3	Homo sapiens	116-121
34445170-6	2021	We found an inhibitory effect of GTN on the activation of the JAK2/STAT3 signaling, migration and invasion of TNBC cells.	Nitroglycerin	33-36	Janus kinase 2	Homo sapiens	62-66
34445170-6	2021	We found an inhibitory effect of GTN on the activation of the JAK2/STAT3 signaling, migration and invasion of TNBC cells.	Nitroglycerin	33-36	signal transducer and activator of transcription 3	Homo sapiens	67-72
34445170-7	2021	We discovered that GTN inhibits the activation of JAK2, the upstream activator of STAT3, and mediates the S-nitrosylation of JAK2.	Nitroglycerin	19-22	Janus kinase 2	Homo sapiens	50-54
34445170-7	2021	We discovered that GTN inhibits the activation of JAK2, the upstream activator of STAT3, and mediates the S-nitrosylation of JAK2.	Nitroglycerin	19-22	signal transducer and activator of transcription 3	Homo sapiens	82-87
34445170-7	2021	We discovered that GTN inhibits the activation of JAK2, the upstream activator of STAT3, and mediates the S-nitrosylation of JAK2.	Nitroglycerin	19-22	Janus kinase 2	Homo sapiens	125-129
34319490-0	2021	Berberine Reverses Nitroglycerin Tolerance through Suppressing Protein Kinase C Alpha Activity in Vascular Smooth Muscle Cells.	Nitroglycerin	19-32	protein kinase C, alpha	Rattus norvegicus	63-85
34319490-6	2021	RESULTS: NTG tolerance induced by either prior exposure of rat aortas to NTG in vitro or pretreatment with an NTG patch in vivo was reversed by co-treatment with berberine, as well as the inhibitors of protein kinase C (PKC) and protein kinase C alpha (PKCalpha).	Nitroglycerin	9-12	protein kinase C, alpha	Rattus norvegicus	220-223
34319490-6	2021	RESULTS: NTG tolerance induced by either prior exposure of rat aortas to NTG in vitro or pretreatment with an NTG patch in vivo was reversed by co-treatment with berberine, as well as the inhibitors of protein kinase C (PKC) and protein kinase C alpha (PKCalpha).	Nitroglycerin	9-12	protein kinase C, alpha	Rattus norvegicus	229-251
34319490-6	2021	RESULTS: NTG tolerance induced by either prior exposure of rat aortas to NTG in vitro or pretreatment with an NTG patch in vivo was reversed by co-treatment with berberine, as well as the inhibitors of protein kinase C (PKC) and protein kinase C alpha (PKCalpha).	Nitroglycerin	9-12	protein kinase C, alpha	Rattus norvegicus	253-261
34319490-7	2021	The mechanistic study revealed that PKCalpha participated in the development of NTG tolerance as NTG increased the activity of PKCalpha with enriched PKCalpha membrane localization and elevated phosphorylation of PKCalpha in VSMCs, which was reversed by berberine or PKCalpha inhibitors.	Nitroglycerin	80-83	protein kinase C, alpha	Rattus norvegicus	36-44
34319490-7	2021	The mechanistic study revealed that PKCalpha participated in the development of NTG tolerance as NTG increased the activity of PKCalpha with enriched PKCalpha membrane localization and elevated phosphorylation of PKCalpha in VSMCs, which was reversed by berberine or PKCalpha inhibitors.	Nitroglycerin	80-83	protein kinase C, alpha	Rattus norvegicus	127-135
34319490-7	2021	The mechanistic study revealed that PKCalpha participated in the development of NTG tolerance as NTG increased the activity of PKCalpha with enriched PKCalpha membrane localization and elevated phosphorylation of PKCalpha in VSMCs, which was reversed by berberine or PKCalpha inhibitors.	Nitroglycerin	80-83	protein kinase C, alpha	Rattus norvegicus	150-158
34319490-7	2021	The mechanistic study revealed that PKCalpha participated in the development of NTG tolerance as NTG increased the activity of PKCalpha with enriched PKCalpha membrane localization and elevated phosphorylation of PKCalpha in VSMCs, which was reversed by berberine or PKCalpha inhibitors.	Nitroglycerin	80-83	protein kinase C, alpha	Rattus norvegicus	213-221
34319490-7	2021	The mechanistic study revealed that PKCalpha participated in the development of NTG tolerance as NTG increased the activity of PKCalpha with enriched PKCalpha membrane localization and elevated phosphorylation of PKCalpha in VSMCs, which was reversed by berberine or PKCalpha inhibitors.	Nitroglycerin	80-83	protein kinase C, alpha	Rattus norvegicus	267-275
34319490-7	2021	The mechanistic study revealed that PKCalpha participated in the development of NTG tolerance as NTG increased the activity of PKCalpha with enriched PKCalpha membrane localization and elevated phosphorylation of PKCalpha in VSMCs, which was reversed by berberine or PKCalpha inhibitors.	Nitroglycerin	97-100	protein kinase C, alpha	Rattus norvegicus	36-44
34319490-7	2021	The mechanistic study revealed that PKCalpha participated in the development of NTG tolerance as NTG increased the activity of PKCalpha with enriched PKCalpha membrane localization and elevated phosphorylation of PKCalpha in VSMCs, which was reversed by berberine or PKCalpha inhibitors.	Nitroglycerin	97-100	protein kinase C, alpha	Rattus norvegicus	127-135
34319490-7	2021	The mechanistic study revealed that PKCalpha participated in the development of NTG tolerance as NTG increased the activity of PKCalpha with enriched PKCalpha membrane localization and elevated phosphorylation of PKCalpha in VSMCs, which was reversed by berberine or PKCalpha inhibitors.	Nitroglycerin	97-100	protein kinase C, alpha	Rattus norvegicus	150-158
34319490-7	2021	The mechanistic study revealed that PKCalpha participated in the development of NTG tolerance as NTG increased the activity of PKCalpha with enriched PKCalpha membrane localization and elevated phosphorylation of PKCalpha in VSMCs, which was reversed by berberine or PKCalpha inhibitors.	Nitroglycerin	97-100	protein kinase C, alpha	Rattus norvegicus	213-221
34319490-7	2021	The mechanistic study revealed that PKCalpha participated in the development of NTG tolerance as NTG increased the activity of PKCalpha with enriched PKCalpha membrane localization and elevated phosphorylation of PKCalpha in VSMCs, which was reversed by berberine or PKCalpha inhibitors.	Nitroglycerin	97-100	protein kinase C, alpha	Rattus norvegicus	267-275
34319490-8	2021	CONCLUSION: This study is probably the first demonstration that berberine reverses NTG tolerance through inhibiting PKCalpha activity in VSMCs and PKCalpha is an important contributor to the development of NTG tolerance.	Nitroglycerin	83-86	protein kinase C, alpha	Rattus norvegicus	116-124
34319490-8	2021	CONCLUSION: This study is probably the first demonstration that berberine reverses NTG tolerance through inhibiting PKCalpha activity in VSMCs and PKCalpha is an important contributor to the development of NTG tolerance.	Nitroglycerin	83-86	protein kinase C, alpha	Rattus norvegicus	147-155
34319490-8	2021	CONCLUSION: This study is probably the first demonstration that berberine reverses NTG tolerance through inhibiting PKCalpha activity in VSMCs and PKCalpha is an important contributor to the development of NTG tolerance.	Nitroglycerin	206-209	protein kinase C, alpha	Rattus norvegicus	116-124
34319490-8	2021	CONCLUSION: This study is probably the first demonstration that berberine reverses NTG tolerance through inhibiting PKCalpha activity in VSMCs and PKCalpha is an important contributor to the development of NTG tolerance.	Nitroglycerin	206-209	protein kinase C, alpha	Rattus norvegicus	147-155
34319490-9	2021	These new findings suggest that berberine could become a promising drug for prevention of NTG tolerance and that targeting PKCalpha in VSMCs is likely to be a potential therapeutic strategy for reversal of NTG tolerance in blood vessels.	Nitroglycerin	206-209	protein kinase C, alpha	Rattus norvegicus	123-131
35189405-8	2022	Our study proposed and validated the mechanism to counteract VEGFR inhibition, providing GTN as the potential treatment to MKI-induced HFSR, which may further improve the therapeutic window of various MKI based cancer therapies.	Nitroglycerin	89-92	kinase insert domain receptor	Homo sapiens	61-66
35563235-9	2022	Our results demonstrated that the SP and SB treatments attenuated hyperalgesia and pain following NTG injection.	Nitroglycerin	98-101	trefoil factor 2 (spasmolytic protein 1)	Mus musculus	34-36
35362954-7	2022	NG-497 binds ATGL within a hydrophobic cavity near the active site.	Nitroglycerin	0-2	patatin like phospholipase domain containing 2	Homo sapiens	13-17
35297026-13	2022	CONCLUSIONS: In Spain, the usability advantage of NG over IG translates to potential cost savings per SHE in three populations with insulin-treated diabetes, and the introduction of NG was associated with a lower budget impact versus IG in each group.	Nitroglycerin	50-52	insulin	Homo sapiens	132-139
35353773-0	2022	Transient receptor potential melastatin 8 (TRPM8) is required for nitroglycerin and calcitonin gene-related peptide induced migraine-like pain behaviors in mice.	Nitroglycerin	66-79	transient receptor potential cation channel, subfamily M, member 8	Mus musculus	0-41
35353773-0	2022	Transient receptor potential melastatin 8 (TRPM8) is required for nitroglycerin and calcitonin gene-related peptide induced migraine-like pain behaviors in mice.	Nitroglycerin	66-79	transient receptor potential cation channel, subfamily M, member 8	Mus musculus	43-48
35157994-2	2022	Nitroglycerin (NTG) can reduce HIF-1 in tissues, and this may have anti-angiogenic, pro-apoptotic, and anti-efflux effects.	Nitroglycerin	0-13	hypoxia inducible factor 1 subunit alpha	Homo sapiens	31-36
35157994-2	2022	Nitroglycerin (NTG) can reduce HIF-1 in tissues, and this may have anti-angiogenic, pro-apoptotic, and anti-efflux effects.	Nitroglycerin	15-18	hypoxia inducible factor 1 subunit alpha	Homo sapiens	31-36
34445170-0	2021	Nitric Oxide-Releasing Drug Glyceryl Trinitrate Targets JAK2/STAT3 Signaling, Migration and Invasion of Triple-Negative Breast Cancer Cells.	Nitroglycerin	28-47	Janus kinase 2	Homo sapiens	56-60
34325647-0	2021	Activation of microglial GLP-1R in the trigeminal nucleus caudalis suppresses central sensitization of chronic migraine after recurrent nitroglycerin stimulation.	Nitroglycerin	136-149	glucagon-like peptide 1 receptor	Mus musculus	25-31
34325647-13	2021	RESULTS: The protein expression of GLP-1R was increased in the TNC after nitroglycerin injection.	Nitroglycerin	73-86	glucagon-like peptide 1 receptor	Mus musculus	35-41
34325647-17	2021	In addition, activating GLP-1R reduced Iba-1, IL-1beta and TNF-alpha release and inhibited TNC microglial number and morphological changes (process retraction) following nitroglycerin administration.	Nitroglycerin	170-183	glucagon-like peptide 1 receptor	Mus musculus	24-30
34325647-17	2021	In addition, activating GLP-1R reduced Iba-1, IL-1beta and TNF-alpha release and inhibited TNC microglial number and morphological changes (process retraction) following nitroglycerin administration.	Nitroglycerin	170-183	induction of brown adipocytes 1	Mus musculus	39-44
34325647-17	2021	In addition, activating GLP-1R reduced Iba-1, IL-1beta and TNF-alpha release and inhibited TNC microglial number and morphological changes (process retraction) following nitroglycerin administration.	Nitroglycerin	170-183	interleukin 1 alpha	Mus musculus	46-54
34285277-6	2021	Immunohistochemical analysis revealed strong expression of aggrecan, collagen 2, brachyury and Oct4 in IVD-NPs injected with NTG-101.	Nitroglycerin	125-128	T-box transcription factor T	Rattus norvegicus	81-90
34285277-7	2021	Our results also demonstrated suppression of inflammation induced p38 and NFkappaB resulting in inhibition of catabolic genes, but activation of Smad-2/3, Erk-1/2 and Akt-dependent signaling inducing anabolic genes in IVD-NP on treatment with NTG-101.	Nitroglycerin	243-246	mitogen activated protein kinase 14	Rattus norvegicus	66-69
34285277-7	2021	Our results also demonstrated suppression of inflammation induced p38 and NFkappaB resulting in inhibition of catabolic genes, but activation of Smad-2/3, Erk-1/2 and Akt-dependent signaling inducing anabolic genes in IVD-NP on treatment with NTG-101.	Nitroglycerin	243-246	SMAD family member 2	Rattus norvegicus	145-153
34285277-7	2021	Our results also demonstrated suppression of inflammation induced p38 and NFkappaB resulting in inhibition of catabolic genes, but activation of Smad-2/3, Erk-1/2 and Akt-dependent signaling inducing anabolic genes in IVD-NP on treatment with NTG-101.	Nitroglycerin	243-246	mitogen activated protein kinase 3	Rattus norvegicus	155-162
34285277-7	2021	Our results also demonstrated suppression of inflammation induced p38 and NFkappaB resulting in inhibition of catabolic genes, but activation of Smad-2/3, Erk-1/2 and Akt-dependent signaling inducing anabolic genes in IVD-NP on treatment with NTG-101.	Nitroglycerin	243-246	AKT serine/threonine kinase 1	Rattus norvegicus	167-170
35427818-17	2022	The levels of caspase-9 and IL-1beta in NTG rats showed little fluctuation and were relatively stable; however, their levels in MTG showed a downward trend with time.	Nitroglycerin	40-43	caspase 9	Rattus norvegicus	14-23
35427818-17	2022	The levels of caspase-9 and IL-1beta in NTG rats showed little fluctuation and were relatively stable; however, their levels in MTG showed a downward trend with time.	Nitroglycerin	40-43	interleukin 1 alpha	Rattus norvegicus	28-36
35618045-6	2022	Restoration of epidermal extracellular signal-regulated kinase (ERK) and a reduction in STAT3 signaling via GTN treatment rescued the cellular functions that had been damaged in vitro and further ameliorated the rash in rat models.	Nitroglycerin	108-111	Eph receptor B1	Rattus norvegicus	25-62
35618045-6	2022	Restoration of epidermal extracellular signal-regulated kinase (ERK) and a reduction in STAT3 signaling via GTN treatment rescued the cellular functions that had been damaged in vitro and further ameliorated the rash in rat models.	Nitroglycerin	108-111	Eph receptor B1	Rattus norvegicus	64-67
35618045-6	2022	Restoration of epidermal extracellular signal-regulated kinase (ERK) and a reduction in STAT3 signaling via GTN treatment rescued the cellular functions that had been damaged in vitro and further ameliorated the rash in rat models.	Nitroglycerin	108-111	signal transducer and activator of transcription 3	Rattus norvegicus	88-93
35395139-6	2022	It was found that the weakest PON1 inhibitors are Irbesartan (Ki : 421.73 microM), Glyceryl Trinitrate (Ki : 351.48 microM), and Apixaban (Ki : 333.27 microM).	Nitroglycerin	83-102	paraoxonase 1	Homo sapiens	30-34
35510237-0	2022	Nitroglycerin-induced downregulation of AKT- and ERK1/2-mediated radiation-sensitive 52 expression to enhance pemetrexed-induced cytotoxicity in human lung cancer cells.	Nitroglycerin	0-13	AKT serine/threonine kinase 1	Homo sapiens	40-43
35510237-0	2022	Nitroglycerin-induced downregulation of AKT- and ERK1/2-mediated radiation-sensitive 52 expression to enhance pemetrexed-induced cytotoxicity in human lung cancer cells.	Nitroglycerin	0-13	mitogen-activated protein kinase 3	Homo sapiens	49-55
35510237-6	2022	In 2 NSCLC cell lines (i.e. lung squamous cell carcinoma H520 and lung adenocarcinoma H1975 cells), NTG reduced Rad52 expression; in addition, decreased phospho-AKT and phospho-ERK1/2 protein levels were observed.	Nitroglycerin	100-103	AKT serine/threonine kinase 1	Homo sapiens	161-164
35510237-7	2022	Enhancement of AKT or ERK1/2 activity through transfection with a constitutively active AKT (AKT-CA) vector or constitutively active mitogen-activated protein kinase kinase 1 (MKK1-CA) vector increased the Rad52 protein level and cell survival, which were suppressed by NTG.	Nitroglycerin	270-273	AKT serine/threonine kinase 1	Homo sapiens	15-18
35510237-7	2022	Enhancement of AKT or ERK1/2 activity through transfection with a constitutively active AKT (AKT-CA) vector or constitutively active mitogen-activated protein kinase kinase 1 (MKK1-CA) vector increased the Rad52 protein level and cell survival, which were suppressed by NTG.	Nitroglycerin	270-273	mitogen-activated protein kinase 3	Homo sapiens	22-28
35510237-7	2022	Enhancement of AKT or ERK1/2 activity through transfection with a constitutively active AKT (AKT-CA) vector or constitutively active mitogen-activated protein kinase kinase 1 (MKK1-CA) vector increased the Rad52 protein level and cell survival, which were suppressed by NTG.	Nitroglycerin	270-273	AKT serine/threonine kinase 1	Homo sapiens	88-91
35510237-7	2022	Enhancement of AKT or ERK1/2 activity through transfection with a constitutively active AKT (AKT-CA) vector or constitutively active mitogen-activated protein kinase kinase 1 (MKK1-CA) vector increased the Rad52 protein level and cell survival, which were suppressed by NTG.	Nitroglycerin	270-273	mitogen-activated protein kinase kinase 1	Homo sapiens	133-174
35510237-7	2022	Enhancement of AKT or ERK1/2 activity through transfection with a constitutively active AKT (AKT-CA) vector or constitutively active mitogen-activated protein kinase kinase 1 (MKK1-CA) vector increased the Rad52 protein level and cell survival, which were suppressed by NTG.	Nitroglycerin	270-273	mitogen-activated protein kinase kinase 1	Homo sapiens	176-180
35510237-8	2022	The knockdown of Rad52 expression by using small interfering RNA or by inhibiting AKT and ERK1/2 activity enhanced the cytotoxicity and cell growth inhibition induced by NTG.	Nitroglycerin	170-173	AKT serine/threonine kinase 1	Homo sapiens	82-85
35510237-8	2022	The knockdown of Rad52 expression by using small interfering RNA or by inhibiting AKT and ERK1/2 activity enhanced the cytotoxicity and cell growth inhibition induced by NTG.	Nitroglycerin	170-173	mitogen-activated protein kinase 3	Homo sapiens	90-96
35510237-9	2022	Moreover, NTG synergistically enhanced the cytotoxicity and cell growth inhibition induced by pemetrexed in NSCLC cells; these effects were associated with AKT and ERK1/2 inactivation and, consequently, Rad52 downregulation in H520 and H1975 cells.	Nitroglycerin	10-13	AKT serine/threonine kinase 1	Homo sapiens	156-159
35510237-9	2022	Moreover, NTG synergistically enhanced the cytotoxicity and cell growth inhibition induced by pemetrexed in NSCLC cells; these effects were associated with AKT and ERK1/2 inactivation and, consequently, Rad52 downregulation in H520 and H1975 cells.	Nitroglycerin	10-13	mitogen-activated protein kinase 3	Homo sapiens	164-170
35144528-10	2022	RESULTS: Our results showed that the expression of S1PR1 was increased after NTG injection and S1PR1 was colocalized with in neurons and glial cells in the TCC.	Nitroglycerin	77-80	sphingosine-1-phosphate receptor 1	Mus musculus	51-56
35144528-14	2022	CONCLUSIONS: Our results indicate that inhibiting S1PR1 signal could alleviate central sensitization and inhibit microglia activity caused by chronic NTG administration via STAT3 signal pathway, which provide a new clue for the clinical treatment of CM.	Nitroglycerin	150-153	sphingosine-1-phosphate receptor 1	Mus musculus	50-55
35144528-14	2022	CONCLUSIONS: Our results indicate that inhibiting S1PR1 signal could alleviate central sensitization and inhibit microglia activity caused by chronic NTG administration via STAT3 signal pathway, which provide a new clue for the clinical treatment of CM.	Nitroglycerin	150-153	signal transducer and activator of transcription 3	Mus musculus	173-178
2511136-0	1989	Association of transdermal nitroglycerin to vasopressin infusion in the treatment of variceal hemorrhage: a placebo-controlled clinical trial.	Nitroglycerin	27-40	arginine vasopressin	Homo sapiens	44-55
35087392-6	2021	In addition, the degeneration of PV+ neurons and the expression of NeuN were rarely observed in the SNR of nTg and the other triple transgenic mice.	Nitroglycerin	107-110	RNA binding protein, fox-1 homolog (C. elegans) 3	Mus musculus	67-71
34979902-0	2022	IL-17 crosses the blood-brain barrier to trigger neuroinflammation: a novel mechanism in nitroglycerin-induced chronic migraine.	Nitroglycerin	89-102	interleukin 17A	Rattus norvegicus	0-5
34979902-2	2022	Although the NF-kappaB pathway is involved in an increase in CGRP levels and activation of the trigeminal system in the NTG model, the relationship between NTG and neuroinflammation remains unclear.	Nitroglycerin	120-123	calcitonin-related polypeptide alpha	Rattus norvegicus	61-65
34979902-10	2022	Furthermore, NTG administration increased BBB permeability by altering the levels functional proteins (RAGE, LRP1, AQP4 and MFSD2A) and structural proteins (ZO-1, Occludin and VE-cadherin-2) to increase peripheral IL-17A permeation into the medulla oblongata, activating microglia and neuroinflammation, and eventually causing hyperalgesia and migraine attack.	Nitroglycerin	13-16	advanced glycosylation end product-specific receptor	Rattus norvegicus	103-107
34979902-10	2022	Furthermore, NTG administration increased BBB permeability by altering the levels functional proteins (RAGE, LRP1, AQP4 and MFSD2A) and structural proteins (ZO-1, Occludin and VE-cadherin-2) to increase peripheral IL-17A permeation into the medulla oblongata, activating microglia and neuroinflammation, and eventually causing hyperalgesia and migraine attack.	Nitroglycerin	13-16	LDL receptor related protein 1	Rattus norvegicus	109-113
34979902-10	2022	Furthermore, NTG administration increased BBB permeability by altering the levels functional proteins (RAGE, LRP1, AQP4 and MFSD2A) and structural proteins (ZO-1, Occludin and VE-cadherin-2) to increase peripheral IL-17A permeation into the medulla oblongata, activating microglia and neuroinflammation, and eventually causing hyperalgesia and migraine attack.	Nitroglycerin	13-16	aquaporin 4	Rattus norvegicus	115-119
34979902-10	2022	Furthermore, NTG administration increased BBB permeability by altering the levels functional proteins (RAGE, LRP1, AQP4 and MFSD2A) and structural proteins (ZO-1, Occludin and VE-cadherin-2) to increase peripheral IL-17A permeation into the medulla oblongata, activating microglia and neuroinflammation, and eventually causing hyperalgesia and migraine attack.	Nitroglycerin	13-16	major facilitator superfamily domain containing 2A	Rattus norvegicus	124-130
34979902-10	2022	Furthermore, NTG administration increased BBB permeability by altering the levels functional proteins (RAGE, LRP1, AQP4 and MFSD2A) and structural proteins (ZO-1, Occludin and VE-cadherin-2) to increase peripheral IL-17A permeation into the medulla oblongata, activating microglia and neuroinflammation, and eventually causing hyperalgesia and migraine attack.	Nitroglycerin	13-16	tight junction protein 1	Rattus norvegicus	157-161
34979902-10	2022	Furthermore, NTG administration increased BBB permeability by altering the levels functional proteins (RAGE, LRP1, AQP4 and MFSD2A) and structural proteins (ZO-1, Occludin and VE-cadherin-2) to increase peripheral IL-17A permeation into the medulla oblongata, activating microglia and neuroinflammation, and eventually causing hyperalgesia and migraine attack.	Nitroglycerin	13-16	occludin	Rattus norvegicus	163-171
34979902-10	2022	Furthermore, NTG administration increased BBB permeability by altering the levels functional proteins (RAGE, LRP1, AQP4 and MFSD2A) and structural proteins (ZO-1, Occludin and VE-cadherin-2) to increase peripheral IL-17A permeation into the medulla oblongata, activating microglia and neuroinflammation, and eventually causing hyperalgesia and migraine attack.	Nitroglycerin	13-16	interleukin 17A	Rattus norvegicus	214-220
34979902-13	2022	This process was a novel mechanism in NTG-induced chronic migraine, suggesting that IL-17A might be a novel target in the treatment of migraine.	Nitroglycerin	38-41	interleukin 17A	Rattus norvegicus	84-90
2620324-6	1989	L-NMMA (100 nmol.min-1) stereospecifically inhibited vasodilatation induced by acetylcholine and bradykinin (p less than 0.02) but not that induced by the endothelium independent vasodilator glyceryl trinitrate.	Nitroglycerin	191-210	CD59 molecule (CD59 blood group)	Homo sapiens	17-22
35136961-8	2022	In contrast, glyceryl trinitrate-induced hypersensitivity is dependent on CGRP.	Nitroglycerin	13-32	calcitonin/calcitonin-related polypeptide, alpha	Mus musculus	74-78
35119039-6	2022	Similarly, the immunoreactivities of MMP-2 in the GTN (66.7%) and BM (80.8%) samples were significantly elevated compared to that of the NCV (57.1%) samples (P < .001).	Nitroglycerin	50-53	matrix metallopeptidase 2	Homo sapiens	37-42
35119039-7	2022	The levels of ANG and MMP-2 in the maternal serum of the GTN group were both significantly higher than those of the control group (P < .001).	Nitroglycerin	57-60	angiogenin	Homo sapiens	14-17
35119039-7	2022	The levels of ANG and MMP-2 in the maternal serum of the GTN group were both significantly higher than those of the control group (P < .001).	Nitroglycerin	57-60	matrix metallopeptidase 2	Homo sapiens	22-27
2531047-7	1989	After the larger dose of atrial natriuretic peptide, the administration of nitroglycerin (10 micrograms/kg into the left atrium) caused no further increase of retrograde blood flow, and no further decrease of collateral vascular resistance.	Nitroglycerin	75-88	natriuretic peptide A	Canis lupus familiaris	25-51
2511136-1	1989	The aim of this study was to evaluate, using a double-blind technique, the efficacy of the association of transdermal nitroglycerin to vasopressin infusion for the treatment of variceal bleeding.	Nitroglycerin	118-131	arginine vasopressin	Homo sapiens	135-146
2535309-4	1989	However, the decrease caused by ANF appeared later than that caused by the other vasodilators and lasted longer than with nitroglycerin and sodium nitroprusside.	Nitroglycerin	122-135	natriuretic peptide A	Homo sapiens	32-35
2511136-2	1989	Sixty-nine cirrhotic patients with active variceal bleeding were randomly allocated to receive vasopressin (0.4 to 0.8 unit per min until variceal bleeding has been controlled for 12 hr) associated with nitroglycerin administered transdermically in a slow-release preparation (10 mg in 24 hr) or placebo.	Nitroglycerin	203-216	arginine vasopressin	Homo sapiens	95-106
2511136-8	1989	This study demonstrates that transdermal nitroglycerin improves the effectiveness of vasopressin for controlling variceal hemorrhage.	Nitroglycerin	41-54	arginine vasopressin	Homo sapiens	85-96
2573742-2	1989	Significant increases in excretion of NAG and gamma-GTP were observed in TNG group.	Nitroglycerin	73-76	O-GlcNAcase	Homo sapiens	38-41
2574729-8	1989	Anginal frequency and NTG consumption were significantly reduced, and equally so, by qd and bid regimens.	Nitroglycerin	22-25	BH3 interacting domain death agonist	Homo sapiens	92-95
2573742-2	1989	Significant increases in excretion of NAG and gamma-GTP were observed in TNG group.	Nitroglycerin	73-76	inactive glutathione hydrolase 2	Homo sapiens	46-55
2499616-10	1989	Nitroglycerin ameliorated the increases in systemic and pulmonary artery pressure produced by vasopressin but also tended to reverse the decline in the hepatic venous pressure gradient and markedly increased gastroesophageal flow.	Nitroglycerin	0-13	arginine vasopressin	Homo sapiens	94-105
2506859-5	1989	These data demonstrate that microsomal reductive denitration of glyceryl trinitrate is catalyzed by cytochrome P-450 and can be involved in the formation of the endothelium-derived relaxing factor (EDRF = nitric oxide).	Nitroglycerin	64-83	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	100-116
2545862-2	1989	Biotransformation of 0.1 microM GTN was linear over 30 min and the percentage of glyceryl dinitrate (GDN)/10(6) cells for BAE, BASM, RLF and PK1 at 30 min was 3.1, 2.3, 5.8 and 21.7%, respectively.	Nitroglycerin	32-35	prokineticin 1	Bos taurus	141-144
2545862-5	1989	Upon re-exposure to GTN after treatment of RLF or PK1 cells for 3 hr with 0.1 mM GTN, there was an almost complete loss of the cyclic GMP response, GTN biotransformation was attenuated markedly and the selective formation of 1,2-GDN at low GTN concentration was absent.	Nitroglycerin	20-23	prokineticin 1	Bos taurus	50-53
2545862-5	1989	Upon re-exposure to GTN after treatment of RLF or PK1 cells for 3 hr with 0.1 mM GTN, there was an almost complete loss of the cyclic GMP response, GTN biotransformation was attenuated markedly and the selective formation of 1,2-GDN at low GTN concentration was absent.	Nitroglycerin	81-84	prokineticin 1	Bos taurus	50-53
2545862-5	1989	Upon re-exposure to GTN after treatment of RLF or PK1 cells for 3 hr with 0.1 mM GTN, there was an almost complete loss of the cyclic GMP response, GTN biotransformation was attenuated markedly and the selective formation of 1,2-GDN at low GTN concentration was absent.	Nitroglycerin	81-84	prokineticin 1	Bos taurus	50-53
2545862-5	1989	Upon re-exposure to GTN after treatment of RLF or PK1 cells for 3 hr with 0.1 mM GTN, there was an almost complete loss of the cyclic GMP response, GTN biotransformation was attenuated markedly and the selective formation of 1,2-GDN at low GTN concentration was absent.	Nitroglycerin	81-84	prokineticin 1	Bos taurus	50-53
2757892-9	1989	Glyceryl trinitrate (0.4 microgram min-1) however, completely reversed the constriction to noradrenaline (P less than 0.001).	Nitroglycerin	0-19	CD59 molecule (CD59 blood group)	Homo sapiens	35-40
2521271-3	1989	After 60 minutes of nitroglycerin administration, the mean decrement in wedge pressure was 10.0 +/- 1.7 (standard error) mm Hg (35%) and plasma ANF was 65.3 +/- 13.9 pmol/liter (35%).	Nitroglycerin	20-33	natriuretic peptide A	Homo sapiens	144-147
2468964-2	1989	The present study was performed to elucidate if large oral doses of N-acetylcysteine (NAC, 2,400 mg X 2), a donor of sulfhydryl groups, given together with a single oral dose of the long-acting nitrate, isosorbide-5-mononitrate (5-ISMN, 60 mg), would modify the nitrate effect evaluated by exercise testing before and after additional sublingual doses of nitroglycerin (NTG).	Nitroglycerin	355-368	NACC family member 2	Homo sapiens	68-103
2468964-2	1989	The present study was performed to elucidate if large oral doses of N-acetylcysteine (NAC, 2,400 mg X 2), a donor of sulfhydryl groups, given together with a single oral dose of the long-acting nitrate, isosorbide-5-mononitrate (5-ISMN, 60 mg), would modify the nitrate effect evaluated by exercise testing before and after additional sublingual doses of nitroglycerin (NTG).	Nitroglycerin	370-373	NACC family member 2	Homo sapiens	68-103
2705635-2	1989	Clinical characteristics that occurred more frequently in patients with NCA were: nonexertional pain, pain to the left of the sternum, sharp pain, associated palpitations, absence of typical relief with sublingual nitroglycerin, pain commencing less than one week or more than ten years prior to coronary angiography, a normal electrocardiogram, and negative results from a treadmill stress test or from thallium scintigraphy.	Nitroglycerin	214-227	CEA cell adhesion molecule 6	Homo sapiens	72-75
2563941-6	1989	Similarly, activators of soluble guanylate cyclase, such as glyceryltrinitrate and sodium nitroprusside (10(-5) mol/l) inhibited vasopressin-stimulated corticotropin release by 60%.	Nitroglycerin	60-78	arginine vasopressin	Rattus norvegicus	129-140
2521271-4	1989	The initial decrease, sustained reduction and later increase in plasma ANF levels closely paralleled the changes in pulmonary arterial wedge (r = 0.94, p less than 0.0001) and right atrial pressures (r = 0.91, p less than 0.0001) during and immediately after the nitroglycerin infusion.	Nitroglycerin	263-276	natriuretic peptide A	Homo sapiens	71-74
2473288-4	1989	The coronary vasoconstriction induced by ET-1 subsided after intracoronary administration of nitroglycerin.	Nitroglycerin	93-106	endothelin 1	Canis lupus familiaris	41-45
2491934-0	1989	Simultaneous infusion of nitroglycerin and nitroprusside to offset adverse effects of vasopressin during portosystemic shunting.	Nitroglycerin	25-38	arginine vasopressin	Homo sapiens	86-97
2491934-6	1989	Eleven of 13 patients with vasopressin-induced myocardial ischemia responded to simultaneous infusion of nitroglycerin.	Nitroglycerin	105-118	arginine vasopressin	Homo sapiens	27-38
2491934-7	1989	Further prospective studies are indicated to adequately delineate the dose and duration of therapy with either nitroprusside or nitroglycerin for simultaneous administration with intravenous vasopressin.	Nitroglycerin	128-141	arginine vasopressin	Homo sapiens	191-202
2521284-0	1989	Effects of calcium antagonists and nitroglycerin on atrial natriuretic peptide in normal subjects and patients with essential hypertension.	Nitroglycerin	35-48	natriuretic peptide A	Homo sapiens	52-78
2521284-1	1989	Acute effects of coronary vasodilators (nifedipine, nicardipine, and nitroglycerin) on atrial natriuretic peptide (ANP) and the renin-angiotensin-aldosterone system were studied in normal subjects and patients with essential hypertension.	Nitroglycerin	69-82	natriuretic peptide A	Homo sapiens	87-113
2495813-13	1989	Alinidine administered 2 h before a glyceryl trinitrate challenge reduced (P less than 0.05) the glyceryl trinitrate induced increase in standing heart rate at all time intervals (1 to 6 min); the maximum reduction occurred at 3 min (105.0 +/- 4.3 (glyceryl trinitrate) vs 86.8 +/- 6.7 beats min-1 (combination].	Nitroglycerin	97-116	CD59 molecule (CD59 blood group)	Homo sapiens	292-297
2495813-13	1989	Alinidine administered 2 h before a glyceryl trinitrate challenge reduced (P less than 0.05) the glyceryl trinitrate induced increase in standing heart rate at all time intervals (1 to 6 min); the maximum reduction occurred at 3 min (105.0 +/- 4.3 (glyceryl trinitrate) vs 86.8 +/- 6.7 beats min-1 (combination].	Nitroglycerin	97-116	CD59 molecule (CD59 blood group)	Homo sapiens	292-297
2502445-9	1989	Glutathione S-transferase activity was competitively inhibited by GTN.	Nitroglycerin	66-69	glutathione S-transferase kappa 1	Homo sapiens	0-25
2484698-1	1989	The molecular mechanism of tolerance development to nitrovasodilators, most prominent with nitroglycerin, associated with desensitization of guanylate cyclase is still unclear.	Nitroglycerin	91-104	guanylate cyclase	Bos taurus	141-158
2694666-5	1989	However, even in atherosclerotic arteries, EDRF-mediated vasodilation may contribute considerably to the actual vascular tone, since the release of EDRF upon appropriate stimulation in patients with moderate coronary artery disease appears to result in a vasodilation which is similar to that induced by an intracoronary infusion of nitroglycerin.	Nitroglycerin	333-346	alpha hemoglobin stabilizing protein	Homo sapiens	43-47
2565981-5	1989	NG pre-incubation of GC (in contrast to coronary strips) almost completely abolished the direct and thiol-independent stimulatory effect of 3-morpholinosydnonimine (SIN-1) down to 4.5 +/- 0.2%, whereas pre-incubation with other nitrovasodilators reduced the stimulatory response to SIN-1 to only 59 to 98%.	Nitroglycerin	0-2	MAPK associated protein 1	Homo sapiens	165-170
2565981-5	1989	NG pre-incubation of GC (in contrast to coronary strips) almost completely abolished the direct and thiol-independent stimulatory effect of 3-morpholinosydnonimine (SIN-1) down to 4.5 +/- 0.2%, whereas pre-incubation with other nitrovasodilators reduced the stimulatory response to SIN-1 to only 59 to 98%.	Nitroglycerin	0-2	MAPK associated protein 1	Homo sapiens	282-287
2565981-6	1989	Increasing concentrations of NG during pre-incubation dose-dependently (IC50 = 0.13 mM) reduced the activating effect of SIN-1 during incubation.	Nitroglycerin	29-31	MAPK associated protein 1	Homo sapiens	121-126
2544772-5	1989	These two endothelium-dependent drugs and two endothelium-independent relaxing drugs, nitroprusside and nitroglycerin relaxed the IMA in a dose dependent manner which was associated with an elevation of cyclic GMP.	Nitroglycerin	104-117	5'-nucleotidase, cytosolic II	Homo sapiens	210-213
2555979-3	1989	Nitrate (GTN)-induced relaxation was accompanied by a 2- to 3-fold increase of cyclic GMP content in the vessel walls.	Nitroglycerin	9-12	5'-nucleotidase, cytosolic II	Homo sapiens	86-89
2573982-2	1989	Nitrate tolerance significantly attenuated NTG-induced vasodilation of precontracted (1.0 microM norepinephrine) RA, increase in cyclic GMP in RA and SMC, and activation of guanylate cyclase in homogenates as compared to controls.	Nitroglycerin	43-46	guanylate cyclase	Bos taurus	173-190
2694666-5	1989	However, even in atherosclerotic arteries, EDRF-mediated vasodilation may contribute considerably to the actual vascular tone, since the release of EDRF upon appropriate stimulation in patients with moderate coronary artery disease appears to result in a vasodilation which is similar to that induced by an intracoronary infusion of nitroglycerin.	Nitroglycerin	333-346	alpha hemoglobin stabilizing protein	Homo sapiens	148-152
2836843-4	1988	A polyclonal antibody to IAP counteracted the effect of the toxin on the GTN-response.	Nitroglycerin	73-76	intestinal-type alkaline phosphatase	Bos taurus	25-28
2964972-0	1988	Changes in atrial natriuretic factor during preload reduction with nitroglycerin in patients with congestive heart failure.	Nitroglycerin	67-80	natriuretic peptide A	Homo sapiens	11-36
3126751-6	1988	HDL subfraction mass was significantly reduced in both cardiovascular groups; the HTG group showed a greater reduction in HDL2, whilst the NTG group showed a greater reduction in HDL3.	Nitroglycerin	139-142	HDL3	Homo sapiens	179-183
2964972-4	1988	After nitroglycerin all patients had reductions in right atrial, pulmonary arterial, and pulmonary capillary wedge pressures and a simultaneous decrease in plasma ANF concentrations, reaching lowest values after 10 min.	Nitroglycerin	6-19	natriuretic peptide A	Homo sapiens	163-166
3137071-7	1988	Vasopressin co-infusion decreased both the cardiac output and the arterial nitroglycerin clearance, but it also increased the arteriovenous extraction of nitroglycerin.	Nitroglycerin	75-88	arginine vasopressin	Rattus norvegicus	0-11
3137071-7	1988	Vasopressin co-infusion decreased both the cardiac output and the arterial nitroglycerin clearance, but it also increased the arteriovenous extraction of nitroglycerin.	Nitroglycerin	154-167	arginine vasopressin	Rattus norvegicus	0-11
3137066-3	1988	They were divided into two groups to receive either nitroglycerin (1 microgram kg-1 min-1) or placebo (5% dextrose).	Nitroglycerin	52-65	CD59 molecule (CD59 blood group)	Homo sapiens	84-89
2469867-2	1988	The nitrovasodilators, such as nitroglycerin, generate nitric oxide, which directly activates the soluble isoenzyme of guanylate cyclase resulting in increased intracellular concentrations of cyclic GMP.	Nitroglycerin	31-44	5'-nucleotidase, cytosolic II	Homo sapiens	199-202
2852408-5	1988	GTN suppressed the PAF provoked Mn+2 entering into the cells.	Nitroglycerin	0-3	PCNA clamp associated factor	Homo sapiens	19-22
2441158-2	1987	Prior exposure of rat thoracic aorta to glyceryl trinitrate decreased relaxations to glyceryl trinitrate, sodium nitroprusside, and acetylcholine, whereas relaxations to atriopeptin II and 8-bromo cyclic GMP remained unaltered.	Nitroglycerin	40-59	5'-nucleotidase, cytosolic II	Homo sapiens	204-207
2852408-2	1988	Nitroglycerin (GTN), isosorbide dinitrate (ISDN) and sodium nitroprusside (NP) were found to inhibit dose-dependently the intracellular Ca+2 increase induced by the platelet activating factor (PAF).	Nitroglycerin	0-13	PCNA clamp associated factor	Homo sapiens	193-196
2852408-2	1988	Nitroglycerin (GTN), isosorbide dinitrate (ISDN) and sodium nitroprusside (NP) were found to inhibit dose-dependently the intracellular Ca+2 increase induced by the platelet activating factor (PAF).	Nitroglycerin	15-18	PCNA clamp associated factor	Homo sapiens	193-196
2441158-9	1987	The present results suggest that: glyceryl trinitrate-induced desensitization inhibits relaxation to the nitrogen oxide-containing vasodilators and endothelium-dependent vasodilators in both the rat thoracic aorta and human coronary artery: the inhibition of relaxation is associated with decreased formation of cyclic GMP;(ABSTRACT TRUNCATED AT 250 WORDS)	Nitroglycerin	34-53	5'-nucleotidase, cytosolic II	Homo sapiens	319-322
3115779-3	1987	Doses of 10, 20, 40 and 80 micrograms min-1 of GTN or placebo were infused during treadmill exercise until symptom limiting chest pain or greater than or equal to 3 mm ST segment depression occurred.	Nitroglycerin	47-50	CD59 molecule (CD59 blood group)	Homo sapiens	38-43
3115779-7	1987	These results suggest that 20 micrograms min-1 may be the optimal dose of GTN to achieve significant antianginal effects as demonstrated by the improved exercise tolerance and reduction of myocardial ischaemia.	Nitroglycerin	74-77	CD59 molecule (CD59 blood group)	Homo sapiens	41-46
2441158-6	1987	Pretreatment with glyceryl trinitrate decreased the elevated cyclic GMP levels due to glyceryl trinitrate and acetylcholine in rat thoracic aorta and to glyceryl trinitrate and the Ca2+ ionophore A23187 in human coronary artery.	Nitroglycerin	18-37	5'-nucleotidase, cytosolic II	Homo sapiens	68-71
2441158-6	1987	Pretreatment with glyceryl trinitrate decreased the elevated cyclic GMP levels due to glyceryl trinitrate and acetylcholine in rat thoracic aorta and to glyceryl trinitrate and the Ca2+ ionophore A23187 in human coronary artery.	Nitroglycerin	86-105	5'-nucleotidase, cytosolic II	Homo sapiens	68-71
2441158-6	1987	Pretreatment with glyceryl trinitrate decreased the elevated cyclic GMP levels due to glyceryl trinitrate and acetylcholine in rat thoracic aorta and to glyceryl trinitrate and the Ca2+ ionophore A23187 in human coronary artery.	Nitroglycerin	86-105	5'-nucleotidase, cytosolic II	Homo sapiens	68-71
2447417-10	1987	During rapid atrial pacing, CSF was slightly increased by TNG, but remained unchanged after NC and NF.	Nitroglycerin	58-61	colony stimulating factor 2	Homo sapiens	28-31
2432088-5	1987	Accumulation of cyclic GMP in atherosclerotic strips was suppressed with acetylcholine but unattenuated with A23187 and nitroglycerin.	Nitroglycerin	120-133	5'-nucleotidase, cytosolic II	Homo sapiens	23-26
3090282-5	1986	The renin-angiotensin response at 3 minutes differed between nitroglycerin infusions of 1 and 10 micrograms/kg/min with an initial significant reduction from baseline in plasma renin activity at the lower dose compared with a significant increase from baseline in plasma activity at the higher dose.	Nitroglycerin	61-74	renin	Canis lupus familiaris	4-9
3103560-10	1986	It is concluded that nifedipine as well as nitroglycerin can increase the oxygen saturation level of myocardial myoglobin during hypoxia, suggesting that both drugs may increase the intracellular oxygen tension in the hypoxic heart.	Nitroglycerin	43-56	myoglobin	Rattus norvegicus	112-121
3091286-5	1986	In six additional dogs instrumented with aortic flow probes, nitroglycerin (1.5 micrograms/kg/min) induced a 15 +/- 1% decline in peripheral vascular resistance (PVR) under autonomic blockade, but with reflexes intact these dogs showed no change in PVR and a 21 +/- 10% increase in norepinephrine release rate.	Nitroglycerin	61-74	PVR cell adhesion molecule	Canis lupus familiaris	162-165
3091286-5	1986	In six additional dogs instrumented with aortic flow probes, nitroglycerin (1.5 micrograms/kg/min) induced a 15 +/- 1% decline in peripheral vascular resistance (PVR) under autonomic blockade, but with reflexes intact these dogs showed no change in PVR and a 21 +/- 10% increase in norepinephrine release rate.	Nitroglycerin	61-74	PVR cell adhesion molecule	Canis lupus familiaris	249-252
2877539-0	1986	Development of tolerance to glyceryl trinitrate in an isolated human peripheral vein and its relation to cyclic GMP metabolism.	Nitroglycerin	28-47	5'-nucleotidase, cytosolic II	Homo sapiens	112-115
2877539-4	1986	The relaxant activity as well as the level of intracellular cyclic GMP were restored in GTN-tolerant vessels by dipyridamole (5 microM), an agent with phosphodiesterase inhibiting properties.	Nitroglycerin	88-91	5'-nucleotidase, cytosolic II	Homo sapiens	67-70
2481168-6	1987	The more effective and less costly combination appears to be the association of beta 1-selective blockers and preventive sublingual nitroglycerin.	Nitroglycerin	132-145	potassium calcium-activated channel subfamily M regulatory beta subunit 1	Homo sapiens	80-86
3098960-6	1986	Vasopressin co-infusion decreased both the cardiac output and the arterial NTG plasma clearance, but it also increased the arteriovenous extraction of NTG.	Nitroglycerin	75-78	arginine vasopressin	Rattus norvegicus	0-11
3098960-6	1986	Vasopressin co-infusion decreased both the cardiac output and the arterial NTG plasma clearance, but it also increased the arteriovenous extraction of NTG.	Nitroglycerin	151-154	arginine vasopressin	Rattus norvegicus	0-11
3103112-0	1986	[Effect of nitroglycerin administration on serum lysozyme level during the treatment of acute ischemic heart disease].	Nitroglycerin	11-24	lysozyme	Homo sapiens	49-57
3090282-5	1986	The renin-angiotensin response at 3 minutes differed between nitroglycerin infusions of 1 and 10 micrograms/kg/min with an initial significant reduction from baseline in plasma renin activity at the lower dose compared with a significant increase from baseline in plasma activity at the higher dose.	Nitroglycerin	61-74	renin	Canis lupus familiaris	177-182
3086203-6	1986	The total number of patients with complications during infusions were significantly different statistically in the vasopressin and vasopressin-nitroglycerin groups, respectively (17/19 vs. 7/20, p less than 0.001).	Nitroglycerin	143-156	arginine vasopressin	Homo sapiens	131-142
3085745-5	1986	With reduced glutathione as a co-substrate, platelet glutathione-S-transferase was most active with the synthetic substrate, 1-chloro-2,4-dinitrobenzene, less active with 1,2-dichloro-4-nitrobenzene, and essentially inactive with nitroglycerin and 1,2-epoxy-3-(p-nitrophenoxy)-propane.	Nitroglycerin	230-243	glutathione S-transferase kappa 1	Homo sapiens	53-78
3755137-4	1986	The multiple residues of NG,NG-dimethylarginine (DMA) contained in the nucleolin polypeptide were found to be limited to a segment of less than 10 kDa near the carboxyl-terminal end of the protein.	Nitroglycerin	25-27	nucleolin	Cricetulus griseus	71-80
3104512-7	1986	nitroglycerin, administered continuously at the dose of 0.7 microgram/kg-1/min-1, optimizes myocardial oxygenation during surgery and minimizes the risk of intraoperative myocardial ischemia.	Nitroglycerin	0-13	CD59 molecule (CD59 blood group)	Homo sapiens	75-80
3086204-5	1986	Thus, the addition of nitroglycerin to a vasopressin infusion results in a lower rate of complications and is more effective in controlling variceal hemorrhage.	Nitroglycerin	22-35	arginine vasopressin	Homo sapiens	41-52
3920134-7	1985	Vasopressin caused generalized vasoconstriction, while the addition of NTG reversed the deleterious systemic hemodynamic effects of vasopressin.	Nitroglycerin	71-74	arginine vasopressin	Rattus norvegicus	132-143
3009386-3	1986	Whereas methylene blue, an inhibitor of soluble guanylate cyclase, abolishes endothelium-dependent and independent arterial relaxation and cGMP accumulation in response to acetylcholine and glyceryl trinitrate, respectively, methylene blue failed to alter these responses to atriopeptin II.	Nitroglycerin	190-209	guanylate cyclase	Bos taurus	48-65
3080924-0	1986	Methemoglobin levels following sublingual nitroglycerin in human volunteers.	Nitroglycerin	42-55	hemoglobin subunit gamma 2	Homo sapiens	0-13
3929581-0	1985	Effects of continuous infusion of intravenous nitroglycerin on methemoglobin levels.	Nitroglycerin	46-59	hemoglobin subunit gamma 2	Homo sapiens	63-76
3929581-1	1985	The effect of continuous infusion of intravenous nitroglycerin (NTG) on methemoglobin levels in 24 coronary care unit patients was studied.	Nitroglycerin	49-62	hemoglobin subunit gamma 2	Homo sapiens	72-85
3929581-1	1985	The effect of continuous infusion of intravenous nitroglycerin (NTG) on methemoglobin levels in 24 coronary care unit patients was studied.	Nitroglycerin	64-67	hemoglobin subunit gamma 2	Homo sapiens	72-85
3920134-1	1985	Addition of nitroglycerin (NTG) improves the hemodynamic response to vasopressin and may thus be useful in the treatment of gastrointestinal hemorrhage.	Nitroglycerin	12-25	arginine vasopressin	Rattus norvegicus	69-80
3920134-1	1985	Addition of nitroglycerin (NTG) improves the hemodynamic response to vasopressin and may thus be useful in the treatment of gastrointestinal hemorrhage.	Nitroglycerin	27-30	arginine vasopressin	Rattus norvegicus	69-80
3920134-2	1985	We studied in the rat the influence of vasopressin on the disposition of a constant intravenous infusion of NTG and the cutaneous absorption of NTG ointment.	Nitroglycerin	108-111	arginine vasopressin	Rattus norvegicus	39-50
3084763-0	1986	Requirement for reduced, unliganded hemoprotein for the hemoglobin- and myoglobin-mediated biotransformation of glyceryl trinitrate.	Nitroglycerin	112-131	myoglobin	Homo sapiens	72-81
3084763-1	1986	The biotransformation of glyceryl trinitrate (GTN) by hemoglobin (Hb) and myoglobin (Mb) was assessed using solutions of various forms of the hemoproteins, viz., the oxy-, deoxy-, carbonmonoxy- and met-forms.	Nitroglycerin	25-44	myoglobin	Homo sapiens	74-83
3084763-1	1986	The biotransformation of glyceryl trinitrate (GTN) by hemoglobin (Hb) and myoglobin (Mb) was assessed using solutions of various forms of the hemoproteins, viz., the oxy-, deoxy-, carbonmonoxy- and met-forms.	Nitroglycerin	46-49	myoglobin	Homo sapiens	74-83
2871692-0	1986	The relaxant effect of glyceryltrinitrate on isolated human peripheral vein and its relation to cyclic GMP metabolism.	Nitroglycerin	23-41	5'-nucleotidase, cytosolic II	Homo sapiens	103-106
3084168-8	1986	In hypertensives, only PgI was decreased, with increase after NTG, at rest.	Nitroglycerin	62-65	glucose-6-phosphate isomerase	Homo sapiens	23-26
3084168-9	1986	Thus, PgI is the only humoral indicator participating in blood pressure lowering induced by NTG.	Nitroglycerin	92-95	glucose-6-phosphate isomerase	Homo sapiens	6-9
4084504-1	1985	Protein C23 (Mr 110 000, pI = 5.5), a major phosphoprotein in the nucleolus of mammalian cells, has been shown to contain 1.3 mol% of NG,NG-dimethylarginine (DMA) [Lischwe, M.A., Roberts, K.D., Yeoman, L.C., &amp; Busch, H. (1982) J. Biol.	Nitroglycerin	134-136	nucleolin	Homo sapiens	8-11
3920134-3	1985	The effect of NTG on the pharmacokinetics of vasopressin was also determined.	Nitroglycerin	14-17	arginine vasopressin	Rattus norvegicus	45-56
3925192-0	1985	[Effect of nitroglycerin-induced hypotension on plasma human growth hormone and insulin levels].	Nitroglycerin	11-24	growth hormone 1	Homo sapiens	61-75
3925192-0	1985	[Effect of nitroglycerin-induced hypotension on plasma human growth hormone and insulin levels].	Nitroglycerin	11-24	insulin	Homo sapiens	80-87
3938682-1	1985	An analysis of the cost-effectiveness of two transdermal nitroglycerin systems utilizing adhesive patches, TDN and ND, was performed by a health-care research and management consulting firm.	Nitroglycerin	57-70	triadin	Homo sapiens	107-110
3919521-0	1985	Renin release during controlled hypotension with sodium nitroprusside, nitroglycerin and adenosine: a comparative study in the dog.	Nitroglycerin	71-84	renin	Canis lupus familiaris	0-5
2858501-7	1985	These results give further evidence that a) nicorandil exerts its vasodilating effect via stimulation of guanylate cyclase and b) nitrate esters, such as nitroglycerin or nicorandil, stimulate the enzyme, at least in vitro, only in the presence of cysteine or, to a lesser extent, thiosalicylic acid.	Nitroglycerin	154-167	guanylate cyclase	Bos taurus	105-122
6437206-6	1984	In these patients, NTG caused a marked increase in CSBF (from 112 +/- 64 to 152 +/- 70 ml/min, p less than 0.01) but no consistent change in the concentration of TxB2 in CS blood (141 +/- 132 to 160 +/- 155 pg/ml, difference not significant [NS]).	Nitroglycerin	19-22	chromosome 10 open reading frame 99	Homo sapiens	51-55
6437206-8	1984	In these patients, NTG caused a marked increase in CSBF (from 111 +/- 39 to 180 +/- 63 ml/min, p less than 0.01), even though the concentration of TxB2 in CS blood (8 +/- 10 to 6 +/- 6 pg/ml, NS) was lower (p less than 0.05) than that in control subjects and patients not receiving aspirin.	Nitroglycerin	19-22	chromosome 10 open reading frame 99	Homo sapiens	51-55
6150599-3	1984	The stimulatory action of nitroprusside (NP) or GTN/cysteine on guanylate cyclase (GC) was reduced by 50-60% in GTN-tolerant vessels as compared to control vessels.	Nitroglycerin	48-51	guanylate cyclase	Bos taurus	64-81
6150599-3	1984	The stimulatory action of nitroprusside (NP) or GTN/cysteine on guanylate cyclase (GC) was reduced by 50-60% in GTN-tolerant vessels as compared to control vessels.	Nitroglycerin	48-51	guanylate cyclase	Bos taurus	83-85
6150599-3	1984	The stimulatory action of nitroprusside (NP) or GTN/cysteine on guanylate cyclase (GC) was reduced by 50-60% in GTN-tolerant vessels as compared to control vessels.	Nitroglycerin	112-115	guanylate cyclase	Bos taurus	64-81
6150599-3	1984	The stimulatory action of nitroprusside (NP) or GTN/cysteine on guanylate cyclase (GC) was reduced by 50-60% in GTN-tolerant vessels as compared to control vessels.	Nitroglycerin	112-115	guanylate cyclase	Bos taurus	83-85
6150599-4	1984	The stimulatory action of GTN and NP on GC has been suggested to occur through formation of S-nitrosothiols, probably with a previous denitration step required for GTN.	Nitroglycerin	26-29	guanylate cyclase	Bos taurus	40-42
6150599-4	1984	The stimulatory action of GTN and NP on GC has been suggested to occur through formation of S-nitrosothiols, probably with a previous denitration step required for GTN.	Nitroglycerin	164-167	guanylate cyclase	Bos taurus	40-42
6150599-6	1984	This is suggested to indicate a direct effect of GTN tolerance on GC.	Nitroglycerin	49-52	guanylate cyclase	Bos taurus	66-68
6150599-7	1984	Since the cGMP-phosphodiesterase activity was not affected in GTN-tolerant vessels, the reduced GC activity may be of a crucial importance for the reduced cGMP response in GTN-tolerant BMA as found earlier (Axelsson et al.	Nitroglycerin	172-175	guanylate cyclase	Bos taurus	96-98
6137395-1	1983	The effects of thiols on guanylate cyclase activation by nitroglycerin were studied in bovine heart and the effects of cysteinee and nitroglycerin on the tissue levels of cyclic GMP and lactate were studied in beating rat atria.	Nitroglycerin	57-70	guanylate cyclase	Bos taurus	25-42
6414501-11	1983	The time constants for haemodynamic measurement most sensitive to GTN"s effect, i.e. SPA, PCW and RAP were remarkably similar to the time constant found for GTN concentration.	Nitroglycerin	66-69	surfactant protein A2	Homo sapiens	85-88
6137395-2	1983	Cysteine (2.5 X 10(-3) M) together with nitroglycerin (1 X 10(-3) M), increased 15-fold the activity of guanylate cyclase.	Nitroglycerin	40-53	guanylate cyclase	Bos taurus	104-121
6435951-4	1984	After NTG, a significant prolongation of the pre-ejection period index (PEPI) and isovolumetric relaxation time (IVRT), increase in the PEP/LVET ratio and decrease of the "a" wave of the apexcardiogram were found.	Nitroglycerin	6-9	progestagen associated endometrial protein	Homo sapiens	72-75
6428911-7	1984	With nitroglycerin preload reduction diminished cardiac performance, as shown by a rise in PEPc and PEP/LVET and depression of (dZ/dt)/RZ.	Nitroglycerin	5-18	peptidase C	Homo sapiens	91-95
6428911-7	1984	With nitroglycerin preload reduction diminished cardiac performance, as shown by a rise in PEPc and PEP/LVET and depression of (dZ/dt)/RZ.	Nitroglycerin	5-18	progestagen associated endometrial protein	Homo sapiens	91-94
6083406-2	1984	Cyclic GMP may participate in blood-vessel relaxation caused by drugs such as nitroglycerin and nitroprusside and by agents that require the endothelium for their relaxing effects.	Nitroglycerin	78-91	5'-nucleotidase, cytosolic II	Homo sapiens	7-10
6421007-8	1983	The hemodynamic responses to the two vasodilators were similar, except that NTG reduced PAMP (p less than 0.01) and increased intrapulmonary shunt volume (p less than 0.01).	Nitroglycerin	76-79	adrenomedullin	Homo sapiens	88-92
6413793-0	1983	[Nitroglycerin ointment for numb hands].	Nitroglycerin	1-14	NUMB endocytic adaptor protein	Homo sapiens	28-32
6405071-2	1983	Nitrong and sustac in doses of 2.5 and 2.6 mg, respectively, were effective 1 1/2 and 2 h, on the average; in doses of 6.5 and 6.4 mg--4 1/2 and 3 1/2 h, and in doses of 13 and 12.8 mg--5 1/2 and 4 1/2 h, respectively.	Nitroglycerin	0-7	mucin 7, secreted	Homo sapiens	131-150
6405071-2	1983	Nitrong and sustac in doses of 2.5 and 2.6 mg, respectively, were effective 1 1/2 and 2 h, on the average; in doses of 6.5 and 6.4 mg--4 1/2 and 3 1/2 h, and in doses of 13 and 12.8 mg--5 1/2 and 4 1/2 h, respectively.	Nitroglycerin	0-7	mucin 7, secreted	Homo sapiens	182-201
6405071-2	1983	Nitrong and sustac in doses of 2.5 and 2.6 mg, respectively, were effective 1 1/2 and 2 h, on the average; in doses of 6.5 and 6.4 mg--4 1/2 and 3 1/2 h, and in doses of 13 and 12.8 mg--5 1/2 and 4 1/2 h, respectively.	Nitroglycerin	12-18	mucin 7, secreted	Homo sapiens	131-150
6405071-2	1983	Nitrong and sustac in doses of 2.5 and 2.6 mg, respectively, were effective 1 1/2 and 2 h, on the average; in doses of 6.5 and 6.4 mg--4 1/2 and 3 1/2 h, and in doses of 13 and 12.8 mg--5 1/2 and 4 1/2 h, respectively.	Nitroglycerin	12-18	mucin 7, secreted	Homo sapiens	182-201
6419648-10	1983	In this series, the association of optimal volume loading with a peroperative perfusion of 0.2 micrograms X kg-1 X min-1 NTG gave a good haemodynamic stability.	Nitroglycerin	121-124	CD59 molecule (CD59 blood group)	Homo sapiens	115-120
6794381-0	1981	[Methemoglobin formation in nitroglycerin infusions.	Nitroglycerin	28-41	hemoglobin subunit gamma 2	Homo sapiens	1-14
6815044-0	1982	Nitroglycerin improves the hemodynamic response to vasopressin in portal hypertension.	Nitroglycerin	0-13	arginine vasopressin	Homo sapiens	51-62
6815044-1	1982	This study was designed to investigate whether the addition of nitroglycerin to vasopressin infusion could avoid the deleterious systemic effects of vasopressin while maintaining or enhancing the therapeutic benefits of portal pressure reduction.	Nitroglycerin	63-76	arginine vasopressin	Homo sapiens	149-160
6815044-8	1982	Nitroglycerin when added to the vasopressin infusion reduced portal venous resistance and further decreased portal pressure in dogs.	Nitroglycerin	0-13	arginine vasopressin	Homo sapiens	32-43
6792895-4	1981	Mean plasma nitroglycerin levels were maximal at 2 (1.1 +/- 0.3 ng/ml) and 5 (1.4 +/- 0.6 ng/ml) minutes, when the changes in mean heart rate (+17 +/- 7 and +12 +/- 3 min-1) and decreases in echocardiographic left ventricular diastolic (-4.2 +/- 0.8 mm at 5 minutes) and systolic (-3.1 +/- 0.6 mm at 5 minutes) dimensions were also maximal.	Nitroglycerin	12-25	CD59 molecule (CD59 blood group)	Homo sapiens	167-172
6113801-1	1981	The authors compare the haemodynamic effects of intravenous nitroglycerin (IV TNT) in 14 patients developing hypertension (mean blood pressure greater than 90 mmHg) and in seven normotensive patients (70 less than mean blood pressure less than 90 mmHg) after cardiac surgery with extracorporeal circulation (ECC).	Nitroglycerin	60-73	chromosome 16 open reading frame 82	Homo sapiens	78-81
6167816-2	1981	In 12 normal subjects, NTG significantly increased the plasma norepinephrine concentration in association with a slight reduction in systolic blood pressure and a slight increase in heart rate, plasma cyclic adenosine monophosphate (cyclic AMP) concentration, and renin activity at 1 hr.	Nitroglycerin	23-26	renin	Homo sapiens	264-269
6112057-0	1981	Methylene blue inhibits coronary arterial relaxation and guanylate cyclase activation by nitroglycerin, sodium nitrite, and amyl nitrite.	Nitroglycerin	89-102	guanylate cyclase	Bos taurus	57-74
6112057-2	1981	Methylene blue also inhibited activation of bovine coronary arterial soluble guanylate cyclase by nitroglycerin, which required addition of cysteine.	Nitroglycerin	98-111	guanylate cyclase	Bos taurus	77-94
6769567-7	1980	For prolonged infusions we found that nitroprusside at 1 microgram.kg-1.min-1 and nitroglycerin at 0.5 microgram.kg-1.min-1 were without significant toxicity.	Nitroglycerin	82-95	CD59 molecule (CD59 blood group)	Homo sapiens	118-123
6105889-0	1980	Requirement of thiols for activation of coronary arterial guanylate cyclase by glyceryl trinitrate and sodium nitrite: possible involvement of S-nitrosothiols.	Nitroglycerin	79-98	guanylate cyclase	Bos taurus	58-75
6105889-9	1980	Moreover, these findings suggest that S-nitrosothiols could act as intermediates in the activation of guanylate cyclase by glyceryl trinitrate, NaNO2 and possibly nitroprusside.	Nitroglycerin	123-142	guanylate cyclase	Bos taurus	102-119
6769361-2	1980	When infused alone, TNG, 19 microgram/kg/min, decreased MAP 19 per cent and increased PR 33 per cent from control values (P less than 0.05), but did not significantly change UBF or UVC.	Nitroglycerin	20-23	MBL associated serine protease 2	Homo sapiens	56-62
7319689-6	1981	FIAT increased approximately linearly with increasing medium FA concentrations in both NTG and HTG patients.	Nitroglycerin	87-90	taxilin gamma	Homo sapiens	0-4
6779029-13	1981	And by comparing with radionuclide angiography obtained before and after NTG administration, NTG-loading myocardial imaging and ECG findings in 20 patients with CAD, we demonstrated that the transient defective myocardial segments were underperfused but viable.	Nitroglycerin	93-96	aconitate decarboxylase 1	Homo sapiens	161-164
230369-7	1979	Group II, including nitroglycerin and isosorbide dinitrate, incrased the concentration of c-GMP and decreased the ratio of c-AMP to c-GMP.	Nitroglycerin	20-33	cathelicidin antimicrobial peptide	Canis lupus familiaris	123-128
6780401-1	1980	The present study was performed to compare hemodynamic effect of intravenous Nitroglycerin (TNT i.v.)	Nitroglycerin	77-90	chromosome 16 open reading frame 82	Homo sapiens	92-95
470321-5	1979	The duration of Sd, Ss -- P and P -- A1 decreased after nitroglycerine and atropine administration but increased after benzodixin administration.	Nitroglycerin	56-70	PAXIP1 associated glutamate rich protein 1	Homo sapiens	32-39
115635-0	1979	Allergic contact dermatitis secondary to nitroglycerin in Nitro-Bid ointment.	Nitroglycerin	41-54	BH3 interacting domain death agonist	Homo sapiens	64-67
235996-0	1975	The conversion of glyceraldehyde-3-phosphate dehydrogenase to an acylphosphatase by trinitroglycerin and inactivation of this activity by azide and ascorbate.	Nitroglycerin	84-100	glyceraldehyde-3-phosphate dehydrogenase	Sus scrofa	18-58
120016-0	1979	Intravenous nitroglycerin to improve coronary blood flow and left ventricular performance during vasopressin therapy.	Nitroglycerin	12-25	arginine vasopressin	Homo sapiens	97-108
235996-1	1975	Trinitroglycerin oxidizes the essential sulfhydryl group, Cys-149, of pig muscle glyceraldehyde-3-phosphate dehydrogenase (D-glyceraldehyde-3-phosphate : NAD+ oxidoreductase(phosphorylating) EC 1.2.1.12) TO A SLUFENIC ACID, NOT TO A DISULFIDE.	Nitroglycerin	0-16	glyceraldehyde-3-phosphate dehydrogenase	Sus scrofa	81-121
814761-3	1975	The use of nitroglycerin sample permitted to reveal in practically healthy relatives certain REG changes which exceeded the normal limits.	Nitroglycerin	11-24	regenerating family member 1 alpha	Homo sapiens	93-96
4961855-0	1967	[Effect of sodium nitrate and nitroglycerine on incorporation of P-32 into energetic phosphates in the heart--antagonism to noradrenaline].	Nitroglycerin	30-44	inhibitor of growth family member 2	Homo sapiens	65-69
33252452-3	2021	In a mouse model of chronic migraine, repeated nitroglycerin (NTG) administration significantly increased the number of CGRP-R and PACAP-R neurons in TG but not dorsal root ganglia.	Nitroglycerin	47-60	calcitonin receptor like receptor	Homo sapiens	120-126
33252452-3	2021	In a mouse model of chronic migraine, repeated nitroglycerin (NTG) administration significantly increased the number of CGRP-R and PACAP-R neurons in TG but not dorsal root ganglia.	Nitroglycerin	62-65	calcitonin receptor like receptor	Homo sapiens	120-126
33252452-4	2021	In TG neurons that express endogenous alphaCGRP, repeated NTG led to a 7-fold increase in the number of neurons that respond to both CGRP and PACAP (CGRP-R&PACAP-R).	Nitroglycerin	58-61	calcitonin/calcitonin-related polypeptide, alpha	Mus musculus	43-47
33252452-4	2021	In TG neurons that express endogenous alphaCGRP, repeated NTG led to a 7-fold increase in the number of neurons that respond to both CGRP and PACAP (CGRP-R&PACAP-R).	Nitroglycerin	58-61	adenylate cyclase activating polypeptide 1	Mus musculus	142-147
33252452-4	2021	In TG neurons that express endogenous alphaCGRP, repeated NTG led to a 7-fold increase in the number of neurons that respond to both CGRP and PACAP (CGRP-R&PACAP-R).	Nitroglycerin	58-61	adenylate cyclase activating polypeptide 1	Mus musculus	149-163
33713748-0	2021	Insulin-Like Growth Factor-1 Inhibits Nitroglycerin-Induced Trigeminal Activation of Oxidative Stress, Calcitonin Gene-Related Peptide and c-Fos Expression.	Nitroglycerin	38-51	insulin-like growth factor 1	Rattus norvegicus	0-28
33713748-0	2021	Insulin-Like Growth Factor-1 Inhibits Nitroglycerin-Induced Trigeminal Activation of Oxidative Stress, Calcitonin Gene-Related Peptide and c-Fos Expression.	Nitroglycerin	38-51	calcitonin-related polypeptide alpha	Rattus norvegicus	103-134
33713748-0	2021	Insulin-Like Growth Factor-1 Inhibits Nitroglycerin-Induced Trigeminal Activation of Oxidative Stress, Calcitonin Gene-Related Peptide and c-Fos Expression.	Nitroglycerin	38-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-144
33713748-9	2021	Measurements taken two hours later after nitroglycerin alone showed increased surrogate markers of trigeminal activation - oxidative stress and CGRP in the trigeminal ganglion and c-Fos in the trigeminocervical complex compared to vehicle control.	Nitroglycerin	41-54	calcitonin-related polypeptide alpha	Rattus norvegicus	144-148
33883930-10	2021	Both TA-MS-HP-beta-CD and TA-MS-M-beta-CD used at 50 mg/kg more effectively attenuated tactile allodynia in NTG-treated mice than the same dose of pure TA.	Nitroglycerin	108-111	adrenocortical dysplasia	Mus musculus	14-21
33856345-5	2021	The human migraine trigger, nitroglycerin, produced chronic migraine-associated pain and decreased neurite growth in headache-processing regions, which were reversed by HDAC6 inhibition.	Nitroglycerin	28-41	histone deacetylase 6	Homo sapiens	169-174
33883930-10	2021	Both TA-MS-HP-beta-CD and TA-MS-M-beta-CD used at 50 mg/kg more effectively attenuated tactile allodynia in NTG-treated mice than the same dose of pure TA.	Nitroglycerin	108-111	adrenocortical dysplasia	Mus musculus	34-41
33486763-6	2021	Treatment of patients with high dose N-acetylcysteine (NAC) plus glyceryl trinitrate rapidly increased platelet responsiveness to SNP and decreased plasma syndecan-1 concentrations.	Nitroglycerin	65-84	syndecan 1	Homo sapiens	155-165
33256564-7	2021	We find that the normalized diffusion and release of hEGF increases with free water content in injectable hydrogels: ranging from 0.176 at 41% free water in HA-Tyr to 0.2 at 53% free water in Gtn-HPA, while it is decreasing with hydrogel stiffness: 600 Pa for Gtn-HPA and 1440 Pa for HA-Tyr.	Nitroglycerin	192-195	epidermal growth factor	Homo sapiens	53-57
33605657-8	2021	In addition, a corresponding increase in CGRP expression in the trigeminal ganglia and trigeminal nucleus caudalis was observed after chronic nitroglycerin, an augmentation that was blocked by SNC80.	Nitroglycerin	142-155	calcitonin related polypeptide alpha	Homo sapiens	41-45
33597821-12	2021	GTN stimulation increased both CRLR/CGRPR1 expression, and immunostaining was apparent in microglia and meningeal cells.	Nitroglycerin	0-3	calcitonin receptor like receptor	Homo sapiens	31-35
33587406-4	2021	By contrast, after NTG administration, PEA levels increased in the MIG group at T120 (p=0.004), while remaining stable in the HC group.NTG administration induced central sensitization in the MIG group, which was recorded as reductions in RTh (p=0.046) at T30 and T120, and in TST (p=0.001) at all time points.	Nitroglycerin	135-138	thiosulfate sulfurtransferase	Homo sapiens	276-279
33534356-5	2021	Chronic glyceryl trinitrate (GTN, 10 mg/kg) administration led to increased sensitivity to mechanical stimuli, and increased expression of phosphorylated protein kinase A (p-PKA), neuronal nitric oxide synthase (nNOS), and transient receptor potential ankyrin 1 (TRPA1) proteins in trigeminal ganglia.	Nitroglycerin	8-27	nitric oxide synthase 1, neuronal	Mus musculus	180-210
33534356-5	2021	Chronic glyceryl trinitrate (GTN, 10 mg/kg) administration led to increased sensitivity to mechanical stimuli, and increased expression of phosphorylated protein kinase A (p-PKA), neuronal nitric oxide synthase (nNOS), and transient receptor potential ankyrin 1 (TRPA1) proteins in trigeminal ganglia.	Nitroglycerin	8-27	nitric oxide synthase 1, neuronal	Mus musculus	212-216
33534356-5	2021	Chronic glyceryl trinitrate (GTN, 10 mg/kg) administration led to increased sensitivity to mechanical stimuli, and increased expression of phosphorylated protein kinase A (p-PKA), neuronal nitric oxide synthase (nNOS), and transient receptor potential ankyrin 1 (TRPA1) proteins in trigeminal ganglia.	Nitroglycerin	8-27	transient receptor potential cation channel, subfamily A, member 1	Mus musculus	223-261
33534356-5	2021	Chronic glyceryl trinitrate (GTN, 10 mg/kg) administration led to increased sensitivity to mechanical stimuli, and increased expression of phosphorylated protein kinase A (p-PKA), neuronal nitric oxide synthase (nNOS), and transient receptor potential ankyrin 1 (TRPA1) proteins in trigeminal ganglia.	Nitroglycerin	8-27	transient receptor potential cation channel, subfamily A, member 1	Mus musculus	263-268
33534356-5	2021	Chronic glyceryl trinitrate (GTN, 10 mg/kg) administration led to increased sensitivity to mechanical stimuli, and increased expression of phosphorylated protein kinase A (p-PKA), neuronal nitric oxide synthase (nNOS), and transient receptor potential ankyrin 1 (TRPA1) proteins in trigeminal ganglia.	Nitroglycerin	29-32	nitric oxide synthase 1, neuronal	Mus musculus	180-210
33534356-5	2021	Chronic glyceryl trinitrate (GTN, 10 mg/kg) administration led to increased sensitivity to mechanical stimuli, and increased expression of phosphorylated protein kinase A (p-PKA), neuronal nitric oxide synthase (nNOS), and transient receptor potential ankyrin 1 (TRPA1) proteins in trigeminal ganglia.	Nitroglycerin	29-32	nitric oxide synthase 1, neuronal	Mus musculus	212-216
33534356-5	2021	Chronic glyceryl trinitrate (GTN, 10 mg/kg) administration led to increased sensitivity to mechanical stimuli, and increased expression of phosphorylated protein kinase A (p-PKA), neuronal nitric oxide synthase (nNOS), and transient receptor potential ankyrin 1 (TRPA1) proteins in trigeminal ganglia.	Nitroglycerin	29-32	transient receptor potential cation channel, subfamily A, member 1	Mus musculus	223-261
33534356-5	2021	Chronic glyceryl trinitrate (GTN, 10 mg/kg) administration led to increased sensitivity to mechanical stimuli, and increased expression of phosphorylated protein kinase A (p-PKA), neuronal nitric oxide synthase (nNOS), and transient receptor potential ankyrin 1 (TRPA1) proteins in trigeminal ganglia.	Nitroglycerin	29-32	transient receptor potential cation channel, subfamily A, member 1	Mus musculus	263-268
33534356-10	2021	Subsequent challenge with a previously ineffective low-dose GTN (0.1-0.3 mg/kg) revealed latent behavioral sensitization and increased expression of p-PKA, nNOS, and TRPA1 proteins in trigeminal ganglia.	Nitroglycerin	60-63	nitric oxide synthase 1, neuronal	Mus musculus	156-160
33534356-10	2021	Subsequent challenge with a previously ineffective low-dose GTN (0.1-0.3 mg/kg) revealed latent behavioral sensitization and increased expression of p-PKA, nNOS, and TRPA1 proteins in trigeminal ganglia.	Nitroglycerin	60-63	transient receptor potential cation channel, subfamily A, member 1	Mus musculus	166-171
33450066-10	2021	In contrast, inhibition of ALDH2 by benomyl (10 muM) inhibited NTG-induced nitrite production and relaxation and deletion of POR did not modulate this response.	Nitroglycerin	63-66	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	27-32
33040175-0	2021	Presence of the aldehyde dehydrogenase 2 variant ALDH2*2 considerably increases EC50 of nitroglycerin.	Nitroglycerin	88-101	aldehyde dehydrogenase 2 family member	Homo sapiens	16-40
33040175-0	2021	Presence of the aldehyde dehydrogenase 2 variant ALDH2*2 considerably increases EC50 of nitroglycerin.	Nitroglycerin	88-101	aldehyde dehydrogenase 2 family member	Homo sapiens	49-54
33256564-7	2021	We find that the normalized diffusion and release of hEGF increases with free water content in injectable hydrogels: ranging from 0.176 at 41% free water in HA-Tyr to 0.2 at 53% free water in Gtn-HPA, while it is decreasing with hydrogel stiffness: 600 Pa for Gtn-HPA and 1440 Pa for HA-Tyr.	Nitroglycerin	260-263	epidermal growth factor	Homo sapiens	53-57
33402188-0	2021	P2X7R-mediated autophagic impairment contributes to central sensitization in a chronic migraine model with recurrent nitroglycerin stimulation in mice.	Nitroglycerin	117-130	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	0-5
33402188-12	2021	RESULTS: The expression of P2X7R was increased and was mainly colocalized with microglia in the TNC following recurrent NTG administration.	Nitroglycerin	120-123	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	27-32
33336110-3	2021	In this study, we fabricated a Carbomer-based contraceptive gel consisting of three agents: tenofovir, gossypol acetate, and nitroglycerin (TGN), with pH adjusted to 4.5 (to be compatible with the vagina).	Nitroglycerin	125-138	thyroglobulin	Rattus norvegicus	140-143
33326598-0	2021	A non-convulsant delta-opioid receptor agonist, KNT-127, reduces cortical spreading depression and nitroglycerin-induced allodynia.	Nitroglycerin	99-112	opioid receptor, delta 1	Mus musculus	17-38
33129939-2	2021	We have previously shown that the peripherally restricted FAAH inhibitor, URB937, prevents nitroglycerin-induced hyperalgesia - an animal model of migraine - and attenuates the activation of brain areas that are relevant for migraine pain, e.g. trigeminal nucleus caudalis and locus coeruleus.	Nitroglycerin	91-104	fatty acid amide hydrolase	Homo sapiens	58-62
33129939-10	2021	The results show that peripheral FAAH inhibition by URB937 effectively reduces both acute and chronic NTG-induced trigeminal hyperalgesia, likely via augmented anandamide-mediated CB1 receptor activation.	Nitroglycerin	102-105	fatty-acid amide hydrolase-like	Rattus norvegicus	33-37
33459716-6	2021	Aggregated tau pathology in the bilateral hippocampus was more prominent in Tg601 mice than in NTg mice.	Nitroglycerin	95-98	microtubule associated protein tau	Homo sapiens	11-14
33128338-6	2021	In Apoe-/- mice, nitroglycerine infusion increased both Akt S-Nitrosylation and infarct size, reduced Akt activity and capillary density, and delayed the recovery of cardiac function in ischaemic hearts, compared with mice infused with vehicle.	Nitroglycerin	17-31	apolipoprotein E	Mus musculus	3-7
33128338-6	2021	In Apoe-/- mice, nitroglycerine infusion increased both Akt S-Nitrosylation and infarct size, reduced Akt activity and capillary density, and delayed the recovery of cardiac function in ischaemic hearts, compared with mice infused with vehicle.	Nitroglycerin	17-31	thymoma viral proto-oncogene 1	Mus musculus	56-59
33128338-6	2021	In Apoe-/- mice, nitroglycerine infusion increased both Akt S-Nitrosylation and infarct size, reduced Akt activity and capillary density, and delayed the recovery of cardiac function in ischaemic hearts, compared with mice infused with vehicle.	Nitroglycerin	17-31	thymoma viral proto-oncogene 1	Mus musculus	102-105
33128338-7	2021	Importantly, these in vivo effects of nitroglycerine in Apoe-/- mice were remarkably prevented by adenovirus-mediated enforced expression of Akt-C296/344A mutant.	Nitroglycerin	38-52	apolipoprotein E	Mus musculus	56-60
33128338-7	2021	Importantly, these in vivo effects of nitroglycerine in Apoe-/- mice were remarkably prevented by adenovirus-mediated enforced expression of Akt-C296/344A mutant.	Nitroglycerin	38-52	thymoma viral proto-oncogene 1	Mus musculus	141-144
33179114-4	2021	The pharmacological effects of nitroglycerine and rutaecarpine have been demonstrated to be associated with an increase in the synthesis and release of CGRP.	Nitroglycerin	31-45	calcitonin related polypeptide alpha	Homo sapiens	152-156
33111258-7	2021	After 5 sessions of NTG injections, the GABA-synthesizing enzyme, 65-kDa glutamate decarboxylase (GAD65), but not the GABA transporter 1 (GAT1) or the alpha6 subunit-containing GABAA receptors (alpha6GABAARs), was downregulated in mouse TG tissues.	Nitroglycerin	20-23	glutamic acid decarboxylase 2	Mus musculus	98-103
32777344-6	2020	The number and size of Ang II-induced aorta collateral aneurysms and atherosclerotic lesions in the renal artery and aortic root of SDN mice were significantly decreased compared to NTg mice, and directly correlated with a decrease in OPN expression.	Nitroglycerin	182-185	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	23-29
33261640-10	2020	We found that VPS35 D620N Tg mice displayed a significantly higher dopamine level than NTg counterparts.	Nitroglycerin	87-90	VPS35 retromer complex component	Mus musculus	14-19
33323164-9	2020	However, mice given NG had a significant reduction in IL6 and TNFalpha in BAL fluid and no significant differences in CCL2, IL4, IL10, CXCL1, CXCL2, and VEGF.	Nitroglycerin	20-22	interleukin 6	Mus musculus	54-57
33323164-9	2020	However, mice given NG had a significant reduction in IL6 and TNFalpha in BAL fluid and no significant differences in CCL2, IL4, IL10, CXCL1, CXCL2, and VEGF.	Nitroglycerin	20-22	tumor necrosis factor	Mus musculus	62-70
32644795-2	2020	In the present study, by coating ~ 3 nm MoSx on nitrogen-doped graphene (NG) pre-engrafted on a flexible carbon cloth (MNG) as a model system, an extremely low Tafel slope of 39.6 mV dec-1 with cyclic stability up to 5000 cycles is obtained.	Nitroglycerin	73-75	deleted in esophageal cancer 1	Homo sapiens	183-188
32686605-10	2020	Besides, NTG administration increased CGRP expression in the Vc of rats.	Nitroglycerin	9-12	calcitonin-related polypeptide alpha	Rattus norvegicus	38-42
33077757-3	2020	In a model of chronic migraine-associated pain using the human migraine trigger, nitroglycerin, we observed increased expression of DOR in cortex, hippocampus, and striatum; suggesting a role for these forebrain regions in the regulation of migraine.	Nitroglycerin	81-94	opioid receptor, delta 1	Mus musculus	132-135
32745488-7	2020	NTG caused significant freezing behavior, which was prevented by all OrxA doses.	Nitroglycerin	0-3	hypocretin neuropeptide precursor	Rattus norvegicus	69-73
32745488-8	2020	Moreover, OrxA (100 pM) could obstruct NTG-induced increases in facial rubbing and decreases in climbing and body grooming.	Nitroglycerin	39-42	hypocretin neuropeptide precursor	Rattus norvegicus	10-14
32745488-9	2020	Furthermore, NTG-induced light aversion and thermal hyperalgesia were attenuated by OrxA at doses of 50 and 100 pM.	Nitroglycerin	13-16	hypocretin neuropeptide precursor	Rattus norvegicus	84-88
32745488-11	2020	Besides, OrxA (100 pM) decreased NTG-induced CGRP upregulation.	Nitroglycerin	33-36	hypocretin neuropeptide precursor	Rattus norvegicus	9-13
32745488-11	2020	Besides, OrxA (100 pM) decreased NTG-induced CGRP upregulation.	Nitroglycerin	33-36	calcitonin-related polypeptide alpha	Rattus norvegicus	45-49
32745488-12	2020	The data revealed that the activation of Orx1Rs in the vlPAG is effective in relieving NTG-induced migraine symptoms mainly by the downregulation of CGRP in the Vc of rats.	Nitroglycerin	87-90	calcitonin-related polypeptide alpha	Rattus norvegicus	149-153
32706883-7	2020	RESULTS: Greater IL-6 reactivity to stress, measured with baseline-adjusted area under the curve, predicted 12-month decrease in flow-mediated dilatation of the brachial artery (P = 0.0005), a measure of endothelial-dependent vascular function, but not in endothelial-independent function measured with nitroglycerin-mediated dilatation (P = 0.17).	Nitroglycerin	303-316	interleukin 6	Homo sapiens	17-21
32505063-10	2020	Change in SBP from baseline after 2 h of drug administration was significantly higher with labetalol (p = 0.028 for patients eligible for reperfusion), amlodipine (p = 0.014), and nitroglycerine (p = 0.044).	Nitroglycerin	180-194	selenium binding protein 1	Homo sapiens	10-13
32639078-7	2022	Methanandamide attenuated nitroglycerin-induced CGRP increments in in-vivo plasma, trigeminal ganglia and brainstem and also in ex-vivo hemiskull preparations.	Nitroglycerin	26-39	calcitonin-related polypeptide alpha	Rattus norvegicus	48-52
32173888-1	2020	This study aimed to assess the protective effect of nitroglycerin, a commonly used drug in cardiovascular diseases, on mice with acute liver injury induced by carbon tetrachloride (CCl4 ).	Nitroglycerin	52-65	chemokine (C-C motif) ligand 4	Mus musculus	181-185
32173888-5	2020	Analysis of the amounts of serum alanine aminotransferase (ALT)/aspartate aminotransferase (AST), hepatic glutathione (GSH), and malondialdehyde (MDA) showed that nitroglycerin protected against CCl4 -induced acute liver injury.	Nitroglycerin	163-176	glutamic pyruvic transaminase, soluble	Mus musculus	33-57
32173888-5	2020	Analysis of the amounts of serum alanine aminotransferase (ALT)/aspartate aminotransferase (AST), hepatic glutathione (GSH), and malondialdehyde (MDA) showed that nitroglycerin protected against CCl4 -induced acute liver injury.	Nitroglycerin	163-176	chemokine (C-C motif) ligand 4	Mus musculus	195-199
32173888-7	2020	Furthermore, we found that nitroglycerin suppressed the increase of T helper 17 (Th17) cells in CCl4 -induced acute liver injury mice.	Nitroglycerin	27-40	chemokine (C-C motif) ligand 4	Mus musculus	96-100
32366615-15	2020	CONCLUSION: The observed rate of relief after oral nitroglycerin solution for EFI is disappointing but comparable to previous glucagon, benzodiazepines and effervescent beverage studies, and that of placebo.	Nitroglycerin	51-64	glucagon	Homo sapiens	126-134
32326776-5	2020	We observed additive impairment of noise exposure and genetic Ogg1 deficiency on endothelium-independent relaxation (nitroglycerine), which may be due to exacerbated oxidative DNA damage leading to leukocyte activation and oxidative aldehyde dehydrogenase inhibition.Conclusions: The finding that chronic noise exposure causes oxidative DNA damage in mice is worrisome since these potential mutagenic lesions could contribute to cancer progression.	Nitroglycerin	117-131	8-oxoguanine DNA-glycosylase 1	Mus musculus	62-66
32278976-8	2020	In addition, Ro 64-6198 can dose dependently block NTG-induced paw and head allodynia, an effect that is blocked by the NOP antagonist, SB-612111.	Nitroglycerin	51-54	opioid related nociceptin receptor 1	Homo sapiens	120-123
32516986-9	2020	MMTL pretreatment significantly upregulated the protein level of CGRP in the spinal trigeminal nucleus caudalis after NTG injection.	Nitroglycerin	118-121	calcitonin/calcitonin-related polypeptide, alpha	Mus musculus	65-69
32516986-10	2020	Our results indicate that a pre-existing myogenic TMD can upregulate NTG-induced trigeminal CGRP and enhance migraine-like hypersensitivity.	Nitroglycerin	69-72	calcitonin/calcitonin-related polypeptide, alpha	Mus musculus	92-96
32147481-0	2020	Evodiamine via targeting nNOS and AMPA receptor GluA1 inhibits nitroglycerin-induced migraine-like response.	Nitroglycerin	63-76	nitric oxide synthase 1	Rattus norvegicus	25-29
32147481-0	2020	Evodiamine via targeting nNOS and AMPA receptor GluA1 inhibits nitroglycerin-induced migraine-like response.	Nitroglycerin	63-76	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	48-53
32275117-3	2020	In this study, we demonstrated that tumor necrosis factor receptor-associated factor 3 (TRAF3) regulates mitochondrial ROS production and promotes TLR agonist LPS plus nigericin (LPS/Ng)-induced inflammasome and pyroptosis in mouse primary macrophages and human monocyte THP-1 cells.	Nitroglycerin	183-185	TNF receptor-associated factor 3	Mus musculus	36-86
32275117-3	2020	In this study, we demonstrated that tumor necrosis factor receptor-associated factor 3 (TRAF3) regulates mitochondrial ROS production and promotes TLR agonist LPS plus nigericin (LPS/Ng)-induced inflammasome and pyroptosis in mouse primary macrophages and human monocyte THP-1 cells.	Nitroglycerin	183-185	TNF receptor-associated factor 3	Mus musculus	88-93
31991513-3	2020	During rewarming period, patients were given intravenous nitroglycerin with an infusion rate 5 and 1 microg kg-1  min-1 in high-dose and low-dose groups, respectively.	Nitroglycerin	57-70	CD59 molecule (CD59 blood group)	Homo sapiens	114-119
31991513-8	2020	CONCLUSIONS: High-dose nitroglycerin administered during cardiopulmonary bypass improves erythrocyte deformability through activating phosphorylation of aquaporin 1, vasodilator-stimulated phosphoprotein and focal adhesion kinase in erythrocytes.	Nitroglycerin	23-36	aquaporin 1 (Colton blood group)	Homo sapiens	153-164
31991513-8	2020	CONCLUSIONS: High-dose nitroglycerin administered during cardiopulmonary bypass improves erythrocyte deformability through activating phosphorylation of aquaporin 1, vasodilator-stimulated phosphoprotein and focal adhesion kinase in erythrocytes.	Nitroglycerin	23-36	vasodilator stimulated phosphoprotein	Homo sapiens	166-203
31522561-4	2020	Thus, we investigated the relationship between ASB10 and NTG in a Korean cohort.	Nitroglycerin	57-60	ankyrin repeat and SOCS box containing 10	Homo sapiens	47-52
31522561-5	2020	METHODS: Whole-exome sequencing was performed to identify the ASB10 variants in one patient with a strong NTG family history.	Nitroglycerin	106-109	ankyrin repeat and SOCS box containing 10	Homo sapiens	62-67
31794788-16	2020	IHC experiments further showed that RYZBPTM up-regulated SP expression levels and enhanced NK1R levels in the NTG-induced migraine rats (P < 0.05).	Nitroglycerin	110-113	tachykinin receptor 1	Rattus norvegicus	91-95
32062367-0	2020	GC-MS and LC-MS/MS pilot studies on the guanidine (NG)-dimethylation in native, asymmetrically and symmetrically NG-dimethylated arginine-vasopressin peptides and proteins in human red blood cells.	Nitroglycerin	51-53	arginine vasopressin	Homo sapiens	138-149
31640402-10	2020	The protein levels of PD-L1 were significantly increased 2 h, 4 h and 6 h after treatment, and PD-1 was significantly increased at 2 h and 6 h. The blockade of PD-1 increased acute nitroglycerin-induced hyperalgesia, and this effect was accompanied by a more significant increase in calcitonin gene-related peptide, IL-1beta, TNF-alpha, IL-6 and IL-18 in the trigeminal ganglia.	Nitroglycerin	181-194	interleukin 6	Mus musculus	337-341
31640402-10	2020	The protein levels of PD-L1 were significantly increased 2 h, 4 h and 6 h after treatment, and PD-1 was significantly increased at 2 h and 6 h. The blockade of PD-1 increased acute nitroglycerin-induced hyperalgesia, and this effect was accompanied by a more significant increase in calcitonin gene-related peptide, IL-1beta, TNF-alpha, IL-6 and IL-18 in the trigeminal ganglia.	Nitroglycerin	181-194	interleukin 18	Mus musculus	346-351
31868992-0	2020	Automated Dynamic Clamp for Simulation of IK1 in Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes in Real Time Using Patchliner Dynamite8.	Nitroglycerin	138-147	IKAROS family zinc finger 1	Homo sapiens	42-45
31594384-4	2020	METHODS: In 16 women with migraine without aura and 10 age- and gender-matched controls without headache, intravenous nitroglycerin (0.5 microg kg-1 min-1) was administered.	Nitroglycerin	118-131	CD59 molecule (CD59 blood group)	Homo sapiens	149-154
31640402-9	2020	The mRNA levels of PD-L1 and PD-1 were significantly elevated 2 h, 4 h and 6 h after acute nitroglycerin treatment (p &lt; 0.05).	Nitroglycerin	91-104	CD274 antigen	Mus musculus	19-24
31640402-9	2020	The mRNA levels of PD-L1 and PD-1 were significantly elevated 2 h, 4 h and 6 h after acute nitroglycerin treatment (p &lt; 0.05).	Nitroglycerin	91-104	programmed cell death 1	Mus musculus	29-33
31640402-10	2020	The protein levels of PD-L1 were significantly increased 2 h, 4 h and 6 h after treatment, and PD-1 was significantly increased at 2 h and 6 h. The blockade of PD-1 increased acute nitroglycerin-induced hyperalgesia, and this effect was accompanied by a more significant increase in calcitonin gene-related peptide, IL-1beta, TNF-alpha, IL-6 and IL-18 in the trigeminal ganglia.	Nitroglycerin	181-194	CD274 antigen	Mus musculus	22-27
31640402-10	2020	The protein levels of PD-L1 were significantly increased 2 h, 4 h and 6 h after treatment, and PD-1 was significantly increased at 2 h and 6 h. The blockade of PD-1 increased acute nitroglycerin-induced hyperalgesia, and this effect was accompanied by a more significant increase in calcitonin gene-related peptide, IL-1beta, TNF-alpha, IL-6 and IL-18 in the trigeminal ganglia.	Nitroglycerin	181-194	programmed cell death 1	Mus musculus	95-99
31640402-10	2020	The protein levels of PD-L1 were significantly increased 2 h, 4 h and 6 h after treatment, and PD-1 was significantly increased at 2 h and 6 h. The blockade of PD-1 increased acute nitroglycerin-induced hyperalgesia, and this effect was accompanied by a more significant increase in calcitonin gene-related peptide, IL-1beta, TNF-alpha, IL-6 and IL-18 in the trigeminal ganglia.	Nitroglycerin	181-194	programmed cell death 1	Mus musculus	160-164
31640402-10	2020	The protein levels of PD-L1 were significantly increased 2 h, 4 h and 6 h after treatment, and PD-1 was significantly increased at 2 h and 6 h. The blockade of PD-1 increased acute nitroglycerin-induced hyperalgesia, and this effect was accompanied by a more significant increase in calcitonin gene-related peptide, IL-1beta, TNF-alpha, IL-6 and IL-18 in the trigeminal ganglia.	Nitroglycerin	181-194	interleukin 1 beta	Mus musculus	316-324
31640402-10	2020	The protein levels of PD-L1 were significantly increased 2 h, 4 h and 6 h after treatment, and PD-1 was significantly increased at 2 h and 6 h. The blockade of PD-1 increased acute nitroglycerin-induced hyperalgesia, and this effect was accompanied by a more significant increase in calcitonin gene-related peptide, IL-1beta, TNF-alpha, IL-6 and IL-18 in the trigeminal ganglia.	Nitroglycerin	181-194	tumor necrosis factor	Mus musculus	326-335
31794788-18	2020	Both RT-qPCR and western blotting trials indicated that RYZBP treatment significantly decreased CCK and CGRP expression levels (P < 0.01 or P < 0.05) in the NTG-induced migraine rats.	Nitroglycerin	157-160	cholecystokinin	Rattus norvegicus	96-99
31937253-11	2020	5-BDBD or ANA-12 prevented hyperalgesia induced by NTG, which was associated with a significant inhibition of the NTG-induced increase in phosphorylated extracellular regulated protein kinases (p-ERK) and calcitonin gene related peptide (CGRP) release in the TNC.	Nitroglycerin	114-117	mitogen-activated protein kinase 1	Mus musculus	196-199
32185753-10	2020	Significantly more intense staining for CD 34 was found in the nitroglycerin group compared with the other groups.	Nitroglycerin	63-76	CD34 molecule	Homo sapiens	40-45
32009064-1	2020	BACKGROUND: Aldehyde dehydrogenase 2 (ALDH2) plays a central role in the biotransformation of glyceryl trinitrate (GTN) or nitroglycerin, which is widely used for the treatment of coronary artery disease (CAD).	Nitroglycerin	94-113	aldehyde dehydrogenase 2 family member	Homo sapiens	12-36
32009064-1	2020	BACKGROUND: Aldehyde dehydrogenase 2 (ALDH2) plays a central role in the biotransformation of glyceryl trinitrate (GTN) or nitroglycerin, which is widely used for the treatment of coronary artery disease (CAD).	Nitroglycerin	94-113	aldehyde dehydrogenase 2 family member	Homo sapiens	38-43
32009064-1	2020	BACKGROUND: Aldehyde dehydrogenase 2 (ALDH2) plays a central role in the biotransformation of glyceryl trinitrate (GTN) or nitroglycerin, which is widely used for the treatment of coronary artery disease (CAD).	Nitroglycerin	115-118	aldehyde dehydrogenase 2 family member	Homo sapiens	12-36
32009064-1	2020	BACKGROUND: Aldehyde dehydrogenase 2 (ALDH2) plays a central role in the biotransformation of glyceryl trinitrate (GTN) or nitroglycerin, which is widely used for the treatment of coronary artery disease (CAD).	Nitroglycerin	115-118	aldehyde dehydrogenase 2 family member	Homo sapiens	38-43
32009064-1	2020	BACKGROUND: Aldehyde dehydrogenase 2 (ALDH2) plays a central role in the biotransformation of glyceryl trinitrate (GTN) or nitroglycerin, which is widely used for the treatment of coronary artery disease (CAD).	Nitroglycerin	123-136	aldehyde dehydrogenase 2 family member	Homo sapiens	12-36
32009064-1	2020	BACKGROUND: Aldehyde dehydrogenase 2 (ALDH2) plays a central role in the biotransformation of glyceryl trinitrate (GTN) or nitroglycerin, which is widely used for the treatment of coronary artery disease (CAD).	Nitroglycerin	123-136	aldehyde dehydrogenase 2 family member	Homo sapiens	38-43
32009064-6	2020	CONCLUSIONS: Continuous administration of GTN produced endothelial dysfunction as well as nitrate tolerance in bothALDH2*1/1andALDH2*2patients with CSA.ALDH2*2attenuated GTN response and exacerbated GTN tolerance, but not endothelial dysfunction, as compared toALDH2*1/*1in patients with CSA.	Nitroglycerin	42-45	aldehyde dehydrogenase 2 family member	Homo sapiens	115-120
31912870-6	2020	Concentrations of GTN known to primarily activate the NO/cGMP pathway (100 nM-1 microM) inhibited hypoxia-induced HIF-1alpha protein accumulation in a time-dependent manner.	Nitroglycerin	18-21	hypoxia inducible factor 1 subunit alpha	Homo sapiens	114-124
31912870-8	2020	Furthermore, treatment of cells with the calpain (Ca2+-activated proteinase) inhibitor calpastatin attenuated the effects of GTN and 8-Bromo-cGMP on HIF-1alpha accumulation.	Nitroglycerin	125-128	hypoxia inducible factor 1 subunit alpha	Homo sapiens	149-159
32062637-0	2020	Nitroglycerin Tolerance in Patients With ALDH2 Variant.	Nitroglycerin	0-13	aldehyde dehydrogenase 2 family member	Homo sapiens	41-46
32066464-13	2020	CONCLUSION: These results provided the evidence that DMF, by Nrf-2 modulation, has a protective effect on central sensitization induced by NTG, suggesting a new insight into the potential application of DMF as novel candidates in drug development for migraine.	Nitroglycerin	139-142	NFE2 like bZIP transcription factor 2	Homo sapiens	61-66
31707574-5	2020	Anti-inflammatory thymoquinone ameliorated GTN-stimulated CGRP levels in plasma, and migraine-related structures including trigeminal ganglion and brainstem; moreover, thymoquinone inhibited degranulation of MMCs and prevented the increase in the number of MMCs in GTN-induced in vivo migraine model.	Nitroglycerin	43-46	calcitonin-related polypeptide alpha	Rattus norvegicus	58-62
31629892-2	2020	We previously reported that the peripherally restricted FAAH inhibitor URB937, which selectively increases AEA levels outside the central nervous system, reduces hyperalgesia and c-Fos expression in the trigeminal nucleus caudalis (TNC) and the locus coeruleus in an animal model of migraine based on nitroglycerin (NTG) administration.	Nitroglycerin	301-314	fatty-acid amide hydrolase-like	Rattus norvegicus	56-60
31629892-2	2020	We previously reported that the peripherally restricted FAAH inhibitor URB937, which selectively increases AEA levels outside the central nervous system, reduces hyperalgesia and c-Fos expression in the trigeminal nucleus caudalis (TNC) and the locus coeruleus in an animal model of migraine based on nitroglycerin (NTG) administration.	Nitroglycerin	316-319	fatty-acid amide hydrolase-like	Rattus norvegicus	56-60
31912870-0	2020	Inhibition of Hypoxia-Inducible Factor 1 Alpha Accumulation by Glyceryl Trinitrate and Cyclic Guanosine Monophosphate.	Nitroglycerin	63-82	hypoxia inducible factor 1 subunit alpha	Homo sapiens	14-46
31912870-5	2020	Using human DU145 prostate cancer cells, we assessed the effect of the NO mimetic glyceryl trinitrate (GTN) and the cGMP analogue 8-Bromo-cGMP on hypoxic accumulation of HIF-1alpha.	Nitroglycerin	82-101	hypoxia inducible factor 1 subunit alpha	Homo sapiens	170-180
31937253-0	2020	Microglia P2X4R-BDNF signalling contributes to central sensitization in a recurrent nitroglycerin-induced chronic migraine model.	Nitroglycerin	84-97	brain derived neurotrophic factor	Mus musculus	16-20
31937253-10	2020	RESULTS: Chronic intermittent administration of NTG resulted in chronic mechanical and thermal hyperalgesia, accompanied by the upregulation of P2X4Rs and BDNF expression.	Nitroglycerin	48-51	brain derived neurotrophic factor	Mus musculus	155-159
31937253-11	2020	5-BDBD or ANA-12 prevented hyperalgesia induced by NTG, which was associated with a significant inhibition of the NTG-induced increase in phosphorylated extracellular regulated protein kinases (p-ERK) and calcitonin gene related peptide (CGRP) release in the TNC.	Nitroglycerin	51-54	mitogen-activated protein kinase 1	Mus musculus	196-199
31937253-11	2020	5-BDBD or ANA-12 prevented hyperalgesia induced by NTG, which was associated with a significant inhibition of the NTG-induced increase in phosphorylated extracellular regulated protein kinases (p-ERK) and calcitonin gene related peptide (CGRP) release in the TNC.	Nitroglycerin	51-54	calcitonin/calcitonin-related polypeptide, alpha	Mus musculus	205-236
31937253-11	2020	5-BDBD or ANA-12 prevented hyperalgesia induced by NTG, which was associated with a significant inhibition of the NTG-induced increase in phosphorylated extracellular regulated protein kinases (p-ERK) and calcitonin gene related peptide (CGRP) release in the TNC.	Nitroglycerin	51-54	calcitonin/calcitonin-related polypeptide, alpha	Mus musculus	238-242
31937253-11	2020	5-BDBD or ANA-12 prevented hyperalgesia induced by NTG, which was associated with a significant inhibition of the NTG-induced increase in phosphorylated extracellular regulated protein kinases (p-ERK) and calcitonin gene related peptide (CGRP) release in the TNC.	Nitroglycerin	114-117	calcitonin/calcitonin-related polypeptide, alpha	Mus musculus	205-236
31937794-9	2020	For gene-based testing, METTL20 showed a significant association in POAG (Pcombined = 0.002) and in the subgroup of NTG (Pcombined = 0.02), whereas ZNF677 were significantly associated with only in the subgroup of high-tension glaucoma (Pcombined = 1.5E-06).	Nitroglycerin	116-119	electron transfer flavoprotein subunit beta lysine methyltransferase	Homo sapiens	24-31
31937253-11	2020	5-BDBD or ANA-12 prevented hyperalgesia induced by NTG, which was associated with a significant inhibition of the NTG-induced increase in phosphorylated extracellular regulated protein kinases (p-ERK) and calcitonin gene related peptide (CGRP) release in the TNC.	Nitroglycerin	114-117	calcitonin/calcitonin-related polypeptide, alpha	Mus musculus	238-242
32082393-6	2019	Conclusion: The antimigraine effect of DCXF could be achieved by improving the metabolic profile and increasing the expressions of GS and EAAT1 to promote the glutamate cycle of TCC and serum samples in NTG-induced migraine rats to a certain extent.	Nitroglycerin	203-206	solute carrier family 1 member 3	Rattus norvegicus	138-143
33499643-3	2020	In the first place are the results of OCT angiography, which verify the pathology of NTG to the anterior part of optic nerve.	Nitroglycerin	85-88	plexin A2	Homo sapiens	38-41
31378003-4	2020	We observed that antibiotics treatment-prolonged nitroglycerin (NTG)-induced acute migraine-like pain in wild-type (WT) mice and the pain prolongation was completely blocked by genetic deletion of tumor necrosis factor-alpha (TNFalpha) or intra-spinal trigeminal nucleus caudalis (Sp5C) injection of TNFalpha receptor antagonist.	Nitroglycerin	49-62	tumor necrosis factor	Mus musculus	197-224
31378003-4	2020	We observed that antibiotics treatment-prolonged nitroglycerin (NTG)-induced acute migraine-like pain in wild-type (WT) mice and the pain prolongation was completely blocked by genetic deletion of tumor necrosis factor-alpha (TNFalpha) or intra-spinal trigeminal nucleus caudalis (Sp5C) injection of TNFalpha receptor antagonist.	Nitroglycerin	49-62	tumor necrosis factor	Mus musculus	226-234
31378003-4	2020	We observed that antibiotics treatment-prolonged nitroglycerin (NTG)-induced acute migraine-like pain in wild-type (WT) mice and the pain prolongation was completely blocked by genetic deletion of tumor necrosis factor-alpha (TNFalpha) or intra-spinal trigeminal nucleus caudalis (Sp5C) injection of TNFalpha receptor antagonist.	Nitroglycerin	64-67	tumor necrosis factor	Mus musculus	197-224
31378003-4	2020	We observed that antibiotics treatment-prolonged nitroglycerin (NTG)-induced acute migraine-like pain in wild-type (WT) mice and the pain prolongation was completely blocked by genetic deletion of tumor necrosis factor-alpha (TNFalpha) or intra-spinal trigeminal nucleus caudalis (Sp5C) injection of TNFalpha receptor antagonist.	Nitroglycerin	64-67	tumor necrosis factor	Mus musculus	226-234
31378003-4	2020	We observed that antibiotics treatment-prolonged nitroglycerin (NTG)-induced acute migraine-like pain in wild-type (WT) mice and the pain prolongation was completely blocked by genetic deletion of tumor necrosis factor-alpha (TNFalpha) or intra-spinal trigeminal nucleus caudalis (Sp5C) injection of TNFalpha receptor antagonist.	Nitroglycerin	64-67	tumor necrosis factor	Mus musculus	300-308
31378003-5	2020	The antibiotics treatment extended NTG-induced TNFalpha upregulation in the Sp5C.	Nitroglycerin	35-38	tumor necrosis factor	Mus musculus	47-55
31630149-0	2020	Nitroglycerin Enhances Cisplatin-Induced Cytotoxicity via AKT Inactivation and Thymidylate Synthase Downregulation in Human Lung Cancer Cells.	Nitroglycerin	0-13	thymidylate synthetase	Homo sapiens	79-99
31630149-3	2020	However, whether NTG and cisplatin could induce synergistic cytotoxicity in nonsmall cell lung cancer (NSCLC) cells through modulating TS expression is unknown.	Nitroglycerin	17-20	thymidylate synthetase	Homo sapiens	135-137
31630149-4	2020	In this study, NTG decreased TS expression in an AKT, also known as Protein kinase B (PKB) inactivation dependent manner in human lung adenocarcinoma A549 and squamous cell carcinoma H1703 cells.	Nitroglycerin	15-18	thymidylate synthetase	Homo sapiens	29-31
31630149-4	2020	In this study, NTG decreased TS expression in an AKT, also known as Protein kinase B (PKB) inactivation dependent manner in human lung adenocarcinoma A549 and squamous cell carcinoma H1703 cells.	Nitroglycerin	15-18	AKT serine/threonine kinase 1	Homo sapiens	49-52
31630149-4	2020	In this study, NTG decreased TS expression in an AKT, also known as Protein kinase B (PKB) inactivation dependent manner in human lung adenocarcinoma A549 and squamous cell carcinoma H1703 cells.	Nitroglycerin	15-18	protein tyrosine kinase 2 beta	Homo sapiens	68-84
31630149-4	2020	In this study, NTG decreased TS expression in an AKT, also known as Protein kinase B (PKB) inactivation dependent manner in human lung adenocarcinoma A549 and squamous cell carcinoma H1703 cells.	Nitroglycerin	15-18	protein tyrosine kinase 2 beta	Homo sapiens	86-89
31630149-5	2020	Enhancement of AKT activity by transfection with constitutive active AKT vectors increased the TS expression level as well as the cell survival pretreated by NTG.	Nitroglycerin	158-161	AKT serine/threonine kinase 1	Homo sapiens	15-18
31630149-5	2020	Enhancement of AKT activity by transfection with constitutive active AKT vectors increased the TS expression level as well as the cell survival pretreated by NTG.	Nitroglycerin	158-161	AKT serine/threonine kinase 1	Homo sapiens	69-72
31630149-6	2020	Moreover, NTG synergistically enhanced cytotoxicity and cell growth inhibition by cisplatin treatment in NSCLC cells, which were associated with downregulation of TS expression and inactivation of AKT in A549 and H1703 cells.	Nitroglycerin	10-13	thymidylate synthetase	Homo sapiens	163-165
31630149-6	2020	Moreover, NTG synergistically enhanced cytotoxicity and cell growth inhibition by cisplatin treatment in NSCLC cells, which were associated with downregulation of TS expression and inactivation of AKT in A549 and H1703 cells.	Nitroglycerin	10-13	AKT serine/threonine kinase 1	Homo sapiens	197-200
31327485-8	2020	High-dose NTG may be appropriate in H-AHF patients presenting with severe respiratory distress and SBP &gt;=160 mmHg or MAP &gt;=120 mmHg.	Nitroglycerin	10-13	selenium binding protein 1	Homo sapiens	99-102
31242931-0	2019	Multicentre Randomised trial of Acute Stroke treatment in the Ambulance with a nitroglycerin Patch (MR ASAP): study protocol for a randomised controlled trial.	Nitroglycerin	79-92	microtubule associated protein 9	Homo sapiens	103-107
31885641-0	2019	Auricular Electrical Stimulation Alleviates Headache through CGRP/COX-2/TRPV1/TRPA1 Signaling Pathways in a Nitroglycerin-Induced Migraine Rat Model.	Nitroglycerin	108-121	calcitonin-related polypeptide alpha	Rattus norvegicus	61-65
31885641-0	2019	Auricular Electrical Stimulation Alleviates Headache through CGRP/COX-2/TRPV1/TRPA1 Signaling Pathways in a Nitroglycerin-Induced Migraine Rat Model.	Nitroglycerin	108-121	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	66-71
31885641-0	2019	Auricular Electrical Stimulation Alleviates Headache through CGRP/COX-2/TRPV1/TRPA1 Signaling Pathways in a Nitroglycerin-Induced Migraine Rat Model.	Nitroglycerin	108-121	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	72-77
31885641-0	2019	Auricular Electrical Stimulation Alleviates Headache through CGRP/COX-2/TRPV1/TRPA1 Signaling Pathways in a Nitroglycerin-Induced Migraine Rat Model.	Nitroglycerin	108-121	transient receptor potential cation channel, subfamily A, member 1	Rattus norvegicus	78-83
31885641-7	2019	The CGRP, COX-2, TRPV1, and TRPA1 immunoreactive cells in the trigeminal ganglion increased in the NTG group compared with the control group (all p &lt; 0.0001); this increase could, however, be reduced by auricular ES pretreatment (27.8 +- 2.6 vs 63.0 +- 4.2, p &lt; 0.0001; 21.7 +- 1.2 vs 61.8 +- 4.0, p &lt; 0.0001; 24.3 +- 1.0 vs 36.5 +- 1.7, p=0.0003; and 20.7 +- 1.9 vs 90.8 +- 6.5, p &lt; 0.0001, respectively).	Nitroglycerin	99-102	calcitonin-related polypeptide alpha	Rattus norvegicus	4-8
31885641-7	2019	The CGRP, COX-2, TRPV1, and TRPA1 immunoreactive cells in the trigeminal ganglion increased in the NTG group compared with the control group (all p &lt; 0.0001); this increase could, however, be reduced by auricular ES pretreatment (27.8 +- 2.6 vs 63.0 +- 4.2, p &lt; 0.0001; 21.7 +- 1.2 vs 61.8 +- 4.0, p &lt; 0.0001; 24.3 +- 1.0 vs 36.5 +- 1.7, p=0.0003; and 20.7 +- 1.9 vs 90.8 +- 6.5, p &lt; 0.0001, respectively).	Nitroglycerin	99-102	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	10-15
31885641-7	2019	The CGRP, COX-2, TRPV1, and TRPA1 immunoreactive cells in the trigeminal ganglion increased in the NTG group compared with the control group (all p &lt; 0.0001); this increase could, however, be reduced by auricular ES pretreatment (27.8 +- 2.6 vs 63.0 +- 4.2, p &lt; 0.0001; 21.7 +- 1.2 vs 61.8 +- 4.0, p &lt; 0.0001; 24.3 +- 1.0 vs 36.5 +- 1.7, p=0.0003; and 20.7 +- 1.9 vs 90.8 +- 6.5, p &lt; 0.0001, respectively).	Nitroglycerin	99-102	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	17-22
31885641-7	2019	The CGRP, COX-2, TRPV1, and TRPA1 immunoreactive cells in the trigeminal ganglion increased in the NTG group compared with the control group (all p &lt; 0.0001); this increase could, however, be reduced by auricular ES pretreatment (27.8 +- 2.6 vs 63.0 +- 4.2, p &lt; 0.0001; 21.7 +- 1.2 vs 61.8 +- 4.0, p &lt; 0.0001; 24.3 +- 1.0 vs 36.5 +- 1.7, p=0.0003; and 20.7 +- 1.9 vs 90.8 +- 6.5, p &lt; 0.0001, respectively).	Nitroglycerin	99-102	transient receptor potential cation channel, subfamily A, member 1	Rattus norvegicus	28-33
31742594-7	2019	Using the chronic nitroglycerine rodent migraine model, we demonstrate that mice lacking TRESK develop exaggerated nitroglycerine-induced mechanical and thermal hyperalgesia, and furthermore, show that cloxyquin conversely is able to prevent sensitization.	Nitroglycerin	115-129	potassium channel, subfamily K, member 18	Mus musculus	89-94
31722730-11	2019	RESULTS: The protein levels of P2Y12R, GTP-RhoA, ROCK2, CGRP, c-fos, and inducible nitric oxide synthase (iNOS) in the TNC were increased after recurrent NTG injection.	Nitroglycerin	154-157	nitric oxide synthase 2, inducible	Mus musculus	73-104
31722730-11	2019	RESULTS: The protein levels of P2Y12R, GTP-RhoA, ROCK2, CGRP, c-fos, and inducible nitric oxide synthase (iNOS) in the TNC were increased after recurrent NTG injection.	Nitroglycerin	154-157	nitric oxide synthase 2, inducible	Mus musculus	106-110
31638891-7	2019	In a model of migraine induced by intravenous systemic infusion of nitroglycerin (NTG), rats with chronic exposure to acetaminophen exhibited significantly more frequent neuronal firing in the TNC and greater Fos-IR than those without the acetaminophen treatment.	Nitroglycerin	67-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	209-212
31638891-7	2019	In a model of migraine induced by intravenous systemic infusion of nitroglycerin (NTG), rats with chronic exposure to acetaminophen exhibited significantly more frequent neuronal firing in the TNC and greater Fos-IR than those without the acetaminophen treatment.	Nitroglycerin	82-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	209-212
30605506-7	2019	In both 12-mo-old NTG and AC8TG, PLN and GSK3alpha/beta phosphorylation was increased together with main localization of phospho-PKA substrates in Z-line interspaces.	Nitroglycerin	18-21	phospholamban	Mus musculus	33-36
30605506-7	2019	In both 12-mo-old NTG and AC8TG, PLN and GSK3alpha/beta phosphorylation was increased together with main localization of phospho-PKA substrates in Z-line interspaces.	Nitroglycerin	18-21	glycogen synthase kinase 3 alpha	Mus musculus	41-50
31250045-0	2019	Influence of the aldehyde dehydrogenase 2 polymorphism on the vasodilatory effect of nitroglycerin in infants with congenital heart disease and pulmonary arterial hypertension.	Nitroglycerin	85-98	aldehyde dehydrogenase 2 family member	Homo sapiens	17-41
31250045-1	2019	PURPOSE: The influence of the aldehyde dehydrogenase 2 (ALDH2) gene polymorphism on the pharmacokinetics and haemodynamics of nitroglycerin (GTN) was determined in human subjects.	Nitroglycerin	126-139	aldehyde dehydrogenase 2 family member	Homo sapiens	30-54
31250045-1	2019	PURPOSE: The influence of the aldehyde dehydrogenase 2 (ALDH2) gene polymorphism on the pharmacokinetics and haemodynamics of nitroglycerin (GTN) was determined in human subjects.	Nitroglycerin	126-139	aldehyde dehydrogenase 2 family member	Homo sapiens	56-61
31250045-1	2019	PURPOSE: The influence of the aldehyde dehydrogenase 2 (ALDH2) gene polymorphism on the pharmacokinetics and haemodynamics of nitroglycerin (GTN) was determined in human subjects.	Nitroglycerin	141-144	aldehyde dehydrogenase 2 family member	Homo sapiens	30-54
31250045-1	2019	PURPOSE: The influence of the aldehyde dehydrogenase 2 (ALDH2) gene polymorphism on the pharmacokinetics and haemodynamics of nitroglycerin (GTN) was determined in human subjects.	Nitroglycerin	141-144	aldehyde dehydrogenase 2 family member	Homo sapiens	56-61
31250045-5	2019	RESULTS: Plasma GTN concentrations were significantly higher in patients with the ALDH2 gene polymorphism than in those without the polymorphism.	Nitroglycerin	16-19	aldehyde dehydrogenase 2 family member	Homo sapiens	82-87
31250045-7	2019	CONCLUSIONS: These data suggest that the ALDH2 gene polymorphism influences the pharmacokinetics and haemodynamics of GTN in human subjects.	Nitroglycerin	118-121	aldehyde dehydrogenase 2 family member	Homo sapiens	41-46
31330139-13	2019	In chronic model, WIN 55,212-2 (0.33, 1 and 3 mg/kg) significantly attenuated NTG-induced hyperalgesia through both CB1 and CB2 receptors.	Nitroglycerin	78-81	cannabinoid receptor 1	Rattus norvegicus	116-119
31330139-13	2019	In chronic model, WIN 55,212-2 (0.33, 1 and 3 mg/kg) significantly attenuated NTG-induced hyperalgesia through both CB1 and CB2 receptors.	Nitroglycerin	78-81	cannabinoid receptor 2	Rattus norvegicus	124-127
31883320-0	2019	Is the mechanism of nitroglycerin tolerance associated with aldehyde dehydrogenase activity?	Nitroglycerin	20-33	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	60-82
31883320-2	2019	The aim of the study presented here was an attempt to answer the question posed in the title: Is the mechanism of nitroglycerin tolerance associated with aldehyde dehydrogenase (ALDH) activity?	Nitroglycerin	114-127	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	154-176
31883320-2	2019	The aim of the study presented here was an attempt to answer the question posed in the title: Is the mechanism of nitroglycerin tolerance associated with aldehyde dehydrogenase (ALDH) activity?	Nitroglycerin	114-127	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	178-182
31883320-5	2019	Our data revealed that not only DSF and GTN inhibited the total ALDH activity in the rat liver, but LA also proved to be an inhibitor of this enzyme.	Nitroglycerin	40-43	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	64-68
31733648-13	2019	p-Stat3 expression was increased in both Ntg and GET-1 mice in the ischemia brain at 7 days after tMCAO.	Nitroglycerin	41-44	signal transducer and activator of transcription 3	Mus musculus	2-7
31733648-14	2019	p-Stat3 expression was significantly upregulated in the ipsilateral side in the GET-1 brain than that in the Ntg brain at 7 days after tMCAO.	Nitroglycerin	109-112	signal transducer and activator of transcription 3	Mus musculus	2-7
31722730-15	2019	In addition, inhibiting P2Y12R and ROCK2 activities suppressed NTG-induced microglial morphological changes (process retraction) and iNOS production in the TNC.	Nitroglycerin	63-66	Rho-associated coiled-coil containing protein kinase 2	Mus musculus	35-40
31722730-15	2019	In addition, inhibiting P2Y12R and ROCK2 activities suppressed NTG-induced microglial morphological changes (process retraction) and iNOS production in the TNC.	Nitroglycerin	63-66	nitric oxide synthase 2, inducible	Mus musculus	133-137
31420791-0	2019	Rhynchophylline attenuates migraine in trigeminal nucleus caudalis in nitroglycerin-induced rat model by inhibiting MAPK/NF-kB signaling.	Nitroglycerin	70-83	RELA proto-oncogene, NF-kB subunit	Rattus norvegicus	121-126
31420791-7	2019	The results showed that NTG induced EEG and behavior disorders in rats, which was associated with the initiation of oxidative stress and increased expression of CGRP.	Nitroglycerin	24-27	calcitonin-related polypeptide alpha	Rattus norvegicus	161-165
31487370-8	2019	Conclusions: These results suggest that alphaRGC and ipRGC are highly tolerant to NMDA-induced neurotoxicity and NTG-like neurodegeneration in GLAST KO mice.	Nitroglycerin	113-116	solute carrier family 1 (glial high affinity glutamate transporter), member 3	Mus musculus	143-148
31242931-2	2019	The Multicentre Randomised trial of Acute Stroke treatment in the Ambulance with a nitroglycerin Patch (MR ASAP) aims to assess the effect of transdermal GTN, started within 3 h after stroke onset in the prehospital setting, on functional outcome at 90 days in patients with acute ischaemic stroke or intracerebral haemorrhage.	Nitroglycerin	154-157	microtubule associated protein 9	Homo sapiens	107-111
31242931-9	2019	DISCUSSION: MR ASAP will assess whether very early administration of GTN improves outcome after stroke in a setting where rates of intravenous thrombolysis and endovascular treatment for acute ischaemic stroke are high.	Nitroglycerin	69-72	microtubule associated protein 9	Homo sapiens	15-19
31159375-3	2019	The hemispherical punch stretching test of commercially pure titanium (TA1) sheet is simulated by a plastic constitutive formula derived from the GTN model.	Nitroglycerin	146-149	trace amine associated receptor 1	Homo sapiens	71-74
31316651-2	2019	Nitroglycerin, N-acetyl cysteine and Metoprolol in acute liver injury induced by CCL4.	Nitroglycerin	0-13	C-C motif chemokine 4	Oryctolagus cuniculus	81-85
31497516-9	2019	Conclusions: For the first time, we showed that more than half of the patients undergoing surgery suffered from methemoglobin level above 2% after prescribing nitroglycerin, and the only predictor of abnormal methemoglobin level was the rate of nitroglycerin prescription.	Nitroglycerin	159-172	hemoglobin subunit gamma 2	Homo sapiens	112-125
31497516-9	2019	Conclusions: For the first time, we showed that more than half of the patients undergoing surgery suffered from methemoglobin level above 2% after prescribing nitroglycerin, and the only predictor of abnormal methemoglobin level was the rate of nitroglycerin prescription.	Nitroglycerin	245-258	hemoglobin subunit gamma 2	Homo sapiens	209-222
31162244-2	2019	More recently, aldehyde dehydrogenase-2 (ALDH-2) has been reported as the important enzyme involved in the bioactivation of nitroglycerin at therapeutically relevant concentrations.	Nitroglycerin	124-137	aldehyde dehydrogenase 2 family member	Homo sapiens	15-39
31162244-2	2019	More recently, aldehyde dehydrogenase-2 (ALDH-2) has been reported as the important enzyme involved in the bioactivation of nitroglycerin at therapeutically relevant concentrations.	Nitroglycerin	124-137	aldehyde dehydrogenase 2 family member	Homo sapiens	41-47
31159375-6	2019	The results show that the GTN model determined by the finite element reverse calibration method can be used to predict the forming limit of the TA1 sheet metal.	Nitroglycerin	26-29	trace amine associated receptor 1	Homo sapiens	144-147
31120979-5	2019	We genotyped 300 patients with severe AKI (KDIGO 2 or 3) and 353 controls without AKI (KDIGO 0) for the guanine-thymine (GTn) repeat in the promoter region of the HMOX1 gene.	Nitroglycerin	121-124	heme oxygenase 1	Homo sapiens	163-168
31179338-10	2019	In conclusion, AG and NG synergistically ameliorated diabetic podocyte injury partly through upregulation of nephrin, alpha-dystroglycan, and Bcl-xl, as well as downregulation of Bax and Nox4.	Nitroglycerin	22-24	NPHS1 adhesion molecule, nephrin	Rattus norvegicus	109-116
30843200-3	2019	The concurrent presence of a low capillary density and high microvascular reactivity to topical nitroglycerin at sea level was found to be associated with a failure to reach the summit, whereas the presence of a high baseline capillary density with the ability to further increase maximum recruitable capillary density upon ascent to an extreme altitude was associated with summit success.	Nitroglycerin	96-109	S13 erythroblastosis (avian) oncogene homolog	Homo sapiens	113-116
31179338-10	2019	In conclusion, AG and NG synergistically ameliorated diabetic podocyte injury partly through upregulation of nephrin, alpha-dystroglycan, and Bcl-xl, as well as downregulation of Bax and Nox4.	Nitroglycerin	22-24	dystroglycan 1	Rattus norvegicus	118-136
31179338-10	2019	In conclusion, AG and NG synergistically ameliorated diabetic podocyte injury partly through upregulation of nephrin, alpha-dystroglycan, and Bcl-xl, as well as downregulation of Bax and Nox4.	Nitroglycerin	22-24	Bcl2-like 1	Rattus norvegicus	142-148
31179338-10	2019	In conclusion, AG and NG synergistically ameliorated diabetic podocyte injury partly through upregulation of nephrin, alpha-dystroglycan, and Bcl-xl, as well as downregulation of Bax and Nox4.	Nitroglycerin	22-24	BCL2 associated X, apoptosis regulator	Rattus norvegicus	179-182
31179338-10	2019	In conclusion, AG and NG synergistically ameliorated diabetic podocyte injury partly through upregulation of nephrin, alpha-dystroglycan, and Bcl-xl, as well as downregulation of Bax and Nox4.	Nitroglycerin	22-24	NADPH oxidase 4	Rattus norvegicus	187-191
30720069-7	2019	Furthermore, it was observed that GTN differentially regulates the level of the precursor form of GDF-15 between resistant and parental cells, and that recombinant GDF-15 can modulate the expression of CLU isoforms and counteract GTN-induced cytotoxicity in resistant cells.	Nitroglycerin	230-233	growth differentiation factor 15	Homo sapiens	164-170
30971286-0	2019	Microglial NLRP3 inflammasome activation mediates IL-1beta release and contributes to central sensitization in a recurrent nitroglycerin-induced migraine model.	Nitroglycerin	123-136	NLR family, pyrin domain containing 3	Mus musculus	11-16
30971286-9	2019	RESULTS: Repeated NTG administration induced acute and chronic mechanical hyperalgesia and increased expression of NLRP3 and IL-1beta.	Nitroglycerin	18-21	NLR family, pyrin domain containing 3	Mus musculus	115-120
30971286-9	2019	RESULTS: Repeated NTG administration induced acute and chronic mechanical hyperalgesia and increased expression of NLRP3 and IL-1beta.	Nitroglycerin	18-21	interleukin 1 beta	Mus musculus	125-133
30971286-10	2019	Blockade of NLRP3 or IL-1beta reduced NTG-induced hyperalgesia, and this effect was accompanied by a significant inhibition of the NTG-induced increase in p-ERK, c-Fos and CGRP levels in the TNC.	Nitroglycerin	38-41	NLR family, pyrin domain containing 3	Mus musculus	12-17
30971286-10	2019	Blockade of NLRP3 or IL-1beta reduced NTG-induced hyperalgesia, and this effect was accompanied by a significant inhibition of the NTG-induced increase in p-ERK, c-Fos and CGRP levels in the TNC.	Nitroglycerin	38-41	interleukin 1 beta	Mus musculus	21-29
30971286-10	2019	Blockade of NLRP3 or IL-1beta reduced NTG-induced hyperalgesia, and this effect was accompanied by a significant inhibition of the NTG-induced increase in p-ERK, c-Fos and CGRP levels in the TNC.	Nitroglycerin	131-134	NLR family, pyrin domain containing 3	Mus musculus	12-17
30971286-10	2019	Blockade of NLRP3 or IL-1beta reduced NTG-induced hyperalgesia, and this effect was accompanied by a significant inhibition of the NTG-induced increase in p-ERK, c-Fos and CGRP levels in the TNC.	Nitroglycerin	131-134	interleukin 1 beta	Mus musculus	21-29
30971286-10	2019	Blockade of NLRP3 or IL-1beta reduced NTG-induced hyperalgesia, and this effect was accompanied by a significant inhibition of the NTG-induced increase in p-ERK, c-Fos and CGRP levels in the TNC.	Nitroglycerin	131-134	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	155-160
30971286-10	2019	Blockade of NLRP3 or IL-1beta reduced NTG-induced hyperalgesia, and this effect was accompanied by a significant inhibition of the NTG-induced increase in p-ERK, c-Fos and CGRP levels in the TNC.	Nitroglycerin	131-134	FBJ osteosarcoma oncogene	Mus musculus	162-167
30971286-10	2019	Blockade of NLRP3 or IL-1beta reduced NTG-induced hyperalgesia, and this effect was accompanied by a significant inhibition of the NTG-induced increase in p-ERK, c-Fos and CGRP levels in the TNC.	Nitroglycerin	131-134	calcitonin/calcitonin-related polypeptide, alpha	Mus musculus	172-176
30720069-0	2019	Glyceryl trinitrate-induced cytotoxicity of docetaxel-resistant prostatic cancer cells is associated with differential regulation of clusterin.	Nitroglycerin	0-19	clusterin	Homo sapiens	133-142
30720069-5	2019	It is also demonstrated that GTN modulates the level of expression of clusterin (CLU) which is dependent of GDF-15, two markers associated with docetaxel resistance in prostate cancer.	Nitroglycerin	29-32	clusterin	Homo sapiens	70-79
30720069-5	2019	It is also demonstrated that GTN modulates the level of expression of clusterin (CLU) which is dependent of GDF-15, two markers associated with docetaxel resistance in prostate cancer.	Nitroglycerin	29-32	clusterin	Homo sapiens	81-84
30720069-5	2019	It is also demonstrated that GTN modulates the level of expression of clusterin (CLU) which is dependent of GDF-15, two markers associated with docetaxel resistance in prostate cancer.	Nitroglycerin	29-32	growth differentiation factor 15	Homo sapiens	108-114
30720069-6	2019	The results indicate that GTN represses the level of expression of the cytoprotective isoform of CLU (sCLU) and can increase the level of expression of the cytotoxic isoform (nuclear CLU) in docetaxel resistant cells.	Nitroglycerin	26-29	clusterin	Homo sapiens	97-100
30720069-6	2019	The results indicate that GTN represses the level of expression of the cytoprotective isoform of CLU (sCLU) and can increase the level of expression of the cytotoxic isoform (nuclear CLU) in docetaxel resistant cells.	Nitroglycerin	26-29	clusterin	Homo sapiens	103-106
30720069-7	2019	Furthermore, it was observed that GTN differentially regulates the level of the precursor form of GDF-15 between resistant and parental cells, and that recombinant GDF-15 can modulate the expression of CLU isoforms and counteract GTN-induced cytotoxicity in resistant cells.	Nitroglycerin	34-37	growth differentiation factor 15	Homo sapiens	98-104
30831484-11	2019	Then, we found that the ERK and GSK3beta/beta-catenin signaling pathway were noticeably blocked in CRC cells after treatment with NG.	Nitroglycerin	130-132	mitogen-activated protein kinase 1	Homo sapiens	24-27
30831484-11	2019	Then, we found that the ERK and GSK3beta/beta-catenin signaling pathway were noticeably blocked in CRC cells after treatment with NG.	Nitroglycerin	130-132	glycogen synthase kinase 3 beta	Homo sapiens	32-40
30831484-11	2019	Then, we found that the ERK and GSK3beta/beta-catenin signaling pathway were noticeably blocked in CRC cells after treatment with NG.	Nitroglycerin	130-132	catenin beta 1	Homo sapiens	41-53
30569164-2	2019	Considering the involvement of dimethylarginine dimethylaminohydrolase 2 (DDAH2) in diabetes, it was hypothesized that DDAH2 may be beneficial to cardiac function and myocardial fibrosis during the progression of DCM with involvement of the DDAH/asymmetric NG, NGdimethyl-L-arginine (ADMA)/nitric oxide synthase (NOS)/nitric oxide (NO) signaling pathway.	Nitroglycerin	257-259	dimethylarginine dimethylaminohydrolase 2	Rattus norvegicus	31-72
30165375-0	2019	Nitroglycerine limits infarct size through S-nitrosation of cyclophilin D: a novel mechanism for an old drug.	Nitroglycerin	0-14	peptidylprolyl isomerase F (cyclophilin F)	Mus musculus	60-73
30165375-5	2019	Mechanistically, NTG was shown to nitrosate and inhibit cyclophilin D (CypD), and NTG administration failed to limit infarct size in CypD knockout mice.	Nitroglycerin	17-20	peptidylprolyl isomerase F (cyclophilin F)	Mus musculus	56-69
30165375-5	2019	Mechanistically, NTG was shown to nitrosate and inhibit cyclophilin D (CypD), and NTG administration failed to limit infarct size in CypD knockout mice.	Nitroglycerin	17-20	peptidylprolyl isomerase F (cyclophilin F)	Mus musculus	71-75
30165375-8	2019	Moreover, NTG retained its cardioprotective effects in a model of endothelial dysfunction (ApoE knockout) by preserving CypD nitrosation.	Nitroglycerin	10-13	apolipoprotein E	Mus musculus	91-95
30165375-8	2019	Moreover, NTG retained its cardioprotective effects in a model of endothelial dysfunction (ApoE knockout) by preserving CypD nitrosation.	Nitroglycerin	10-13	peptidylprolyl isomerase F (cyclophilin F)	Mus musculus	120-124
30165375-10	2019	CONCLUSION: Low-dose NTG given prior to reperfusion reduces myocardial infarct size by preserving eNOS function, and the subsequent eNOS-dependent S-nitrosation of CypD, inhibiting cardiomyocyte necrosis.	Nitroglycerin	21-24	peptidylprolyl isomerase F (cyclophilin F)	Mus musculus	164-168
30569164-2	2019	Considering the involvement of dimethylarginine dimethylaminohydrolase 2 (DDAH2) in diabetes, it was hypothesized that DDAH2 may be beneficial to cardiac function and myocardial fibrosis during the progression of DCM with involvement of the DDAH/asymmetric NG, NGdimethyl-L-arginine (ADMA)/nitric oxide synthase (NOS)/nitric oxide (NO) signaling pathway.	Nitroglycerin	257-259	dimethylarginine dimethylaminohydrolase 2	Rattus norvegicus	74-79
30569164-2	2019	Considering the involvement of dimethylarginine dimethylaminohydrolase 2 (DDAH2) in diabetes, it was hypothesized that DDAH2 may be beneficial to cardiac function and myocardial fibrosis during the progression of DCM with involvement of the DDAH/asymmetric NG, NGdimethyl-L-arginine (ADMA)/nitric oxide synthase (NOS)/nitric oxide (NO) signaling pathway.	Nitroglycerin	257-259	dimethylarginine dimethylaminohydrolase 2	Rattus norvegicus	119-124
30554658-0	2019	Decreased PKG transcription mediated by PI3K/Akt/FoxO1 pathway is involved in the development of nitroglycerin tolerance.	Nitroglycerin	97-110	thymoma viral proto-oncogene 1	Mus musculus	45-48
30827356-10	2019	In contrast, protein S100-A11 and l-lactate dehydrogenase A chain, were down-regulated in molar tissue from most patients in the GTN group.	Nitroglycerin	129-132	S100 calcium binding protein A11	Homo sapiens	21-29
30554658-0	2019	Decreased PKG transcription mediated by PI3K/Akt/FoxO1 pathway is involved in the development of nitroglycerin tolerance.	Nitroglycerin	97-110	forkhead box O1	Mus musculus	49-54
30554658-2	2019	The present study is to determine whether PI3K/Akt pathway in vascular smooth muscle cells is involved in nitroglycerin (NTG) tolerance and the underlying mechanism.	Nitroglycerin	106-119	thymoma viral proto-oncogene 1	Mus musculus	47-50
30554658-2	2019	The present study is to determine whether PI3K/Akt pathway in vascular smooth muscle cells is involved in nitroglycerin (NTG) tolerance and the underlying mechanism.	Nitroglycerin	121-124	thymoma viral proto-oncogene 1	Mus musculus	47-50
30554658-13	2019	The level of phosphorylated FoxO1 at Ser256 and its translocation from the nucleus to the cytosol were both increased in NTG tolerance and were also inhibited by LY294002.	Nitroglycerin	121-124	forkhead box O1	Mus musculus	28-33
30554658-15	2019	In conclusion, the present study suggests that PI3K/Akt in vascular smooth muscle is involved in the development of NTG tolerance via inhibiting PKG transcription and the effect is mediated by FoxO1.	Nitroglycerin	116-119	thymoma viral proto-oncogene 1	Mus musculus	52-55
30554658-15	2019	In conclusion, the present study suggests that PI3K/Akt in vascular smooth muscle is involved in the development of NTG tolerance via inhibiting PKG transcription and the effect is mediated by FoxO1.	Nitroglycerin	116-119	forkhead box O1	Mus musculus	193-198
29672839-7	2019	Inhibition of cyclooxygenase 1 by aspirin, supplementation of PGI2 by beraprost, and inhibition of PGIS S-nitrosylation by N-acetyl-cysteine improved GTN-induced nitrate cross-tolerance in rats.	Nitroglycerin	150-153	prostaglandin-endoperoxide synthase 1	Rattus norvegicus	14-30
30608494-1	2019	A combination of a preexfoliated nanographene (NG) dispersion and fused electron donor-acceptor tetrathiafulvalene-perylenediimide (TTF-PDI) results in a noncovalent functionalization of NG.	Nitroglycerin	47-49	ras homolog family member H	Homo sapiens	132-135
30608494-1	2019	A combination of a preexfoliated nanographene (NG) dispersion and fused electron donor-acceptor tetrathiafulvalene-perylenediimide (TTF-PDI) results in a noncovalent functionalization of NG.	Nitroglycerin	47-49	peptidyl arginine deiminase 1	Homo sapiens	136-139
29672839-3	2019	This study aimed to determine the role of PGIS S-nitrosylation in nitrate tolerance induced by nitroglycerin (GTN).	Nitroglycerin	95-108	prostaglandin I2 synthase	Homo sapiens	42-46
29672839-3	2019	This study aimed to determine the role of PGIS S-nitrosylation in nitrate tolerance induced by nitroglycerin (GTN).	Nitroglycerin	110-113	prostaglandin I2 synthase	Homo sapiens	42-46
29672839-7	2019	Inhibition of cyclooxygenase 1 by aspirin, supplementation of PGI2 by beraprost, and inhibition of PGIS S-nitrosylation by N-acetyl-cysteine improved GTN-induced nitrate cross-tolerance in rats.	Nitroglycerin	150-153	prostaglandin I2 synthase	Rattus norvegicus	99-103
29672839-4	2019	In endothelial cells, GTN increased PGIS S-nitrosylation and disturbed PGH2 metabolism, which were normalized by mutants of PGIS cysteine 231/441 to alanine (C231/441A).	Nitroglycerin	22-25	prostaglandin I2 synthase	Homo sapiens	36-40
29672839-4	2019	In endothelial cells, GTN increased PGIS S-nitrosylation and disturbed PGH2 metabolism, which were normalized by mutants of PGIS cysteine 231/441 to alanine (C231/441A).	Nitroglycerin	22-25	prostaglandin I2 synthase	Homo sapiens	124-128
29672839-5	2019	Clearance of nitric oxide by carboxy-PTIO or inhibition of S-nitrosylation by N-acetyl-cysteine decreased GTN-induced PGIS S-nitrosylation.	Nitroglycerin	106-109	prostaglandin I2 synthase	Homo sapiens	118-122
29672839-6	2019	Enforced expression of mutated PGIS with C231/441A markedly abolished GTN-induced PGIS S-nitrosylation and nitrate cross-tolerance in Apoe-/- mice.	Nitroglycerin	70-73	prostaglandin I2 (prostacyclin) synthase	Mus musculus	31-35
29672839-6	2019	Enforced expression of mutated PGIS with C231/441A markedly abolished GTN-induced PGIS S-nitrosylation and nitrate cross-tolerance in Apoe-/- mice.	Nitroglycerin	70-73	prostaglandin I2 synthase	Homo sapiens	82-86
29672839-6	2019	Enforced expression of mutated PGIS with C231/441A markedly abolished GTN-induced PGIS S-nitrosylation and nitrate cross-tolerance in Apoe-/- mice.	Nitroglycerin	70-73	apolipoprotein E	Mus musculus	134-138
31539705-6	2019	We identified Isl1 and Lhx2 as two transcription factors that label neuronal subpopulations in the forming TNG, distinct from GnRH1+ cells, thereby revealing a diversity of cell types during the formation of the TNG.	Nitroglycerin	107-110	ISL LIM homeobox 1	Gallus gallus	14-18
31539705-6	2019	We identified Isl1 and Lhx2 as two transcription factors that label neuronal subpopulations in the forming TNG, distinct from GnRH1+ cells, thereby revealing a diversity of cell types during the formation of the TNG.	Nitroglycerin	107-110	LIM homeobox 2	Gallus gallus	23-27
31539705-6	2019	We identified Isl1 and Lhx2 as two transcription factors that label neuronal subpopulations in the forming TNG, distinct from GnRH1+ cells, thereby revealing a diversity of cell types during the formation of the TNG.	Nitroglycerin	212-215	ISL LIM homeobox 1	Gallus gallus	14-18
31539705-6	2019	We identified Isl1 and Lhx2 as two transcription factors that label neuronal subpopulations in the forming TNG, distinct from GnRH1+ cells, thereby revealing a diversity of cell types during the formation of the TNG.	Nitroglycerin	212-215	LIM homeobox 2	Gallus gallus	23-27
29672839-9	2019	In conclusion, GTN induces nitrate cross-tolerance through PGIS S-nitrosylation at cysteine 231/441.	Nitroglycerin	15-18	prostaglandin I2 synthase	Homo sapiens	59-63
29237283-0	2018	Ghrelin attenuated hyperalgesia induced by chronic nitroglycerin: CGRP and TRPV1 as targets for migraine management.	Nitroglycerin	51-64	ghrelin and obestatin prepropeptide	Rattus norvegicus	0-7
30687454-4	2018	Methods and Results: Organic nitrates (ISMN, ISDN, and nitroglycerin (GTN)) augmented the oxidative burst and interleukin-6 release in cultured macrophages, whereas macitentan decreased the oxidative burst in isolated human leukocytes.	Nitroglycerin	55-68	interleukin 6	Homo sapiens	110-123
30687454-4	2018	Methods and Results: Organic nitrates (ISMN, ISDN, and nitroglycerin (GTN)) augmented the oxidative burst and interleukin-6 release in cultured macrophages, whereas macitentan decreased the oxidative burst in isolated human leukocytes.	Nitroglycerin	70-73	interleukin 6	Homo sapiens	110-123
30618656-5	2018	Among the 109 genes that exhibited an NTG treatment-by-region interaction, solute carrier family 32 (GABA vesicular transporter) member 1 (Slc32a1) and preproenkephalin (Penk) exhibited reversal of expression patterns between the NTG and CON groups.	Nitroglycerin	230-233	preproenkephalin	Mus musculus	152-168
30618656-5	2018	Among the 109 genes that exhibited an NTG treatment-by-region interaction, solute carrier family 32 (GABA vesicular transporter) member 1 (Slc32a1) and preproenkephalin (Penk) exhibited reversal of expression patterns between the NTG and CON groups.	Nitroglycerin	230-233	preproenkephalin	Mus musculus	170-174
29859998-1	2018	BACKGROUND: Addition of nitroglycerine (NTG) to transcatheter arterial embolization/transarterial chemoembolization (TAE/TACE) has been shown to increase deposition of Lipiodol emulsion in hepatocellular carcinoma (HCC) tumors.	Nitroglycerin	24-38	ADAM metallopeptidase domain 17	Homo sapiens	121-125
29859998-1	2018	BACKGROUND: Addition of nitroglycerine (NTG) to transcatheter arterial embolization/transarterial chemoembolization (TAE/TACE) has been shown to increase deposition of Lipiodol emulsion in hepatocellular carcinoma (HCC) tumors.	Nitroglycerin	40-43	ADAM metallopeptidase domain 17	Homo sapiens	121-125
30345159-10	2018	In conclusion, routine monitoring of methemoglobin levels should be undertaken when GTN patches are used in very prematurely born infants.	Nitroglycerin	84-87	hemoglobin subunit gamma 2	Homo sapiens	37-50
30618656-5	2018	Among the 109 genes that exhibited an NTG treatment-by-region interaction, solute carrier family 32 (GABA vesicular transporter) member 1 (Slc32a1) and preproenkephalin (Penk) exhibited reversal of expression patterns between the NTG and CON groups.	Nitroglycerin	38-41	solute carrier family 32 (GABA vesicular transporter), member 1	Mus musculus	75-137
30618656-5	2018	Among the 109 genes that exhibited an NTG treatment-by-region interaction, solute carrier family 32 (GABA vesicular transporter) member 1 (Slc32a1) and preproenkephalin (Penk) exhibited reversal of expression patterns between the NTG and CON groups.	Nitroglycerin	38-41	solute carrier family 32 (GABA vesicular transporter), member 1	Mus musculus	139-146
30618656-5	2018	Among the 109 genes that exhibited an NTG treatment-by-region interaction, solute carrier family 32 (GABA vesicular transporter) member 1 (Slc32a1) and preproenkephalin (Penk) exhibited reversal of expression patterns between the NTG and CON groups.	Nitroglycerin	38-41	preproenkephalin	Mus musculus	152-168
30618656-5	2018	Among the 109 genes that exhibited an NTG treatment-by-region interaction, solute carrier family 32 (GABA vesicular transporter) member 1 (Slc32a1) and preproenkephalin (Penk) exhibited reversal of expression patterns between the NTG and CON groups.	Nitroglycerin	38-41	preproenkephalin	Mus musculus	170-174
30618656-5	2018	Among the 109 genes that exhibited an NTG treatment-by-region interaction, solute carrier family 32 (GABA vesicular transporter) member 1 (Slc32a1) and preproenkephalin (Penk) exhibited reversal of expression patterns between the NTG and CON groups.	Nitroglycerin	230-233	solute carrier family 32 (GABA vesicular transporter), member 1	Mus musculus	75-137
30618656-5	2018	Among the 109 genes that exhibited an NTG treatment-by-region interaction, solute carrier family 32 (GABA vesicular transporter) member 1 (Slc32a1) and preproenkephalin (Penk) exhibited reversal of expression patterns between the NTG and CON groups.	Nitroglycerin	230-233	solute carrier family 32 (GABA vesicular transporter), member 1	Mus musculus	139-146
29237283-0	2018	Ghrelin attenuated hyperalgesia induced by chronic nitroglycerin: CGRP and TRPV1 as targets for migraine management.	Nitroglycerin	51-64	calcitonin-related polypeptide alpha	Rattus norvegicus	66-70
29985973-11	2018	Early periorbital vasodilatation evoked by glyceryl trinitrate was attenuated by ALDH2 inhibition but was unaffected by TRPA1 blockade.	Nitroglycerin	43-62	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	81-86
30184561-8	2018	Higher NAMPT/visfatin serum concentration was found in patients with GD comparing with patients with TNG (p=0.03855).	Nitroglycerin	101-104	nicotinamide phosphoribosyltransferase	Homo sapiens	7-12
30184561-8	2018	Higher NAMPT/visfatin serum concentration was found in patients with GD comparing with patients with TNG (p=0.03855).	Nitroglycerin	101-104	nicotinamide phosphoribosyltransferase	Homo sapiens	13-21
30165876-0	2018	Microglia P2X4 receptor contributes to central sensitization following recurrent nitroglycerin stimulation.	Nitroglycerin	81-94	purinergic receptor P2X 4	Homo sapiens	10-23
30165876-10	2018	RESULTS: Chronic intermittent administration of NTG resulted in acute and chronic basal mechanical hyperalgesia, accompanied with microglia activation and upregulation of P2X4R expression.	Nitroglycerin	48-51	purinergic receptor P2X 4	Homo sapiens	171-176
30165876-14	2018	This effect was associated with a significant inhibition of the NTG-induced increase in c-Fos protein and CGRP release in the TNC.	Nitroglycerin	64-67	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	88-93
30165876-14	2018	This effect was associated with a significant inhibition of the NTG-induced increase in c-Fos protein and CGRP release in the TNC.	Nitroglycerin	64-67	calcitonin related polypeptide alpha	Homo sapiens	106-110
29985973-0	2018	TRPA1/NOX in the soma of trigeminal ganglion neurons mediates migraine-related pain of glyceryl trinitrate in mice.	Nitroglycerin	87-106	transient receptor potential cation channel, subfamily A, member 1	Mus musculus	0-5
29985973-5	2018	Herein, we explored the role of TRPA1 in glyceryl trinitrate-evoked allodynia.	Nitroglycerin	41-60	transient receptor potential cation channel, subfamily A, member 1	Mus musculus	32-37
29985973-15	2018	The autocrine pathway, sustained by TRPA1 and NOX1/2 within neuronal cell bodies of trigeminal ganglia, may sensitize meningeal nociceptors and second order trigeminal neurons to elicit periorbital allodynia, and could be of relevance for migraine-like headaches evoked by glyceryl trinitrate in humans.	Nitroglycerin	273-292	transient receptor potential cation channel subfamily A member 1	Homo sapiens	36-41
29985973-15	2018	The autocrine pathway, sustained by TRPA1 and NOX1/2 within neuronal cell bodies of trigeminal ganglia, may sensitize meningeal nociceptors and second order trigeminal neurons to elicit periorbital allodynia, and could be of relevance for migraine-like headaches evoked by glyceryl trinitrate in humans.	Nitroglycerin	273-292	NADPH oxidase 1	Homo sapiens	46-50
29766604-9	2018	This study quantified the effect of an exogenous NO donor [sodium nitroglycerin (NTG); 0.4 mg sublingual spray] on the right middle cerebral artery (rMCA) cross-sectional area (CSA), blood velocity and overall blood flow.	Nitroglycerin	81-84	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	177-180
29766604-11	2018	The CSA increased in the rMCA [BL, 5.2 +- 1.2 mm2 ; PLO, 5.4 +- 1.5 mm2 ; NTG, 6.6 +- 1.5 mm2 , P &lt; 0.05; mean +- SD].	Nitroglycerin	74-77	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	4-7
30003352-0	2018	Chronic and intermittent administration of systemic nitroglycerin in the rat induces an increase in the gene expression of CGRP in central areas: potential contribution to pain processing.	Nitroglycerin	52-65	calcitonin-related polypeptide alpha	Rattus norvegicus	123-127
29431644-4	2018	METHODS: Nitrovasodilator resistance was induced by nitroglycerin (100 mg kg-1 d-1, 3 days) infusion in Apoe-/- mice.	Nitroglycerin	52-65	apolipoprotein E	Mus musculus	104-108
29431644-10	2018	Furthermore, nitroglycerin-decreased PTGIS gene expression was prevented by miR-199a/b antagomirs or was mirrored by the enforced expression of miR-199a/b in human umbilical vein endothelial cells.	Nitroglycerin	13-26	prostaglandin I2 synthase	Homo sapiens	37-42
29431644-11	2018	In Apoe-/- mice, nitroglycerin induced the ectopic expression of miR-199a/b in the carotid arterial endothelium, decreased PTGIS gene expression, and instigated nitrovasodilator resistance, all of which were abrogated by miR-199a/b antagomirs or LNA-anti-miR-199.	Nitroglycerin	17-30	apolipoprotein E	Mus musculus	3-7
29431644-11	2018	In Apoe-/- mice, nitroglycerin induced the ectopic expression of miR-199a/b in the carotid arterial endothelium, decreased PTGIS gene expression, and instigated nitrovasodilator resistance, all of which were abrogated by miR-199a/b antagomirs or LNA-anti-miR-199.	Nitroglycerin	17-30	prostaglandin I2 (prostacyclin) synthase	Mus musculus	123-128
29431644-14	2018	Finally, indomethacin, iloprost, and SQ29548 improved vasorelaxation in nitroglycerin-infused Apoe-/- mice, whereas U51605 induced nitrovasodilator resistance.	Nitroglycerin	72-85	apolipoprotein E	Mus musculus	94-98
30003352-10	2018	RESULTS: NTG administration induced spinal hyperalgesia and orofacial allodynia, together with a significant increase in the expression of CGRP and c-Fos genes in trigeminal ganglia and central areas.	Nitroglycerin	9-12	calcitonin-related polypeptide alpha	Rattus norvegicus	139-143
30003352-10	2018	RESULTS: NTG administration induced spinal hyperalgesia and orofacial allodynia, together with a significant increase in the expression of CGRP and c-Fos genes in trigeminal ganglia and central areas.	Nitroglycerin	9-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	148-153
29344989-9	2018	The results showed that GTN triggered the increase in CGRP levels in plasma, trigeminal ganglion neurons and ex vivo meningeal preparations.	Nitroglycerin	24-27	calcitonin-related polypeptide alpha	Rattus norvegicus	54-58
29871702-0	2018	Sublingual nitroglycerin for early blood pressure control in hypertensive emergencies: observations from an emergency department clinical audit in Sri Lanka.	Nitroglycerin	11-24	sorcin	Homo sapiens	147-150
29344989-10	2018	Likewise, GTN-induced c-fos expression in TNC.	Nitroglycerin	10-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
29696345-4	2018	Subsequently, HUT testing, either drug-free or, if necessary, with pharmacological provocation (usually nitroglycerin) has proven to be a useful and safe modality for identifying susceptibility to VVS.	Nitroglycerin	104-117	VVS	Homo sapiens	197-200
29486167-0	2018	AMPA receptor GluA1 Ser831 phosphorylation is critical for nitroglycerin-induced migraine-like pain.	Nitroglycerin	59-72	glutamate ionotropic receptor AMPA type subunit 1	Homo sapiens	14-19
29773813-7	2018	Mechanistically, NTG-A-009 suppressed Th1 and Th17 cells differentiation via the modulation of JAK/STAT signaling pathway.	Nitroglycerin	17-20	negative elongation factor complex member C/D	Homo sapiens	38-41
28738691-0	2018	Selective cephalic upregulation of p-ERK, CamKII and p-CREB in response to glyceryl trinitrate infusion.	Nitroglycerin	75-94	cAMP responsive element binding protein 1	Rattus norvegicus	55-59
28816506-2	2018	Methods We investigated the anti-nociceptive effects of inhibition of monoacylglycerol lipase (MGL), a key enzyme in the hydrolysis of the 2-arachidonoylglycerol, in a rat model of migraine based on nitroglycerin (NTG) administration.	Nitroglycerin	199-212	monoglyceride lipase	Rattus norvegicus	70-93
28816506-2	2018	Methods We investigated the anti-nociceptive effects of inhibition of monoacylglycerol lipase (MGL), a key enzyme in the hydrolysis of the 2-arachidonoylglycerol, in a rat model of migraine based on nitroglycerin (NTG) administration.	Nitroglycerin	199-212	monoglyceride lipase	Rattus norvegicus	95-98
28816506-2	2018	Methods We investigated the anti-nociceptive effects of inhibition of monoacylglycerol lipase (MGL), a key enzyme in the hydrolysis of the 2-arachidonoylglycerol, in a rat model of migraine based on nitroglycerin (NTG) administration.	Nitroglycerin	214-217	monoglyceride lipase	Rattus norvegicus	70-93
28816506-2	2018	Methods We investigated the anti-nociceptive effects of inhibition of monoacylglycerol lipase (MGL), a key enzyme in the hydrolysis of the 2-arachidonoylglycerol, in a rat model of migraine based on nitroglycerin (NTG) administration.	Nitroglycerin	214-217	monoglyceride lipase	Rattus norvegicus	95-98
29486167-3	2018	In the present study, we observed that AMPA receptor GluA1 Ser831 phosphorylation was enhanced in the spinal trigeminal nucleus caudalis (Sp5C) after intraperitoneal injection of nitroglycerin (NTG).	Nitroglycerin	179-192	glutamate ionotropic receptor AMPA type subunit 1	Homo sapiens	53-58
29486167-3	2018	In the present study, we observed that AMPA receptor GluA1 Ser831 phosphorylation was enhanced in the spinal trigeminal nucleus caudalis (Sp5C) after intraperitoneal injection of nitroglycerin (NTG).	Nitroglycerin	194-197	glutamate ionotropic receptor AMPA type subunit 1	Homo sapiens	53-58
29486167-5	2018	Interestingly, targeted mutation of GluA1 Ser831 site to prevent phosphorylation significantly inhibited NTG-induced migraine-like pain.	Nitroglycerin	105-108	glutamate ionotropic receptor AMPA type subunit 1	Homo sapiens	36-41
29486167-6	2018	Moreover, NTG incubation caused a robust Ca2+ influx in cultured brainstem neurons, which was dramatically inhibited by GluA1 S831A (serine at the 831 site of GluA1 is mutated to alanine) phospho-deficient mutation, and treatment with 1-naphthyl acetyl spermine (NASPM), a selective Ca2+-permeable AMPA receptor channel blocker, dose-dependently blocked the NTG-evoked increase of Ca2+ influx in the cultured neurons.	Nitroglycerin	10-13	glutamate ionotropic receptor AMPA type subunit 1	Homo sapiens	120-125
29486167-6	2018	Moreover, NTG incubation caused a robust Ca2+ influx in cultured brainstem neurons, which was dramatically inhibited by GluA1 S831A (serine at the 831 site of GluA1 is mutated to alanine) phospho-deficient mutation, and treatment with 1-naphthyl acetyl spermine (NASPM), a selective Ca2+-permeable AMPA receptor channel blocker, dose-dependently blocked the NTG-evoked increase of Ca2+ influx in the cultured neurons.	Nitroglycerin	10-13	glutamate ionotropic receptor AMPA type subunit 1	Homo sapiens	159-164
29486167-6	2018	Moreover, NTG incubation caused a robust Ca2+ influx in cultured brainstem neurons, which was dramatically inhibited by GluA1 S831A (serine at the 831 site of GluA1 is mutated to alanine) phospho-deficient mutation, and treatment with 1-naphthyl acetyl spermine (NASPM), a selective Ca2+-permeable AMPA receptor channel blocker, dose-dependently blocked the NTG-evoked increase of Ca2+ influx in the cultured neurons.	Nitroglycerin	358-361	glutamate ionotropic receptor AMPA type subunit 1	Homo sapiens	120-125
29486167-6	2018	Moreover, NTG incubation caused a robust Ca2+ influx in cultured brainstem neurons, which was dramatically inhibited by GluA1 S831A (serine at the 831 site of GluA1 is mutated to alanine) phospho-deficient mutation, and treatment with 1-naphthyl acetyl spermine (NASPM), a selective Ca2+-permeable AMPA receptor channel blocker, dose-dependently blocked the NTG-evoked increase of Ca2+ influx in the cultured neurons.	Nitroglycerin	358-361	glutamate ionotropic receptor AMPA type subunit 1	Homo sapiens	159-164
29431638-3	2018	We report here that the nitric oxide (NO) donor glyceryl trinitrate (GTN) converts TNFalpha, generated from immune cells or cancer cells stimulated by chemotherapy, into a prodeath mediator in colon and mammary cancer cells.	Nitroglycerin	48-67	tumor necrosis factor	Homo sapiens	83-91
29431638-3	2018	We report here that the nitric oxide (NO) donor glyceryl trinitrate (GTN) converts TNFalpha, generated from immune cells or cancer cells stimulated by chemotherapy, into a prodeath mediator in colon and mammary cancer cells.	Nitroglycerin	69-72	tumor necrosis factor	Homo sapiens	83-91
29431638-4	2018	GTN-mediated S-nitrosylation of cIAP1 on cysteines 571 and 574 inhibited its E3 ubiquitin ligase activity, which in turn reduced Lys63-linked ubiquitination of RIP1 and initiated assembly of a death complex.	Nitroglycerin	0-3	baculoviral IAP repeat containing 2	Homo sapiens	32-37
29431638-4	2018	GTN-mediated S-nitrosylation of cIAP1 on cysteines 571 and 574 inhibited its E3 ubiquitin ligase activity, which in turn reduced Lys63-linked ubiquitination of RIP1 and initiated assembly of a death complex.	Nitroglycerin	0-3	receptor interacting serine/threonine kinase 1	Homo sapiens	160-164
29408867-6	2018	Surprisingly, only 52  FosB gene targets were shared between NTG and APP mice; the vast majority of targets were unique to one genotype or the other.	Nitroglycerin	61-64	FBJ osteosarcoma oncogene B	Mus musculus	23-27
29358221-0	2018	Sustained Formation of Nitroglycerin-Derived Nitric Oxide by Aldehyde Dehydrogenase-2 in Vascular Smooth Muscle without Added Reductants: Implications for the Development of Nitrate Tolerance.	Nitroglycerin	23-36	aldehyde dehydrogenase 2 family member	Homo sapiens	61-85
29358221-1	2018	According to current views, oxidation of aldehyde dehydrogenase-2 (ALDH2) during glyceryltrinitrate (GTN) biotransformation is essentially involved in vascular nitrate tolerance and explains the dependence of this reaction on added thiols.	Nitroglycerin	81-99	aldehyde dehydrogenase 2 family member	Homo sapiens	41-65
29358221-1	2018	According to current views, oxidation of aldehyde dehydrogenase-2 (ALDH2) during glyceryltrinitrate (GTN) biotransformation is essentially involved in vascular nitrate tolerance and explains the dependence of this reaction on added thiols.	Nitroglycerin	81-99	aldehyde dehydrogenase 2 family member	Homo sapiens	67-72
29358221-1	2018	According to current views, oxidation of aldehyde dehydrogenase-2 (ALDH2) during glyceryltrinitrate (GTN) biotransformation is essentially involved in vascular nitrate tolerance and explains the dependence of this reaction on added thiols.	Nitroglycerin	101-104	aldehyde dehydrogenase 2 family member	Homo sapiens	41-65
29358221-1	2018	According to current views, oxidation of aldehyde dehydrogenase-2 (ALDH2) during glyceryltrinitrate (GTN) biotransformation is essentially involved in vascular nitrate tolerance and explains the dependence of this reaction on added thiols.	Nitroglycerin	101-104	aldehyde dehydrogenase 2 family member	Homo sapiens	67-72
29358221-2	2018	Using a novel fluorescent intracellular nitric oxide (NO) probe expressed in vascular smooth muscle cells (VSMCs), we observed ALDH2-catalyzed formation of NO from GTN in the presence of exogenously added dithiothreitol (DTT), whereas only a short burst of NO, corresponding to a single turnover of ALDH2, occurred in the absence of DTT.	Nitroglycerin	164-167	aldehyde dehydrogenase 2 family member	Homo sapiens	127-132
29358221-2	2018	Using a novel fluorescent intracellular nitric oxide (NO) probe expressed in vascular smooth muscle cells (VSMCs), we observed ALDH2-catalyzed formation of NO from GTN in the presence of exogenously added dithiothreitol (DTT), whereas only a short burst of NO, corresponding to a single turnover of ALDH2, occurred in the absence of DTT.	Nitroglycerin	164-167	aldehyde dehydrogenase 2 family member	Homo sapiens	299-304
29358221-7	2018	On a longer time scale, mechanism-based, thiol-refractive irreversible inactivation of ALDH2, and possibly depletion of the endogenous reductant, will render blood vessels tolerant to GTN.	Nitroglycerin	184-187	aldehyde dehydrogenase 2 family member	Homo sapiens	87-92
29431026-4	2018	Mechanistic studies on the nitroglycerin bioactivation process revealed that during bioconversion of nitroglycerin and in the presence of reactive oxygen and nitrogen species the active site thiols of ALDH-2 are oxidized and the enzyme activity is lost.	Nitroglycerin	27-40	aldehyde dehydrogenase 2 family member	Homo sapiens	201-207
29431026-4	2018	Mechanistic studies on the nitroglycerin bioactivation process revealed that during bioconversion of nitroglycerin and in the presence of reactive oxygen and nitrogen species the active site thiols of ALDH-2 are oxidized and the enzyme activity is lost.	Nitroglycerin	101-114	aldehyde dehydrogenase 2 family member	Homo sapiens	201-207
29546048-6	2018	Also, there was statistically significant NAMPT overexpression in patients with TNG (n = 30).	Nitroglycerin	80-83	nicotinamide phosphoribosyltransferase	Homo sapiens	42-47
28990289-5	2018	The NTG administration caused mouse head discomforts, decreased tolerance to cold or hot stimulation and increased content of nitric oxide, calcitonin gene-related peptide and neuropeptide Y in serum, which were ameliorated by intraperitoneal injection of VP.	Nitroglycerin	4-7	neuropeptide Y	Mus musculus	176-190
28990289-6	2018	The levels of two inflammatory factors, interleukin (IL)-1beta and inducible nitric oxide synthase, in dura mater were increased by NTG treatment, while the increase was attenuated by application of VP.	Nitroglycerin	132-135	interleukin 1 beta	Mus musculus	40-62
28990289-7	2018	In addition, the phosphorylation levels of protein kinase C (PKC) alpha, gamma, delta and epsilon were increased by NTG and decreased by VP.	Nitroglycerin	116-119	protein kinase C, alpha	Mus musculus	43-97
28990289-9	2018	Two substrates of PKC, cAMP-response element binding protein 1 and signal transducer and activator of transcription 1 were also phosphorylated by NTG application, and the phosphorylation level was attenuated by VP, consistent with the change of PKC informs.	Nitroglycerin	146-149	signal transducer and activator of transcription 1	Mus musculus	67-117
29408867-7	2018	We also found a functional shift in the repertoire of  FosB gene targets between NTG and APP mice.	Nitroglycerin	81-84	FBJ osteosarcoma oncogene B	Mus musculus	55-59
29375397-15	2017	The exposure of AIA cerebrovascular fractions to GTN increased BDNF levels while the exposure of control fractions to L-NAME decreased BDNF levels.	Nitroglycerin	49-52	brain-derived neurotrophic factor	Rattus norvegicus	63-67
27899434-10	2018	Following the resolution of the concussion-evoked cephalic hypersensitivity, administration of GTN produced a renewed and pronounced cephalic pain hypersensitivity that was inhibited by sumatriptan or anti-CGRP antibody treatment as well as a CGRP-dependent CPA.	Nitroglycerin	95-98	calcitonin-related polypeptide alpha	Rattus norvegicus	206-210
27899434-10	2018	Following the resolution of the concussion-evoked cephalic hypersensitivity, administration of GTN produced a renewed and pronounced cephalic pain hypersensitivity that was inhibited by sumatriptan or anti-CGRP antibody treatment as well as a CGRP-dependent CPA.	Nitroglycerin	95-98	calcitonin-related polypeptide alpha	Rattus norvegicus	243-247
27899434-12	2018	Conclusions Concussion leads to the development of headache and pain-related behaviours, in particular sustained enhanced responses to GTN, that are mediated through a CGRP-dependent mechanism.	Nitroglycerin	135-138	calcitonin-related polypeptide alpha	Rattus norvegicus	168-172
29128404-10	2018	No differences in ZO-1 relative expression patterns were observed in cultured cells, with increased expression in IL-6 in cells exposed to nTg milk than controls, with the Tg group being similar to all groups.	Nitroglycerin	139-142	interleukin 6	Homo sapiens	114-118
29147842-7	2018	In addition, TET pretreatment blocked the activation of S100B and p-ERK in trigeminal ganglion SGCs of NTG-treated rats.	Nitroglycerin	103-106	S100 calcium binding protein B	Rattus norvegicus	56-61
29074411-7	2018	The nitroglycerin stimulated NO production was significantly (P &lt; 0.01) increased by Galphaq-RGS2 loop activator administration in normal rats, too.	Nitroglycerin	4-17	G protein subunit alpha q	Rattus norvegicus	88-95
29074411-7	2018	The nitroglycerin stimulated NO production was significantly (P &lt; 0.01) increased by Galphaq-RGS2 loop activator administration in normal rats, too.	Nitroglycerin	4-17	regulator of G-protein signaling 2	Rattus norvegicus	96-100
28856479-7	2017	Human experimental studies have reported elevated plasma CGRP levels during both spontaneous and glyceryl trinitrate-induced cluster attacks.	Nitroglycerin	97-116	calcitonin related polypeptide alpha	Homo sapiens	57-61
28031354-1	2018	BACKGROUND: Nitroglycerin (also known as glyceryl trinitrate (GTN)), a vasodilator best known for treatment of ischemic heart disease, has also been investigated for its potential therapeutic benefit in ischemic stroke.	Nitroglycerin	12-25	guanine nucleotide binding protein, alpha transducing 3	Mus musculus	41-67
29279024-11	2018	Consistent with this conclusion is the attenuation of NTG-induced relaxation response in young SOD2+/- mice.	Nitroglycerin	54-57	superoxide dismutase 2, mitochondrial	Mus musculus	95-99
29040598-10	2017	On metformin, GTN improved, independent of glycosylated hemoglobin (HbA1c), by 3.3 percentage units [95% confidence interval (CI) 0.3, 6.3, P = 0.03] and insulin dose reduced by 0.2 U/kg/d (95% CI 0.1, 0.3, P = 0.001) during 12 months, with effects from 3 months.	Nitroglycerin	14-17	insulin	Homo sapiens	154-161
27919017-7	2017	Results KYNA-A1 abolished NTG-induced hyperalgesia in both pain models; NTG alone or associated to formalin injection induced an increased mRNA expression of CGRP, nNOS and cytokines in the trigeminal ganglia and central areas, which was reduced by KYNA-A1.	Nitroglycerin	72-75	calcitonin-related polypeptide alpha	Rattus norvegicus	158-162
28830679-1	2017	Nitroglycerin (Gtn) is a treatment for cardiovascular patients due to its vasodilatory actions, but induces tolerance when given chronically.	Nitroglycerin	0-13	guanine nucleotide binding protein, alpha transducing 3	Mus musculus	15-18
27919017-7	2017	Results KYNA-A1 abolished NTG-induced hyperalgesia in both pain models; NTG alone or associated to formalin injection induced an increased mRNA expression of CGRP, nNOS and cytokines in the trigeminal ganglia and central areas, which was reduced by KYNA-A1.	Nitroglycerin	72-75	nitric oxide synthase 1	Rattus norvegicus	164-168
27919017-8	2017	Additionally, NTG caused a significant increase in nNOS immunoreactivity in the NTC, which was prevented by KYNA-A1.	Nitroglycerin	14-17	nitric oxide synthase 1	Rattus norvegicus	51-55
28744782-9	2017	MetHb formed and increased to 6% up to day 1 and then slowly decreased in the HBOC/NTG mixture whereas it remained unchanged in the HBOC/saline mixture.	Nitroglycerin	83-86	hemoglobin subunit gamma 2	Homo sapiens	0-5
28342890-3	2017	ALDH2 has been suggested as a critical factor for nitroglycerin-mediated vasodilation by some human studies and in vitro studies.	Nitroglycerin	50-63	aldehyde dehydrogenase 2 family member	Homo sapiens	0-5
28342890-5	2017	In the present study, the contribution of ALDH2 to the vasodilatory effect of nitroglycerin sublingual tablets was investigated among three genotype groups (ALDH2*1/*1, ALDH2*1/*2, and ALDH2*2/*2) in Japanese.	Nitroglycerin	78-91	aldehyde dehydrogenase 2 family member	Homo sapiens	42-47
28625856-0	2017	Nitroglycerin increases serotonin transporter expression in rat spinal cord but anandamide modulated this effect.	Nitroglycerin	0-13	solute carrier family 6 member 4	Rattus norvegicus	24-45
28625856-6	2017	Our aim was to investigate the effect of an endogenous cannabinoid, anandamide (AEA) on the NTG-induced changes on serotonin transporter (5-HTT) expression in the upper cervical spinal cord (C1-C2) of the rat, where most of the trigeminal nociceptive afferents convey.	Nitroglycerin	92-95	solute carrier family 6 member 4	Rattus norvegicus	115-136
28768233-4	2017	A total of 246 and 1031 differentially expressed genes (DEGs) were identified in the heart of TGL and TGH in relation to NTG littermates at ~ 6 months of age.	Nitroglycerin	121-124	carboxylesterase 1D	Mus musculus	102-105
28827781-2	2017	Flow-mediated vasodilation (FMD) and nitroglycerine-induced vasodilation (NID) were inversely correlated with LDL-C in the 957 statin naive subjects but not in the 392 subjects receiving statin therapy.	Nitroglycerin	37-51	component of oligomeric golgi complex 2	Homo sapiens	110-115
28559108-8	2017	Only GTN elicited phosphorylation of eNOS at Ser1177 and Thr495.	Nitroglycerin	5-8	nitric oxide synthase 3	Homo sapiens	37-41
28884307-7	2017	This effect was associated to a significant inhibition of nitroglycerin-induced increase in c-Fos, TRPA1 and neuropeptides mRNA levels in medulla-pons area, in the cervical spinal cord and in the trigeminal ganglion.	Nitroglycerin	58-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
28884307-7	2017	This effect was associated to a significant inhibition of nitroglycerin-induced increase in c-Fos, TRPA1 and neuropeptides mRNA levels in medulla-pons area, in the cervical spinal cord and in the trigeminal ganglion.	Nitroglycerin	58-71	transient receptor potential cation channel, subfamily A, member 1	Rattus norvegicus	99-104
27758841-2	2017	This study aims to elucidate the effect of exogenous nitric oxide (NO) administration, using GTN, on carbon tetrachloride (CCl4)-induced oxidative stress and liver injury in rats.	Nitroglycerin	93-96	C-C motif chemokine ligand 4	Rattus norvegicus	123-127
27758841-3	2017	The results obtained demonstrated that NO generated by the administration of GTN affords protection against CCl4-induced oxidative stress and liver injury.	Nitroglycerin	77-80	C-C motif chemokine ligand 4	Rattus norvegicus	108-112
28485846-5	2017	Results are also presented which demonstrate that nasal oxytocin inhibits responses of trigeminal nucleus caudalis neurons to noxious stimulation using either noxious facial shock or nitroglycerin infusion.	Nitroglycerin	183-196	oxytocin/neurophysin I prepropeptide	Homo sapiens	56-64
28617840-12	2017	CONCLUSIONS: Treadmill test with administration of sublingual nitroglycerines might be safely used to reproduce syncope in patients with VVS.	Nitroglycerin	62-77	VVS	Homo sapiens	137-140
28343071-11	2017	Meanwhile, immunohistochemistry results showed that NTG treatment significantly activated c-Fos neurons while BAI treatment inhibited the expression of c-Fos.	Nitroglycerin	52-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
28659861-7	2017	A previous study demonstrated a reduction of KAT-II expression following NTG administration in animals.	Nitroglycerin	73-76	aminoadipate aminotransferase	Rattus norvegicus	45-51
28423279-2	2017	MCp+ complexes possess remarkable Ng binding ability, particularly for M = Be and Mg.	Nitroglycerin	34-36	CD46 molecule	Homo sapiens	0-3
28070672-12	2017	These human and rodent data suggest that global PGRN reduction induces microglial TNG expression and increases AD risk by exacerbating neuronal injury and tau pathology, rather than by accelerating Abeta pathology.	Nitroglycerin	82-85	granulin precursor	Homo sapiens	48-52
28423052-4	2017	Our aim here was to determine whether abnormal maternal inflammation causing FGR is linked to placental HIF-1alpha accumulation and whether GTN administration could prevent increases in placental HIF-1alpha.	Nitroglycerin	140-143	hypoxia inducible factor 1 subunit alpha	Rattus norvegicus	196-206
28453571-10	2017	Shenmai injection further ameliorated inhibition of the cGMP/cGK-I signalling pathway triggered by nitroglycerin-induced tolerance through up-regulating the protein expression of sGC, cGK-I, and P-VASP and down- regulating the proteins expression of PDE1A.	Nitroglycerin	99-112	guanylate cyclase 1 soluble subunit alpha 1	Rattus norvegicus	179-182
28453571-10	2017	Shenmai injection further ameliorated inhibition of the cGMP/cGK-I signalling pathway triggered by nitroglycerin-induced tolerance through up-regulating the protein expression of sGC, cGK-I, and P-VASP and down- regulating the proteins expression of PDE1A.	Nitroglycerin	99-112	phosphodiesterase 1A	Rattus norvegicus	250-255
28453571-11	2017	In vitro studies showed that Shenmai injection could recover the attenuated vasodilation response to nitroglycerin following incubation (of aortic rings) with nitroglycerin via activating the enzymes of sGC and cGK-I.	Nitroglycerin	101-114	guanylate cyclase 1 soluble subunit alpha 1	Rattus norvegicus	203-206
28453571-11	2017	In vitro studies showed that Shenmai injection could recover the attenuated vasodilation response to nitroglycerin following incubation (of aortic rings) with nitroglycerin via activating the enzymes of sGC and cGK-I.	Nitroglycerin	159-172	guanylate cyclase 1 soluble subunit alpha 1	Rattus norvegicus	203-206
28423052-12	2017	The GTN-mediated attenuation of placental HIF-1alpha accumulation in LPS-treated rats provides insight into the mechanism by which GTN improves inflammation-induced complications of pregnancy.	Nitroglycerin	4-7	hypoxia inducible factor 1 subunit alpha	Rattus norvegicus	42-52
28423052-12	2017	The GTN-mediated attenuation of placental HIF-1alpha accumulation in LPS-treated rats provides insight into the mechanism by which GTN improves inflammation-induced complications of pregnancy.	Nitroglycerin	131-134	hypoxia inducible factor 1 subunit alpha	Rattus norvegicus	42-52
28425266-9	2017	Immunohistochemistry disclosed significantly increased c-fos-positive neurons in ipsilateral brainstem TNC compared to the contralateral side (brain stem LI ipsilateral 25.4 +- 4.7, contralateral 11.8 +- 1.9, P &lt; 0.05) in chronic NCN-ligated rats exposed to acute NTG.	Nitroglycerin	267-270	tenascin C	Rattus norvegicus	103-106
27778243-9	2016	RESULTS: Total cellular and nuclear levels of the proteins Nrf2, HO1, and NQO1 were elevated in TNC after NTG injection, and Nrf2 was found to be located in the nucleus and cytoplasm of the neurons.	Nitroglycerin	106-109	NFE2 like bZIP transcription factor 2	Rattus norvegicus	59-63
27364224-9	2017	Finally, in vitro exposure of cerebral microvessel-enriched fractions to glycerol trinitrate enhanced BDNF production.	Nitroglycerin	73-92	brain-derived neurotrophic factor	Rattus norvegicus	102-106
28361462-9	2017	HOMA2 for insulin sensitivity (HOMA2-%S) was 48.40 (39.70, 68.70), 110.20 (62.55, 141.95), and 101.20 (79.90, 140.10) in HTG, NTG, and control groups, respectively.	Nitroglycerin	126-129	insulin	Homo sapiens	10-17
28361462-10	2017	HOMA2 for insulin resistance (HOMA2-IR) was 2.09 (1.46, 2.52), 0.92 (0.70, 1.61), and 0.99 (0.71, 1.25) in HTG, NTG, and control groups, respectively.	Nitroglycerin	112-115	insulin	Homo sapiens	10-17
28377719-2	2017	However, prolonged GTN treatment induces tolerance, largely due to increased oxidative stress and reduced aldehyde dehydrogenase-2 (ALDH-2) expression.	Nitroglycerin	19-22	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	106-130
28377719-2	2017	However, prolonged GTN treatment induces tolerance, largely due to increased oxidative stress and reduced aldehyde dehydrogenase-2 (ALDH-2) expression.	Nitroglycerin	19-22	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	132-138
28377719-9	2017	GTN+placebo infusion significantly increased superoxide levels, decreased ALDH-2 and attenuated GTN-mediated vascular relaxation.	Nitroglycerin	0-3	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	74-80
28377719-10	2017	Serelaxin co-treatment with GTN significantly enhanced GTN-mediated vascular relaxation, reduced superoxide levels and increased ALDH-2 expression compared to GTN+placebo-treated rats.	Nitroglycerin	28-31	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	129-135
28377719-11	2017	Conclusion: Our data demonstrate that a combination of serelaxin treatment with low dose GTN attenuates the development of GTN-induced tolerance by reducing superoxide production and increasing ALDH-2 expression in the rat aorta.	Nitroglycerin	89-92	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	194-200
28377719-11	2017	Conclusion: Our data demonstrate that a combination of serelaxin treatment with low dose GTN attenuates the development of GTN-induced tolerance by reducing superoxide production and increasing ALDH-2 expression in the rat aorta.	Nitroglycerin	123-126	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	194-200
27886414-8	2017	We further found that NTG increased the blood levels of PACAP and cortisol, which was significantly reduced by ghrelin treatment.	Nitroglycerin	22-25	adenylate cyclase activating polypeptide 1	Homo sapiens	56-61
27875242-0	2017	Involvement of BDNF/TrkB and ERK/CREB axes in nitroglycerin-induced rat migraine and effects of estrogen on these signals in the migraine.	Nitroglycerin	46-59	brain-derived neurotrophic factor	Rattus norvegicus	15-19
27875242-0	2017	Involvement of BDNF/TrkB and ERK/CREB axes in nitroglycerin-induced rat migraine and effects of estrogen on these signals in the migraine.	Nitroglycerin	46-59	neurotrophic receptor tyrosine kinase 2	Rattus norvegicus	20-24
27875242-0	2017	Involvement of BDNF/TrkB and ERK/CREB axes in nitroglycerin-induced rat migraine and effects of estrogen on these signals in the migraine.	Nitroglycerin	46-59	Eph receptor B1	Rattus norvegicus	29-32
27875242-0	2017	Involvement of BDNF/TrkB and ERK/CREB axes in nitroglycerin-induced rat migraine and effects of estrogen on these signals in the migraine.	Nitroglycerin	46-59	cAMP responsive element binding protein 1	Rattus norvegicus	33-37
27875242-6	2017	Results showed that BDNF, TrkB, phosphor(p)-ERK and p-CREB were up-regulated in the brain neurons of both male and female rats with NTG-induced migraine compared to non-migraine control, whereas their expression levels were decreased in headache-free intervals of the migraine compared to migraine attacks.	Nitroglycerin	132-135	brain-derived neurotrophic factor	Rattus norvegicus	20-24
27875242-6	2017	Results showed that BDNF, TrkB, phosphor(p)-ERK and p-CREB were up-regulated in the brain neurons of both male and female rats with NTG-induced migraine compared to non-migraine control, whereas their expression levels were decreased in headache-free intervals of the migraine compared to migraine attacks.	Nitroglycerin	132-135	neurotrophic receptor tyrosine kinase 2	Rattus norvegicus	26-30
27875242-6	2017	Results showed that BDNF, TrkB, phosphor(p)-ERK and p-CREB were up-regulated in the brain neurons of both male and female rats with NTG-induced migraine compared to non-migraine control, whereas their expression levels were decreased in headache-free intervals of the migraine compared to migraine attacks.	Nitroglycerin	132-135	Eph receptor B1	Rattus norvegicus	44-47
27875242-6	2017	Results showed that BDNF, TrkB, phosphor(p)-ERK and p-CREB were up-regulated in the brain neurons of both male and female rats with NTG-induced migraine compared to non-migraine control, whereas their expression levels were decreased in headache-free intervals of the migraine compared to migraine attacks.	Nitroglycerin	132-135	cAMP responsive element binding protein 1	Rattus norvegicus	54-58
27875242-8	2017	Female ovariectomized rats showed significant reduction in the expression of BDNF, TrkB, p-CREB and p-ERK in both attacks and intervals of NTG-induced migraine, relative to rats that have their ovaries.	Nitroglycerin	139-142	brain-derived neurotrophic factor	Rattus norvegicus	77-81
27875242-8	2017	Female ovariectomized rats showed significant reduction in the expression of BDNF, TrkB, p-CREB and p-ERK in both attacks and intervals of NTG-induced migraine, relative to rats that have their ovaries.	Nitroglycerin	139-142	cAMP responsive element binding protein 1	Rattus norvegicus	91-95
27875242-8	2017	Female ovariectomized rats showed significant reduction in the expression of BDNF, TrkB, p-CREB and p-ERK in both attacks and intervals of NTG-induced migraine, relative to rats that have their ovaries.	Nitroglycerin	139-142	Eph receptor B1	Rattus norvegicus	102-105
27875242-10	2017	Collectively, this study unveiled a positive correlation of BDNF/TrkB and ERK/CREB axes in NTG-induced migraine and promoting effects of estrogen on their signals in the migraine.	Nitroglycerin	91-94	brain-derived neurotrophic factor	Rattus norvegicus	60-64
27875242-10	2017	Collectively, this study unveiled a positive correlation of BDNF/TrkB and ERK/CREB axes in NTG-induced migraine and promoting effects of estrogen on their signals in the migraine.	Nitroglycerin	91-94	neurotrophic receptor tyrosine kinase 2	Rattus norvegicus	65-69
27875242-10	2017	Collectively, this study unveiled a positive correlation of BDNF/TrkB and ERK/CREB axes in NTG-induced migraine and promoting effects of estrogen on their signals in the migraine.	Nitroglycerin	91-94	Eph receptor B1	Rattus norvegicus	74-77
27875242-10	2017	Collectively, this study unveiled a positive correlation of BDNF/TrkB and ERK/CREB axes in NTG-induced migraine and promoting effects of estrogen on their signals in the migraine.	Nitroglycerin	91-94	cAMP responsive element binding protein 1	Rattus norvegicus	78-82
28745655-4	2017	In 46.3% of HTG patients and 38.7% of NTG patients, anti-MBP antibodies were lower than in the controls.	Nitroglycerin	38-41	myelin basic protein	Homo sapiens	57-60
28745655-8	2017	In this aspect, an increase in anti-MBP antibody production at the stage of early hydrodynamic disturbances (NTG) and its decrease at the stage of pronounced changes (HTG) are perfectly natural.	Nitroglycerin	109-112	myelin basic protein	Homo sapiens	36-39
27778243-3	2016	In this study, we aimed to evaluate the role of nuclear factor E2-related factor 2/antioxidant response element (Nrf2/ARE) pathway in regulating the activation of the trigeminovascular system (TGVS) and hypersensitivity in nitroglycerin (NTG)-induced hyperalgesia rats.	Nitroglycerin	223-236	NFE2 like bZIP transcription factor 2	Rattus norvegicus	113-117
27778243-3	2016	In this study, we aimed to evaluate the role of nuclear factor E2-related factor 2/antioxidant response element (Nrf2/ARE) pathway in regulating the activation of the trigeminovascular system (TGVS) and hypersensitivity in nitroglycerin (NTG)-induced hyperalgesia rats.	Nitroglycerin	238-241	NFE2 like bZIP transcription factor 2	Rattus norvegicus	113-117
28224331-0	2017	The interaction of CCl4 with Ng (Ng = He, Ne, Ar), O2, D2O and ND3: rovibrational energies, spectroscopic constants and theoretical calculations.	Nitroglycerin	29-31	C-C motif chemokine ligand 4	Homo sapiens	19-23
27716557-7	2016	RESULTS AND CONCLUSIONS: Univariate regression analysis revealed that serum level of PEDF was significantly correlated with body mass index, high-density lipoprotein cholesterol, glucose, FMD, nitroglycerine-induced vasodilation, and brachial artery IMT.	Nitroglycerin	193-207	serpin family F member 1	Homo sapiens	85-89
27716557-8	2016	Multivariate analysis revealed that serum levels of PEDF remained an independent predictor of nitroglycerine-induced vasodilation (beta=-0.20, P=0.02) and brachial artery IMT (beta=0.14, P=0.03) after adjustment of cardiovascular risk factors, while serum level of PEDF was not associated with FMD (beta=-0.02, P=0.79).	Nitroglycerin	94-108	serpin family F member 1	Homo sapiens	52-56
27778243-9	2016	RESULTS: Total cellular and nuclear levels of the proteins Nrf2, HO1, and NQO1 were elevated in TNC after NTG injection, and Nrf2 was found to be located in the nucleus and cytoplasm of the neurons.	Nitroglycerin	106-109	heme oxygenase 1	Rattus norvegicus	65-68
27778243-9	2016	RESULTS: Total cellular and nuclear levels of the proteins Nrf2, HO1, and NQO1 were elevated in TNC after NTG injection, and Nrf2 was found to be located in the nucleus and cytoplasm of the neurons.	Nitroglycerin	106-109	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	74-78
27366896-10	2016	Moreover, D-OCT quantified evident changes of the blood flow in normal nailfold capillaries after application of nitroglycerine and brimonidine.	Nitroglycerin	113-127	plexin A2	Homo sapiens	12-15
27679490-0	2016	Formation of Nitric Oxide by Aldehyde Dehydrogenase-2 Is Necessary and Sufficient for Vascular Bioactivation of Nitroglycerin.	Nitroglycerin	112-125	aldehyde dehydrogenase 2 family member	Homo sapiens	29-53
27679490-1	2016	Aldehyde dehydrogenase-2 (ALDH2) catalyzes vascular bioactivation of the antianginal drug nitroglycerin (GTN), resulting in activation of soluble guanylate cyclase (sGC) and cGMP-mediated vasodilation.	Nitroglycerin	90-103	aldehyde dehydrogenase 2 family member	Homo sapiens	0-24
27679490-1	2016	Aldehyde dehydrogenase-2 (ALDH2) catalyzes vascular bioactivation of the antianginal drug nitroglycerin (GTN), resulting in activation of soluble guanylate cyclase (sGC) and cGMP-mediated vasodilation.	Nitroglycerin	90-103	aldehyde dehydrogenase 2 family member	Homo sapiens	26-31
27679490-1	2016	Aldehyde dehydrogenase-2 (ALDH2) catalyzes vascular bioactivation of the antianginal drug nitroglycerin (GTN), resulting in activation of soluble guanylate cyclase (sGC) and cGMP-mediated vasodilation.	Nitroglycerin	105-108	aldehyde dehydrogenase 2 family member	Homo sapiens	0-24
27679490-1	2016	Aldehyde dehydrogenase-2 (ALDH2) catalyzes vascular bioactivation of the antianginal drug nitroglycerin (GTN), resulting in activation of soluble guanylate cyclase (sGC) and cGMP-mediated vasodilation.	Nitroglycerin	105-108	aldehyde dehydrogenase 2 family member	Homo sapiens	26-31
27679490-2	2016	We have previously shown that a minor reaction of ALDH2-catalyzed GTN bioconversion, accounting for about 5% of the main clearance-based turnover yielding inorganic nitrite, results in direct NO formation and concluded that this minor pathway could provide the link between vascular GTN metabolism and activation of sGC.	Nitroglycerin	66-69	aldehyde dehydrogenase 2 family member	Homo sapiens	50-55
27679490-2	2016	We have previously shown that a minor reaction of ALDH2-catalyzed GTN bioconversion, accounting for about 5% of the main clearance-based turnover yielding inorganic nitrite, results in direct NO formation and concluded that this minor pathway could provide the link between vascular GTN metabolism and activation of sGC.	Nitroglycerin	283-286	aldehyde dehydrogenase 2 family member	Homo sapiens	50-55
27679490-6	2016	The addition of 1 mum GTN to VSMC expressing either wild-type or C301S/C303S ALDH2 resulted in pronounced intracellular NO elevation, with maximal concentrations of 7 and 17 nm, respectively.	Nitroglycerin	22-25	aldehyde dehydrogenase 2 family member	Homo sapiens	77-82
27679490-7	2016	Formation of GTN-derived NO correlated well with activation of purified sGC in VSMC lysates and cGMP accumulation in intact porcine aortic endothelial cells infected with wild-type or mutant ALDH2.	Nitroglycerin	13-16	aldehyde dehydrogenase 2 family member	Homo sapiens	191-196
27679490-9	2016	The present study demonstrates that ALDH2-catalyzed NO formation is necessary and sufficient for GTN bioactivation in VSMC.	Nitroglycerin	97-100	aldehyde dehydrogenase 2 family member	Homo sapiens	36-41
29634107-3	2016	In this study, we investigated in viti the inactivation of yeast aldehyde dehydrogenase (ALDH) by nitroglycerin (GTN) in the presence and absence of LA and DHLA.	Nitroglycerin	98-111	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	89-93
29634107-3	2016	In this study, we investigated in viti the inactivation of yeast aldehyde dehydrogenase (ALDH) by nitroglycerin (GTN) in the presence and absence of LA and DHLA.	Nitroglycerin	113-116	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	89-93
29634107-5	2016	The results indicated that in vito both LA and DHLA restored and protected ALDH activity against GTN-induced inactivation, while treatment of rats with LA and GTN in combination did not provide any protection against GTN-induced ALDH inhibition.	Nitroglycerin	97-100	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	75-79
27334392-7	2016	Total consumption of regular insulin was significantly lower in the NTG group, median 8 (range 0-50) versus 13 (0-90) international units, p = 0.005.	Nitroglycerin	68-71	insulin	Homo sapiens	29-36
28029666-0	2016	Comparison of Fissure Healing and The Incidence of Headache Among the Patients Treated with Endo- and Perianal Application of 0.2% Glyceryl Trinitrate for Chronic Anal Fissure.	Nitroglycerin	131-150	mannosidase endo-alpha	Homo sapiens	92-96
27366896-12	2016	The quantitative measurements of the blood flow in the D-OCT images of the healthy participant showed significant quantitative differences in blood flow before and after application of nitroglycerine (mean difference, 0.035; 95% CI, 0.008-0.061; P = .02) and brimonidine (mean difference, -0.015; 95% CI, -0.082 to -0.039; P &lt; .001).	Nitroglycerin	185-199	plexin A2	Homo sapiens	57-60
27436480-0	2016	Ghrelin attenuates hyperalgesia and light aversion-induced by nitroglycerin in male rats.	Nitroglycerin	62-75	ghrelin and obestatin prepropeptide	Rattus norvegicus	0-7
27436480-4	2016	Results suggest that the effects of NTG can be largely reversed by administration of ghrelin, which mimics the effects of sumatriptan used as relevant positive therapeutic control in this study.	Nitroglycerin	36-39	ghrelin and obestatin prepropeptide	Rattus norvegicus	85-92
27357950-8	2016	GTN in vivo administration leads to endothelial dysfunction, nitrate tolerance, aortic and cardiac oxidative stress, formation of DNA adducts, stabilization of p53 and apoptotic death of vascular cells in a dose-dependent fashion.	Nitroglycerin	0-3	transformation related protein 53, pseudogene	Mus musculus	160-163
27306299-6	2016	Moreover, we investigated BDNF synthesis in brain slices exposed to the NO donor glyceryl trinitrate.	Nitroglycerin	81-100	brain derived neurotrophic factor	Homo sapiens	26-30
26512068-7	2016	RESULTS AND CONCLUSION: Our results show that NTG is able to increase TRPV1, nNOS, NF-kappaB and COX-2 and decrease KAT-II expression in the C1-C2 segments.	Nitroglycerin	46-49	aminoadipate aminotransferase	Rattus norvegicus	116-122
26512068-7	2016	RESULTS AND CONCLUSION: Our results show that NTG is able to increase TRPV1, nNOS, NF-kappaB and COX-2 and decrease KAT-II expression in the C1-C2 segments.	Nitroglycerin	46-49	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	70-75
26512068-7	2016	RESULTS AND CONCLUSION: Our results show that NTG is able to increase TRPV1, nNOS, NF-kappaB and COX-2 and decrease KAT-II expression in the C1-C2 segments.	Nitroglycerin	46-49	nitric oxide synthase 1	Rattus norvegicus	77-81
26512068-7	2016	RESULTS AND CONCLUSION: Our results show that NTG is able to increase TRPV1, nNOS, NF-kappaB and COX-2 and decrease KAT-II expression in the C1-C2 segments.	Nitroglycerin	46-49	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	97-102
27357950-9	2016	Mice lacking O (6)-methylguanine-DNA methyltransferase displayed more vascular O (6)-methylguanine adducts and oxidative stress under GTN therapy than wild-type mice.	Nitroglycerin	134-137	O-6-methylguanine-DNA methyltransferase	Mus musculus	13-54
27543774-8	2016	As a result of the study, the mean number of neurons in CA1, CA2, and CA3 regions of the hippocampus and the total number of neurons were decreased in the hippocampus samples of the NTG and especially the TG subjects.	Nitroglycerin	182-185	carbonic anhydrase 1	Rattus norvegicus	56-59
26729049-8	2016	administration of nitroglycerine produces an increase in CGRP levels in the brainstem and trigeminal ganglia, which is inhibited by a pre-treatment with lacosamide.	Nitroglycerin	18-32	calcitonin-related polypeptide alpha	Rattus norvegicus	57-61
27323160-0	2016	Aldehyde dehydrogenase 2 protects human umbilical vein endothelial cells against oxidative damage and increases endothelial nitric oxide production to reverse nitroglycerin tolerance.	Nitroglycerin	159-172	aldehyde dehydrogenase 2 family member	Homo sapiens	0-24
27323160-3	2016	In vivo studies have demonstrated that aldehyde dehydrogenase 2 (ALDH2) plays important roles in GTN biotransformation and tolerance.	Nitroglycerin	97-100	aldehyde dehydrogenase 2 family member	Homo sapiens	39-63
27323160-3	2016	In vivo studies have demonstrated that aldehyde dehydrogenase 2 (ALDH2) plays important roles in GTN biotransformation and tolerance.	Nitroglycerin	97-100	aldehyde dehydrogenase 2 family member	Homo sapiens	65-70
27323160-4	2016	Thus, modification of ALDH2 expression represents a potentially effective strategy to prevent and reverse GTN tolerance and endothelial dysfunction.	Nitroglycerin	106-109	aldehyde dehydrogenase 2 family member	Homo sapiens	22-27
27323160-9	2016	Overexpression of ALDH2 increased cell survival against GTN-induced cytotoxicity and conferred protection from oxidative damage resulting from nitrate tolerance, accompanied by decreased production of intracellular reactive oxygen species and reduced expression of heme oxygenase 1.	Nitroglycerin	56-59	aldehyde dehydrogenase 2 family member	Homo sapiens	18-23
27323160-10	2016	Furthermore, ALDH2 overexpression promoted Akt phosphorylation under GTN tolerance conditions.	Nitroglycerin	69-72	aldehyde dehydrogenase 2 family member	Homo sapiens	13-18
27323160-11	2016	ALDH2 gene transfection can reverse and prevent tolerance to GTN through its bioactivation and protect against oxidative damage, preventing the development of endothelial dysfunction.	Nitroglycerin	61-64	aldehyde dehydrogenase 2 family member	Homo sapiens	0-5
27551315-11	2016	In addition to cardiac enlargement, NG37 transgenic mice on high-fat diet also exhibited highly irregular bradycardia not present in either high-fat diet nTG littermates or normal-diet transgenic litter mates.	Nitroglycerin	154-157	von Willebrand factor A domain containing 7	Mus musculus	36-40
27386628-6	2016	Both proteins showed cytoplasmic pattern, whereas the DAB wt% of BCL2A1 and Wnt11 expression was highest in moles that developed to GTN, gradually reduced in spontaneously regressed moles and normal villi (all p &lt; 0.01).	Nitroglycerin	132-135	BCL2 related protein A1	Homo sapiens	65-71
27386628-6	2016	Both proteins showed cytoplasmic pattern, whereas the DAB wt% of BCL2A1 and Wnt11 expression was highest in moles that developed to GTN, gradually reduced in spontaneously regressed moles and normal villi (all p &lt; 0.01).	Nitroglycerin	132-135	Wnt family member 11	Homo sapiens	76-81
26980454-2	2016	MATERIAL &amp; METHODS: Mad2 siRNA was encapsulated in EGFR targeted and nontargeted (NTG) CS nanoparticles by electrostatic interaction.	Nitroglycerin	86-89	mitotic arrest deficient 2 like 1	Homo sapiens	24-28
26779834-7	2016	Furthermore, A-317491, a P2X3 antagonist, which inhibits endothelial cell-dependent hyperalgesia, also prevents GTN and mast cell-mediated hyperalgesia.	Nitroglycerin	112-115	purinergic receptor P2X 3	Rattus norvegicus	25-29
26779834-8	2016	We conclude that delayed-onset mechanical hyperalgesia induced by GTN is mediated by activation of mast cells, which in turn release mediators that stimulate endothelial cells to release ATP, to act on P2X3, a ligand-gated ion channel, in perivascular nociceptors.	Nitroglycerin	66-69	purinergic receptor P2X 3	Rattus norvegicus	202-206
26152915-7	2016	We ascribed the resistance to NTG to the activation of the sympathetic, vasopressin, and renin-angiotensin systems ("neurohormonal activation").	Nitroglycerin	30-33	arginine vasopressin	Homo sapiens	72-83
27420615-1	2016	Human oxyhemoglobin exhibits high resistance to nitroglycerin during incubation of the protein with this compound for 0.3-3 h. Prolonged exposure (24 h) leads to activation of methemoglobin production.	Nitroglycerin	48-61	hemoglobin subunit gamma 2	Homo sapiens	176-189
27420615-2	2016	In the presence of nitroglycerin hemoglobin molecules undergo rapid oxidation during deoxygenation with formation of methemoglobin as the terminal product of human oxyhemoglobin interaction with nitroglycerin.	Nitroglycerin	19-32	hemoglobin subunit gamma 2	Homo sapiens	117-130
27420615-2	2016	In the presence of nitroglycerin hemoglobin molecules undergo rapid oxidation during deoxygenation with formation of methemoglobin as the terminal product of human oxyhemoglobin interaction with nitroglycerin.	Nitroglycerin	195-208	hemoglobin subunit gamma 2	Homo sapiens	117-130
27085197-13	2016	db-cAMP/NTG additive to the preservation solution contributed to the maintenance of VEC expression after reperfusion.	Nitroglycerin	8-11	cadherin 5	Rattus norvegicus	84-87
27328402-10	2016	Furthermore, increased NO production in accompany with reduced ROCK2 expression were observed in both the atorvastatin and nitroglycerin groups, and these benefits were further enhanced by combined therapy (P&lt;0.05).	Nitroglycerin	123-136	rho-associated protein kinase 2	Oryctolagus cuniculus	63-68
27328402-12	2016	CONCLUSION: Nitroglycerin-derived exogenous NO could effectively inhibit ROCK2 expression in rabbits with dyslipidemia which is independent of lipid-modification, and these efficacies could be enhanced by statins therapy.	Nitroglycerin	12-25	rho-associated protein kinase 2	Oryctolagus cuniculus	73-78
27543774-8	2016	As a result of the study, the mean number of neurons in CA1, CA2, and CA3 regions of the hippocampus and the total number of neurons were decreased in the hippocampus samples of the NTG and especially the TG subjects.	Nitroglycerin	182-185	carbonic anhydrase 2	Rattus norvegicus	61-64
27543774-8	2016	As a result of the study, the mean number of neurons in CA1, CA2, and CA3 regions of the hippocampus and the total number of neurons were decreased in the hippocampus samples of the NTG and especially the TG subjects.	Nitroglycerin	182-185	carbonic anhydrase 3	Rattus norvegicus	70-73
27543774-13	2016	In immunohistochemical sections, c-FOS positivity was decreased in the NTG and especially the TG.	Nitroglycerin	71-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
27543774-14	2016	Otherwise, PGC-1  positive cells were increased in the NTG and especially the TG.	Nitroglycerin	55-58	PPARG coactivator 1 alpha	Sus scrofa	11-16
26832618-4	2016	In addition to its dehydrogenase activity, ALDH2 also exhibits esterase and reductase activities, with the main substrates for these three activities being aldehydes, 4-nitrophenyl acetate and nitroglycerin, respectively.	Nitroglycerin	193-206	aldehyde dehydrogenase 2 family member	Homo sapiens	43-48
27150105-0	2016	Valproate ameliorates nitroglycerin-induced migraine in trigeminal nucleus caudalis in rats through inhibition of NF-kB.	Nitroglycerin	22-35	nuclear factor kappa B subunit 1	Rattus norvegicus	114-119
26456070-7	2016	Increased c-Fos expression in the TNC, thermal hyperalgesia, tactile allodynia and orofacial hypersensitivity were apparently good endpoints in mice that were increased by NTG-administration.	Nitroglycerin	172-175	FBJ osteosarcoma oncogene	Mus musculus	10-15
26456070-8	2016	The NTG-induced increase in c-Fos expression was prevented by topiramate but not by sumatriptan treatment.	Nitroglycerin	4-7	FBJ osteosarcoma oncogene	Mus musculus	28-33
26645254-1	2016	BACKGROUND AND PURPOSE: The Efficacy of Nitric Oxide in Stroke (ENOS) trial found that transdermal glyceryl trinitrate (GTN, a nitric oxide donor) lowered blood pressure but did not improve functional outcome in patients with acute stroke.	Nitroglycerin	99-118	nitric oxide synthase 3	Homo sapiens	64-68
26645254-0	2016	Glyceryl Trinitrate for Acute Intracerebral Hemorrhage: Results From the Efficacy of Nitric Oxide in Stroke (ENOS) Trial, a Subgroup Analysis.	Nitroglycerin	0-19	nitric oxide synthase 3	Homo sapiens	109-113
26645254-1	2016	BACKGROUND AND PURPOSE: The Efficacy of Nitric Oxide in Stroke (ENOS) trial found that transdermal glyceryl trinitrate (GTN, a nitric oxide donor) lowered blood pressure but did not improve functional outcome in patients with acute stroke.	Nitroglycerin	120-123	nitric oxide synthase 3	Homo sapiens	64-68
25724914-6	2015	Interestingly, pre-treatment with the effective anti-migraine substances L-nitro-arginine methyl ester and sumatriptan prevented glyceryl trinitrate-induced mast cell degranulation whereas the calcitonin gene-related peptide-receptor antagonist olcegepant and the substance P receptor antagonist L-733,060 did not affect mast cell degranulation.	Nitroglycerin	129-148	tachykinin receptor 1	Homo sapiens	264-284
26839558-0	2016	Endothelium-Independent Hypoxic Contraction Is Prevented Specifically by Nitroglycerin via Inhibition of Akt Kinase in Porcine Coronary Artery.	Nitroglycerin	73-86	AKT serine/threonine kinase 1	Homo sapiens	105-108
26839558-11	2016	The reduction of Akt-p at Ser-473 by NTG, DETA NONOate, and 8-Br-cGMP was significantly inhibited by ODQ, PKG-I.	Nitroglycerin	37-40	AKT serine/threonine kinase 1	Homo sapiens	17-20
26839558-12	2016	The decrease in Akt-p level by NTG and 8-Br-cGMP was prevented by calyculin A but not by okadaic acid.	Nitroglycerin	31-34	AKT serine/threonine kinase 1	Homo sapiens	16-19
26839558-14	2016	These results demonstrated that the endothelium-independent sustained hypoxic vasoconstriction can be prevented by NTG and that the inhibition of PI3K/Akt signaling pathway may be involved.	Nitroglycerin	115-118	AKT serine/threonine kinase 1	Homo sapiens	151-154
26584637-4	2015	Our findings reveal that NTG significantly inhibits human U937 cell adhesion to NO-deficient human microvascular ECs in vitro through an increase in endothelial NO and decrease in endothelial ICAM-1 clustering, as determined by NO analyzer, microfluorimetry, and immunofluorescence staining.	Nitroglycerin	25-28	intercellular adhesion molecule 1	Homo sapiens	192-198
26386799-9	2015	Patients taking versus not taking insulin had 0.83 more episodes of angina and used 1.40 more NTG doses per week, increases evident only in those taking insulin without concomitant metformin (Pinteraction &lt; .05 for both).	Nitroglycerin	94-97	insulin	Homo sapiens	34-41
26347109-1	2015	BACKGROUND: Nitroglycerin (NTG) increases tumor blood flow and oxygenation by inhibiting hypoxia-inducible-factor (HIF)-1.	Nitroglycerin	12-25	hypoxia inducible factor 1 subunit alpha	Homo sapiens	89-121
26347109-1	2015	BACKGROUND: Nitroglycerin (NTG) increases tumor blood flow and oxygenation by inhibiting hypoxia-inducible-factor (HIF)-1.	Nitroglycerin	27-30	hypoxia inducible factor 1 subunit alpha	Homo sapiens	89-121
26386799-11	2015	Patients taking sulfonylureas or insulin had more angina and used more NTG, while metformin was not associated with angina burden.	Nitroglycerin	71-74	insulin	Homo sapiens	33-40
25994587-7	2015	EAAT-2 induction by CEF reduced SNL-induced neuropathic pain in both NTg and GET-1 mice.	Nitroglycerin	69-72	solute carrier family 1 (glial high affinity glutamate transporter), member 2	Mus musculus	0-6
26379783-9	2015	In OB1 group PWV showed correlation with age (r = 0.492, p = 0.001), HR (r = 0.324, p = 0.04), %FM (r = 0.328; p = 0.039), NTG% (r = -0.332, p = 0.036) as well as hsCRP (r = 0.394, p = 0.014).	Nitroglycerin	123-126	HOP homeobox	Homo sapiens	3-6
26379783-12	2015	The values of nitroglycerin-mediated dilatation differed between OB1 and OB2 groups (21.47 +- 8.31 vs. 28.54 +- 8.16 %; p &lt; 0.0001) and were lower as compared with CG (31.42 +- 5.95 %; p = 0.0005).	Nitroglycerin	14-27	HOP homeobox	Homo sapiens	65-68
25608877-6	2015	Furthermore, we investigated whether URB937 affects NTG-induced c-Fos expression in the brain.	Nitroglycerin	52-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
25608877-9	2015	Mapping of brain nuclei activated by NTG indicates that URB937 significantly reduces c-Fos expression in the nucleus trigeminalis caudalis and the locus coeruleus.	Nitroglycerin	37-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
26435741-4	2015	Moreover NTG can reduce HIF-1alpha levels in hypoxic tumour tissues and this may have anti-angiogenic, pro-apoptotic and anti-efflux effects.	Nitroglycerin	9-12	hypoxia inducible factor 1 subunit alpha	Homo sapiens	24-34
25869522-0	2015	Effect of soluble guanylyl cyclase activator and stimulator therapy on nitroglycerin-induced nitrate tolerance in rats.	Nitroglycerin	71-84	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	10-34
25910421-0	2015	Inhibition of FAAH reduces nitroglycerin-induced migraine-like pain and trigeminal neuronal hyperactivity in mice.	Nitroglycerin	27-40	fatty acid amide hydrolase	Mus musculus	14-18
25910421-4	2015	We have therefore investigated mice with a genetic deletion of the two main cannabinoid receptors CB1 and CB2, or the main endocannabinoid degrading enzymes, FAAH and monoacylglycerol lipase (MAGL), which degrades 2-arachidonoylglycerol (2-AG), in a nitroglycerine-induced animal model of migraine.	Nitroglycerin	250-264	monoglyceride lipase	Mus musculus	192-196
28162273-11	2015	Finally, I will discuss our recent efforts to decipher regulatory mechanism of the TNF-alpha/TNFR1 signalling cell death pathway by S-nitrosylation following GTN treatment.	Nitroglycerin	158-161	tumor necrosis factor	Homo sapiens	83-92
28162273-11	2015	Finally, I will discuss our recent efforts to decipher regulatory mechanism of the TNF-alpha/TNFR1 signalling cell death pathway by S-nitrosylation following GTN treatment.	Nitroglycerin	158-161	TNF receptor superfamily member 1A	Homo sapiens	93-98
25892078-7	2015	In the present study, the expression of p-ERK, CGRP and COX-2 was detected in the dura mater, trigeminal ganglion (TG) and spinal trigeminal nucleus caudalis in NTG-induced rats and ESTG models by immunohistochemistry.	Nitroglycerin	161-164	calcitonin-related polypeptide alpha	Rattus norvegicus	47-51
25892078-7	2015	In the present study, the expression of p-ERK, CGRP and COX-2 was detected in the dura mater, trigeminal ganglion (TG) and spinal trigeminal nucleus caudalis in NTG-induced rats and ESTG models by immunohistochemistry.	Nitroglycerin	161-164	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	56-61
25869522-3	2015	Therefore, the present study aims at investigating the effects of the therapy with the sGC activator BAY 60-2770 and the sGC stimulator BAY 41-8543 on side effects induced by chronic nitroglycerin treatment.	Nitroglycerin	183-196	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	121-124
25869522-7	2015	sGC activator therapy improves partially the adverse effects of nitroglycerin therapy whereas sGC stimulation has only minor beneficial effects pointing to a nitroglycerin-dependent sGC oxidation/inactivation mechanism contributing to nitrate tolerance.	Nitroglycerin	64-77	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	0-3
25869522-7	2015	sGC activator therapy improves partially the adverse effects of nitroglycerin therapy whereas sGC stimulation has only minor beneficial effects pointing to a nitroglycerin-dependent sGC oxidation/inactivation mechanism contributing to nitrate tolerance.	Nitroglycerin	158-171	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	94-97
25869522-7	2015	sGC activator therapy improves partially the adverse effects of nitroglycerin therapy whereas sGC stimulation has only minor beneficial effects pointing to a nitroglycerin-dependent sGC oxidation/inactivation mechanism contributing to nitrate tolerance.	Nitroglycerin	158-171	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	94-97
25754766-4	2015	Specifically, we investigated the effects of (i) ALDH2 inhibition by cyanamide or propionaldehyde and the (ii) tolerance-independent inactivation of ALDH2 by glyceryl trinitrate (GTN) on the vasodilator activity of nitrite.	Nitroglycerin	158-177	aldehyde dehydrogenase 2 family member	Homo sapiens	149-154
25754766-4	2015	Specifically, we investigated the effects of (i) ALDH2 inhibition by cyanamide or propionaldehyde and the (ii) tolerance-independent inactivation of ALDH2 by glyceryl trinitrate (GTN) on the vasodilator activity of nitrite.	Nitroglycerin	179-182	aldehyde dehydrogenase 2 family member	Homo sapiens	149-154
25425044-6	2015	GTN resulted in a significant increase in brain cortex and microsomal lipid peroxidation levels although brain calcium, vitamin A, vitamin C, and vitamin E, and brain microsomal-reduced glutathione (GSH), glutathione peroxidase (GSH-Px), and plasma-membrane Ca(2+)-ATPase values decreased through GTN.	Nitroglycerin	0-3	glutathione peroxidase 1	Rattus norvegicus	229-235
25873742-8	2015	A random-effects model revealed that CPAP significantly improved endothelial function as assessed by flow-mediated dilation (weighted mean difference of 2.92, 95% CI 2.21-3.63, P &lt; .001), whereas there was no significant improvement in endothelial function in response to nitroglycerin-mediated dilation (weighted mean difference of 0.90, 95% CI -1.63 to 3.43, P = .48).	Nitroglycerin	275-288	centromere protein J	Homo sapiens	37-41
25638347-7	2015	Nitroglycerin and antihypertensive drugs such as beta-blockers, ACE inhibitors or calcium channel blockers may also be used to lower blood pressure and to improve the oxygen demand of heart.	Nitroglycerin	0-13	angiotensin I converting enzyme	Homo sapiens	64-67
25413692-2	2015	METHODS: Computational-based molecular modeling was used to predict the binding of the substrates propionaldehyde, 4-hydroxynonenal, nitroglycerin, and all-trans retinaldehyde to ALDH1B1.	Nitroglycerin	133-146	aldehyde dehydrogenase 1 family member B1	Homo sapiens	179-186
25413692-3	2015	Based on positive in silico results, the capacity of purified human recombinant ALDH1B1 to metabolize nitroglycerin and all-trans retinaldehyde was explored.	Nitroglycerin	102-115	aldehyde dehydrogenase 1 family member B1	Homo sapiens	80-87
25413692-8	2015	RESULTS: ALDH1B1 metabolizes (and appears to be inhibited by) nitroglycerin and has favorable kinetics for the metabolism of all-trans retinaldehyde.	Nitroglycerin	62-75	aldehyde dehydrogenase 1 family member B1	Homo sapiens	9-16
25413692-13	2015	CONCLUSIONS: ALDH1B1 metabolizes nitroglycerin and all-trans-retinaldehyde.	Nitroglycerin	33-46	aldehyde dehydrogenase 1 family member B1	Homo sapiens	13-20
25459486-7	2015	Increased phosphorylation of ERK and Bcl2, after reperfusion in groups stored in glyceryl-trinitrate, cariporide or both along with increased phospho-STAT3 levels in the glyceryl-trinitrate/cariporide group correlated with functional recovery.	Nitroglycerin	81-100	mitogen-activated protein kinase 1	Homo sapiens	29-32
25762630-3	2015	This synergistic effect requires the generation of reactive oxygen species (ROS) from H89 and NO from GTN treatment that causes cGMP production and PKG activation.	Nitroglycerin	102-105	protein kinase cGMP-dependent 1	Homo sapiens	148-151
25706190-6	2015	Moreover, IKK/nuclear factor-kappaB (NF-kappaB) signaling is found to be activated by NG nanoparticle-induced ROS and serves to antagonize NG nanoparticle-induced apoptosis in HepG2 cells.	Nitroglycerin	86-88	nuclear factor kappa B subunit 1	Homo sapiens	10-35
25706190-6	2015	Moreover, IKK/nuclear factor-kappaB (NF-kappaB) signaling is found to be activated by NG nanoparticle-induced ROS and serves to antagonize NG nanoparticle-induced apoptosis in HepG2 cells.	Nitroglycerin	86-88	nuclear factor kappa B subunit 1	Homo sapiens	37-46
24895375-1	2015	BACKGROUND AND AIMS: Calcitonin gene-related peptide (CGRP) and glyceryl trinitrate (GTN) infusion in migraineurs provokes headache resembling spontaneous migraine, and CGRP receptor antagonists are effective in the treatment of acute migraine.	Nitroglycerin	85-88	calcitonin-related polypeptide alpha	Rattus norvegicus	169-173
25459486-7	2015	Increased phosphorylation of ERK and Bcl2, after reperfusion in groups stored in glyceryl-trinitrate, cariporide or both along with increased phospho-STAT3 levels in the glyceryl-trinitrate/cariporide group correlated with functional recovery.	Nitroglycerin	170-189	signal transducer and activator of transcription 3	Homo sapiens	150-155
25459486-7	2015	Increased phosphorylation of ERK and Bcl2, after reperfusion in groups stored in glyceryl-trinitrate, cariporide or both along with increased phospho-STAT3 levels in the glyceryl-trinitrate/cariporide group correlated with functional recovery.	Nitroglycerin	81-100	BCL2 apoptosis regulator	Homo sapiens	37-41
25459486-7	2015	Increased phosphorylation of ERK and Bcl2, after reperfusion in groups stored in glyceryl-trinitrate, cariporide or both along with increased phospho-STAT3 levels in the glyceryl-trinitrate/cariporide group correlated with functional recovery.	Nitroglycerin	170-189	mitogen-activated protein kinase 1	Homo sapiens	29-32
25098345-1	2014	The aim of this study was to investigate whether N-arachidonic acid ethanolamine (anandamide, AEA) transporter contributed to calcitonin gene-related peptide (CGRP) expression mediated by nitroglycerin (GTN) in peripheral blood mononuclear cells (PBMCs) of healthy volunteers and its association with the mitochondrial aldehyde dehydrogenase-2 (ALDH2) Glu504Lys (ALDH2*2) polymorphism.	Nitroglycerin	188-201	calcitonin related polypeptide alpha	Homo sapiens	126-157
25576686-1	2015	The vascular bioactivation of the antianginal drug nitroglycerin (GTN), yielding 1,2-glycerol dinitrate and nitric oxide or a related activator of soluble guanylate cyclase, is catalyzed by aldehyde dehydrogenase-2 (ALDH2) in rodent and human blood vessels.	Nitroglycerin	51-64	aldehyde dehydrogenase 2 family member	Homo sapiens	190-214
25576686-1	2015	The vascular bioactivation of the antianginal drug nitroglycerin (GTN), yielding 1,2-glycerol dinitrate and nitric oxide or a related activator of soluble guanylate cyclase, is catalyzed by aldehyde dehydrogenase-2 (ALDH2) in rodent and human blood vessels.	Nitroglycerin	51-64	aldehyde dehydrogenase 2 family member	Homo sapiens	216-221
25576686-1	2015	The vascular bioactivation of the antianginal drug nitroglycerin (GTN), yielding 1,2-glycerol dinitrate and nitric oxide or a related activator of soluble guanylate cyclase, is catalyzed by aldehyde dehydrogenase-2 (ALDH2) in rodent and human blood vessels.	Nitroglycerin	66-69	aldehyde dehydrogenase 2 family member	Homo sapiens	190-214
25576686-1	2015	The vascular bioactivation of the antianginal drug nitroglycerin (GTN), yielding 1,2-glycerol dinitrate and nitric oxide or a related activator of soluble guanylate cyclase, is catalyzed by aldehyde dehydrogenase-2 (ALDH2) in rodent and human blood vessels.	Nitroglycerin	66-69	aldehyde dehydrogenase 2 family member	Homo sapiens	216-221
25576686-2	2015	The essential role of ALDH2 has been confirmed in many studies and is considered as general principle of GTN-induced vasodilation in mammals.	Nitroglycerin	105-108	aldehyde dehydrogenase 2 family member	Bos taurus	22-27
25340599-0	2015	Improvement of hepatocyte transplantation efficiency in the mdr2-/- mouse model by glyceryl trinitrate.	Nitroglycerin	83-102	ATP-binding cassette, sub-family B (MDR/TAP), member 4	Mus musculus	60-64
25340599-10	2015	CONCLUSION: The use of GTN improves hepatocyte engraftment and correction of metabolic disease in mdr2 (-/-) mice.	Nitroglycerin	23-26	ATP-binding cassette, sub-family B (MDR/TAP), member 4	Mus musculus	98-102
25135879-4	2014	The results showed that NG had strong cytotoxicity to induce apoptosis, which was characterized by a significant externalization of phosphatidylserine, nuclear morphological changes and enhanced Bax-to-Bcl-2 ratio.	Nitroglycerin	24-26	BCL2 associated X, apoptosis regulator	Homo sapiens	195-198
25135879-4	2014	The results showed that NG had strong cytotoxicity to induce apoptosis, which was characterized by a significant externalization of phosphatidylserine, nuclear morphological changes and enhanced Bax-to-Bcl-2 ratio.	Nitroglycerin	24-26	BCL2 apoptosis regulator	Homo sapiens	202-207
25135879-5	2014	Moreover, the release of cytochrome c (Cyt c) from mitochondria and the activation of caspase-9/3 were also detected, indicating that NG may induce apoptosis through a mitochondrial-mediated pathway.	Nitroglycerin	134-136	cytochrome c, somatic	Homo sapiens	25-37
25135879-5	2014	Moreover, the release of cytochrome c (Cyt c) from mitochondria and the activation of caspase-9/3 were also detected, indicating that NG may induce apoptosis through a mitochondrial-mediated pathway.	Nitroglycerin	134-136	cytochrome c, somatic	Homo sapiens	39-44
25135879-5	2014	Moreover, the release of cytochrome c (Cyt c) from mitochondria and the activation of caspase-9/3 were also detected, indicating that NG may induce apoptosis through a mitochondrial-mediated pathway.	Nitroglycerin	134-136	caspase 9	Homo sapiens	86-95
25591559-0	2015	Effect of aldehyde dehydrogenase 2 gene polymorphism on hemodynamics after nitroglycerin intervention in Northern Chinese Han population.	Nitroglycerin	75-88	aldehyde dehydrogenase 2 family member	Homo sapiens	10-34
25591559-2	2015	Aldehyde dehydrogenase 2 (ALDH2) is a key enzyme in the human body that facilitates the biological metabolism of NTG.	Nitroglycerin	113-116	aldehyde dehydrogenase 2 family member	Homo sapiens	0-24
25591559-2	2015	Aldehyde dehydrogenase 2 (ALDH2) is a key enzyme in the human body that facilitates the biological metabolism of NTG.	Nitroglycerin	113-116	aldehyde dehydrogenase 2 family member	Homo sapiens	26-31
25591559-4	2015	Some reports still contradict the results that the correlation between ALDH2 gene polymorphisms and NTG and its clinical efficacy is different.	Nitroglycerin	100-103	aldehyde dehydrogenase 2 family member	Homo sapiens	71-76
25591559-6	2015	This study aimed to investigate the influence of ALDH2 gene polymorphism on intervention with sublingual NTG using noninvasive hemodynamic parameters of cardiac output (CO) and systemic vascular resistance (SVR) in Northern Chinese Han population.	Nitroglycerin	105-108	aldehyde dehydrogenase 2 family member	Homo sapiens	49-54
25591559-18	2015	CONCLUSION: ALDH2 (G504A) gene polymorphism is associated with changes in noninvasive hemodynamic parameters (i.e. CO and SVR) after intervention with sublingual NTG.	Nitroglycerin	162-165	aldehyde dehydrogenase 2 family member	Homo sapiens	12-17
26334090-6	2015	On the other hand, nitroglycerin-induced relaxation was markedly attenuated by exposing the arteries to H(2)O(2) (pD2: 8.73 +- 0.05 and 8.30 +- 0.05), which was normalized in the presence of catalase (pD2: 8.59 +- 0.05).	Nitroglycerin	19-32	catalase	Rattus norvegicus	191-199
26272684-0	2015	Evaluation of ADMA-DDAH-NOS axis in specific brain areas following nitroglycerin administration: study in an animal model of migraine.	Nitroglycerin	67-80	dimethylarginine dimethylaminohydrolase 1	Homo sapiens	19-23
26272684-4	2015	GTN administration induces an increase in neuronal NOS (nNOS) that is simultaneous with a hyperalgesic condition.	Nitroglycerin	0-3	nitric oxide synthase 1	Homo sapiens	42-54
26272684-4	2015	GTN administration induces an increase in neuronal NOS (nNOS) that is simultaneous with a hyperalgesic condition.	Nitroglycerin	0-3	nitric oxide synthase 1	Homo sapiens	56-60
26272684-14	2015	RESULTS: ADMA levels and nNOS expression increased in the hypothalamus and medulla following GTN administration.	Nitroglycerin	93-96	nitric oxide synthase 1	Homo sapiens	25-29
26272684-18	2015	CONCLUSION: The present data suggest that ADMA accumulates in the brain after GTN administration via the inhibition of DDAH-1.	Nitroglycerin	78-81	dimethylarginine dimethylaminohydrolase 1	Homo sapiens	119-125
26457728-2	2015	Medical professionals and students often use the mnemonic "MONA" (morphine, oxygen, nitroglycerin and aspirin) to recall treatments for ACS; however, this list of therapies is outdated.	Nitroglycerin	84-97	GRB2 related adaptor protein 2	Homo sapiens	59-63
25369080-3	2014	METHODS: Five polymorphisms forming two haplotype blocks within the GTP cyclohydrolase 1 gene, encoding a rate limiting enzyme in tetrahydrobiopterin synthesis, were studied in the context of flow and nitroglycerin mediated dilation (FMD and NMD), intima-media thickness (IMT), and plasma concentrations of von Willebrand factor (vWF) and malondialdehyde (MDA).	Nitroglycerin	201-214	GTP cyclohydrolase 1	Homo sapiens	68-88
25098345-0	2014	Involvement of anandamide transporter in calcitonin gene-related peptide expression stimulated by nitroglycerin and influence of ALDH2 Glu504Lys polymorphism.	Nitroglycerin	98-111	calcitonin related polypeptide alpha	Homo sapiens	41-72
25098345-1	2014	The aim of this study was to investigate whether N-arachidonic acid ethanolamine (anandamide, AEA) transporter contributed to calcitonin gene-related peptide (CGRP) expression mediated by nitroglycerin (GTN) in peripheral blood mononuclear cells (PBMCs) of healthy volunteers and its association with the mitochondrial aldehyde dehydrogenase-2 (ALDH2) Glu504Lys (ALDH2*2) polymorphism.	Nitroglycerin	188-201	calcitonin related polypeptide alpha	Homo sapiens	159-163
25098345-1	2014	The aim of this study was to investigate whether N-arachidonic acid ethanolamine (anandamide, AEA) transporter contributed to calcitonin gene-related peptide (CGRP) expression mediated by nitroglycerin (GTN) in peripheral blood mononuclear cells (PBMCs) of healthy volunteers and its association with the mitochondrial aldehyde dehydrogenase-2 (ALDH2) Glu504Lys (ALDH2*2) polymorphism.	Nitroglycerin	203-206	calcitonin related polypeptide alpha	Homo sapiens	126-157
25098345-1	2014	The aim of this study was to investigate whether N-arachidonic acid ethanolamine (anandamide, AEA) transporter contributed to calcitonin gene-related peptide (CGRP) expression mediated by nitroglycerin (GTN) in peripheral blood mononuclear cells (PBMCs) of healthy volunteers and its association with the mitochondrial aldehyde dehydrogenase-2 (ALDH2) Glu504Lys (ALDH2*2) polymorphism.	Nitroglycerin	203-206	calcitonin related polypeptide alpha	Homo sapiens	159-163
25098345-2	2014	In 10 ALDH2*2-genotyped Chinese volunteers, we assessed the activity of AEA transporter and expression of CGRP messenger ribonucleic acid (mRNA) in cultured PBMCs treated with different concentration of GTN with or without pretreatment with AM404 (the AEA transporter blocker).	Nitroglycerin	203-206	calcitonin related polypeptide alpha	Homo sapiens	106-110
25098345-3	2014	In this study, the activity of AEA transporter and expression of CGRP mRNA elevated with the increase in the concentration of GTN.	Nitroglycerin	126-129	calcitonin related polypeptide alpha	Homo sapiens	65-69
25098345-4	2014	Pretreatment of the cells with AM404 (1 muM) 2 hours before GTN reduced the GTN-induced increase in both AEA transporter activity and CGRP mRNA expression significantly, and cells with the ALDH2*1/*1 homozygote genotype showed significantly higher activity of AEA transporter and CGRP mRNA expression than carriers of the ALDH2*2 allele.	Nitroglycerin	76-79	calcitonin related polypeptide alpha	Homo sapiens	134-138
25098345-4	2014	Pretreatment of the cells with AM404 (1 muM) 2 hours before GTN reduced the GTN-induced increase in both AEA transporter activity and CGRP mRNA expression significantly, and cells with the ALDH2*1/*1 homozygote genotype showed significantly higher activity of AEA transporter and CGRP mRNA expression than carriers of the ALDH2*2 allele.	Nitroglycerin	76-79	calcitonin related polypeptide alpha	Homo sapiens	280-284
25098345-4	2014	Pretreatment of the cells with AM404 (1 muM) 2 hours before GTN reduced the GTN-induced increase in both AEA transporter activity and CGRP mRNA expression significantly, and cells with the ALDH2*1/*1 homozygote genotype showed significantly higher activity of AEA transporter and CGRP mRNA expression than carriers of the ALDH2*2 allele.	Nitroglycerin	76-79	aldehyde dehydrogenase 2 family member	Homo sapiens	322-327
25098345-5	2014	Therefore, we strongly suggested that GTN can stimulate CGRP expression by elevating the AEA transporter activity, which is affected by ALDH2 Glu504Lys polymorphism.	Nitroglycerin	38-41	calcitonin related polypeptide alpha	Homo sapiens	56-60
25098345-5	2014	Therefore, we strongly suggested that GTN can stimulate CGRP expression by elevating the AEA transporter activity, which is affected by ALDH2 Glu504Lys polymorphism.	Nitroglycerin	38-41	aldehyde dehydrogenase 2 family member	Homo sapiens	136-141
25174989-1	2014	Bioconversion of glyceryl trinitrate (GTN) into nitric oxide (NO) by aldehyde dehydrogenase-2 (ALDH-2) is a crucial mechanism which drives vasodilatory and antiplatelet effect of organic nitrates in vitro and in vivo.	Nitroglycerin	17-36	aldehyde dehydrogenase 2 family member	Homo sapiens	69-93
25174989-1	2014	Bioconversion of glyceryl trinitrate (GTN) into nitric oxide (NO) by aldehyde dehydrogenase-2 (ALDH-2) is a crucial mechanism which drives vasodilatory and antiplatelet effect of organic nitrates in vitro and in vivo.	Nitroglycerin	17-36	aldehyde dehydrogenase 2 family member	Homo sapiens	95-101
25174989-1	2014	Bioconversion of glyceryl trinitrate (GTN) into nitric oxide (NO) by aldehyde dehydrogenase-2 (ALDH-2) is a crucial mechanism which drives vasodilatory and antiplatelet effect of organic nitrates in vitro and in vivo.	Nitroglycerin	38-41	aldehyde dehydrogenase 2 family member	Homo sapiens	69-93
25174989-1	2014	Bioconversion of glyceryl trinitrate (GTN) into nitric oxide (NO) by aldehyde dehydrogenase-2 (ALDH-2) is a crucial mechanism which drives vasodilatory and antiplatelet effect of organic nitrates in vitro and in vivo.	Nitroglycerin	38-41	aldehyde dehydrogenase 2 family member	Homo sapiens	95-101
25174989-5	2014	This was expressed by attenuation of platelet aggregation induced by thrombin (40U/mL), an effect accompanied by GTN-related induction of cGMP levels in platelets undergoing thrombin-induced aggregation.	Nitroglycerin	113-116	coagulation factor II, thrombin	Homo sapiens	69-77
25174989-5	2014	This was expressed by attenuation of platelet aggregation induced by thrombin (40U/mL), an effect accompanied by GTN-related induction of cGMP levels in platelets undergoing thrombin-induced aggregation.	Nitroglycerin	113-116	coagulation factor II, thrombin	Homo sapiens	174-182
25174989-6	2014	Both effects were associated to attenuated GTN-induced nitrite formation in platelets supernatants and to prominent nitration of ALDH-2, the GTN to NO metabolizing enzyme, suggesting that GTN tolerance was associated to reduced NO formation via impairment of ALDH-2.	Nitroglycerin	141-144	aldehyde dehydrogenase 2 family member	Homo sapiens	129-135
25174989-6	2014	Both effects were associated to attenuated GTN-induced nitrite formation in platelets supernatants and to prominent nitration of ALDH-2, the GTN to NO metabolizing enzyme, suggesting that GTN tolerance was associated to reduced NO formation via impairment of ALDH-2.	Nitroglycerin	141-144	aldehyde dehydrogenase 2 family member	Homo sapiens	129-135
25174989-11	2014	In conclusion, oxidative stress subsequent to prolonged use of organic nitrates, which occurs via nitration of ALDH-2, represents a key event in GTN tolerance, an effect counteracted both in vitro and in vivo by novel peroxynitrite decomposition catalyst.	Nitroglycerin	145-148	aldehyde dehydrogenase 2 family member	Homo sapiens	111-117
26171326-8	2014	The mean Hb (p=0.035), Hct (p=0.045), and MCH (p=0.032) were decreased by the end of the trial in the Sustac( ), but not in the Dorocontin( ) group, whilst there was no change in other CBC-diff parameters.	Nitroglycerin	102-108	pro-melanin concentrating hormone	Homo sapiens	42-45
24998872-0	2014	Correlation between algogenic effects of calcitonin-gene-related peptide (CGRP) and activation of trigeminal vascular system, in an in vivo experimental model of nitroglycerin-induced sensitization.	Nitroglycerin	162-175	calcitonin-related polypeptide alpha	Rattus norvegicus	41-72
24998872-3	2014	The present study was addressed to investigate CGRP-evoked behavior in nitric oxide (NO) sensitized rats, using an experimental model of nitroglycerin induced sensitization of trigeminal system, looking at neuropeptide release from different cerebral areas after the intra-peritoneal (i.p.)	Nitroglycerin	137-150	calcitonin-related polypeptide alpha	Rattus norvegicus	47-51
24998872-6	2014	On the contrary, CGRP injected in animals pre-treated with 10mg/kg nitroglycerin significantly increased the time spent in face rubbing.	Nitroglycerin	67-80	calcitonin-related polypeptide alpha	Rattus norvegicus	17-21
24998872-9	2014	treatment with nitroglycerin produced an increase of CGRP levels in brainstem and trigeminal ganglia, but not in the hypothalamus and hippocampus.	Nitroglycerin	15-28	calcitonin-related polypeptide alpha	Rattus norvegicus	53-57
24998872-10	2014	The absolute amounts of CGRP produced in the brainstem were lower compared to those in the trigeminal ganglion; however, after nitroglycerin stimulation the percentage increase was higher in the brainstem.	Nitroglycerin	127-140	calcitonin-related polypeptide alpha	Rattus norvegicus	24-28
25112288-9	2014	Meanwhile, VEGF-A expression reached its maximal expression with 7.5 mg/l NTG, but gradually declined by incubation with higher doses of NTG.	Nitroglycerin	74-77	vascular endothelial growth factor A	Homo sapiens	11-17
25112288-9	2014	Meanwhile, VEGF-A expression reached its maximal expression with 7.5 mg/l NTG, but gradually declined by incubation with higher doses of NTG.	Nitroglycerin	137-140	vascular endothelial growth factor A	Homo sapiens	11-17
25158065-0	2014	Nitroglycerin tolerance in caveolin-1 deficient mice.	Nitroglycerin	0-13	caveolin 1, caveolae protein	Mus musculus	27-37
25158065-2	2014	Previously, we have shown that the vasodilatory action of GTN is dependent on endothelial nitric oxide synthase (eNOS/NOS3) activity.	Nitroglycerin	58-61	nitric oxide synthase 3, endothelial cell	Mus musculus	78-111
25158065-2	2014	Previously, we have shown that the vasodilatory action of GTN is dependent on endothelial nitric oxide synthase (eNOS/NOS3) activity.	Nitroglycerin	58-61	nitric oxide synthase 3, endothelial cell	Mus musculus	118-122
25158065-5	2014	Therefore, we hypothesized that nitrate tolerance induced by persistent GTN treatment results from NOS3 dysfunction and vascular toxicity.	Nitroglycerin	72-75	nitric oxide synthase 3, endothelial cell	Mus musculus	99-103
25158065-6	2014	Exposure to GTN for 48-72 h resulted in nitrosation and depletion (&gt;50%) of Cav-1, NOS3 uncoupling as measured by an increase in peroxynitrite production (&gt;100%), and endothelial toxicity in cultured cells.	Nitroglycerin	12-15	caveolin 1, caveolae protein	Mus musculus	79-84
25158065-6	2014	Exposure to GTN for 48-72 h resulted in nitrosation and depletion (&gt;50%) of Cav-1, NOS3 uncoupling as measured by an increase in peroxynitrite production (&gt;100%), and endothelial toxicity in cultured cells.	Nitroglycerin	12-15	nitric oxide synthase 3, endothelial cell	Mus musculus	86-90
25158065-7	2014	In the Cav-1 deficient mice, NOS3 dysfunction was accompanied by GTN tolerance (&gt;50% dilation inhibition at low GTN concentrations).	Nitroglycerin	65-68	caveolin 1, caveolae protein	Mus musculus	7-12
25158065-7	2014	In the Cav-1 deficient mice, NOS3 dysfunction was accompanied by GTN tolerance (&gt;50% dilation inhibition at low GTN concentrations).	Nitroglycerin	115-118	caveolin 1, caveolae protein	Mus musculus	7-12
25158065-7	2014	In the Cav-1 deficient mice, NOS3 dysfunction was accompanied by GTN tolerance (&gt;50% dilation inhibition at low GTN concentrations).	Nitroglycerin	115-118	nitric oxide synthase 3, endothelial cell	Mus musculus	29-33
25158065-8	2014	In conclusion, GTN tolerance results from Cav-1 modification and depletion by GTN that causes persistent NOS3 activation and uncoupling, preventing it from participating in GTN-medicated vasodilation.	Nitroglycerin	15-18	caveolin 1, caveolae protein	Mus musculus	42-47
25158065-8	2014	In conclusion, GTN tolerance results from Cav-1 modification and depletion by GTN that causes persistent NOS3 activation and uncoupling, preventing it from participating in GTN-medicated vasodilation.	Nitroglycerin	15-18	nitric oxide synthase 3, endothelial cell	Mus musculus	105-109
25158065-8	2014	In conclusion, GTN tolerance results from Cav-1 modification and depletion by GTN that causes persistent NOS3 activation and uncoupling, preventing it from participating in GTN-medicated vasodilation.	Nitroglycerin	78-81	nitric oxide synthase 3, endothelial cell	Mus musculus	105-109
25158065-8	2014	In conclusion, GTN tolerance results from Cav-1 modification and depletion by GTN that causes persistent NOS3 activation and uncoupling, preventing it from participating in GTN-medicated vasodilation.	Nitroglycerin	78-81	nitric oxide synthase 3, endothelial cell	Mus musculus	105-109
24366981-0	2014	Effects of CGRP receptor antagonism in nitroglycerin-induced hyperalgesia.	Nitroglycerin	39-52	calcitonin-related polypeptide alpha	Rattus norvegicus	11-15
24997804-0	2014	Nitroglycerin-induced myocardial protection and tolerance: role for CGRP.	Nitroglycerin	0-13	calcitonin related polypeptide alpha	Homo sapiens	68-72
25202948-9	2014	CONCLUSION: Verapamil and nitroglycerin in LPD solution can protect the respiratory function of canine lung grafts by attenuating pulmonary edema and oxidative stress.	Nitroglycerin	26-39	Ras association (RalGDS/AF-6) and pleckstrin homology domains 1	Homo sapiens	43-46
24366981-3	2014	AIM: The aim of this article is to test the analgesic effect of the CGRP receptor antagonist MK-8825 in two animal models of pain that may be relevant for migraine: the tail flick test and the formalin test performed during NTG-induced hyperalgesia.	Nitroglycerin	224-227	calcitonin-related polypeptide alpha	Rattus norvegicus	68-72
24366981-5	2014	Furthermore, the CGRP antagonist proved effective in counteracting NTG-induced hyperalgesia in both tests.	Nitroglycerin	67-70	calcitonin-related polypeptide alpha	Rattus norvegicus	17-21
24480308-9	2014	Younger and older NTG myocytes demonstrated similar contributions from the SR Ca(2+)-ATPase and NCX to restoration of basal Ca(2+).	Nitroglycerin	18-21	T cell leukemia, homeobox 2	Mus musculus	96-99
24799610-4	2014	Individuals with the long allele of a guanine-thymine (GTn) microsatellite repeat located in the promoter region of HMOX1 have a higher risk of cardiometabolic diseases compared with those with the short allele.	Nitroglycerin	55-58	heme oxygenase 1	Homo sapiens	116-121
24385076-6	2014	KYNAa pre-treatment had dose-dependent, mitigating action on nitroglycerine-induced decrease in calcitonin gene-related peptide and increase in c-Fos, neuronal nitric oxide synthase and calmodulin-dependent protein kinase II alpha expression in the C1-C2.	Nitroglycerin	61-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	144-149
24480308-11	2014	Compared to NTG, younger TG-ssTnI myocytes demonstrated a significantly bigger contribution of the NCX (16+-2.7% in TG vs 6.9+-0.9% in NTG) and slow mechanisms (3.3+-0.4% in TG vs 1.4+-0.1% in NTG).	Nitroglycerin	135-138	troponin I, skeletal, slow 1	Mus musculus	28-33
24480308-11	2014	Compared to NTG, younger TG-ssTnI myocytes demonstrated a significantly bigger contribution of the NCX (16+-2.7% in TG vs 6.9+-0.9% in NTG) and slow mechanisms (3.3+-0.4% in TG vs 1.4+-0.1% in NTG).	Nitroglycerin	135-138	troponin I, skeletal, slow 1	Mus musculus	28-33
24885962-3	2014	METHODS: Intraperitoneal NTG injection (15 mg/kg) triggered thermal hyperalgesia in the hindpaws of wild-type C57BL/6J mice, followed by the induction of c-fos in upper cervical spinal cord and trigeminal nucleus caudalis.	Nitroglycerin	25-28	FBJ osteosarcoma oncogene	Mus musculus	154-159
24918292-2	2014	Aorta of TCTP-TG exhibited hypercontractile response compared to that of non-transgenic mice (NTG) suggesting dys-regulation of signaling pathways involved in the vascular contractility by TCTP.	Nitroglycerin	94-97	tumor protein, translationally-controlled 1	Mus musculus	9-13
24884830-6	2014	RESULTS: The positive percentage and expression levels of ERalpha were significantly higher in female PTC patients of reproductive age (18-45 years old; n =50) than age-matched female NTG patients (n =30), while ERbeta1 exhibited the opposite pattern.	Nitroglycerin	184-187	estrogen receptor 1	Homo sapiens	58-65
25295904-8	2014	When compared with the NG group, there was a significant increase in the expression of TNF-alpha (p&lt;0.001) and IL-6 (p=0.002) in the choroid and sclera of animals in the HG group.	Nitroglycerin	23-25	tumor necrosis factor	Oryctolagus cuniculus	87-96
25295904-8	2014	When compared with the NG group, there was a significant increase in the expression of TNF-alpha (p&lt;0.001) and IL-6 (p=0.002) in the choroid and sclera of animals in the HG group.	Nitroglycerin	23-25	interleukin-6	Oryctolagus cuniculus	114-118
24885962-5	2014	RESULTS: NTG decreased the paw withdrawal threshold in both wild-type and P2X7 knockout mice.	Nitroglycerin	9-12	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	74-78
24836861-2	2014	BACKGROUND: Nitroglycerin, a nitric oxide donor agent, reduces the expression of hypoxia-inducible factor-1alpha (HIF-1alpha) and could be a normalizer of the tumor microenvironment.	Nitroglycerin	12-25	hypoxia inducible factor 1 subunit alpha	Homo sapiens	81-112
24836861-2	2014	BACKGROUND: Nitroglycerin, a nitric oxide donor agent, reduces the expression of hypoxia-inducible factor-1alpha (HIF-1alpha) and could be a normalizer of the tumor microenvironment.	Nitroglycerin	12-25	hypoxia inducible factor 1 subunit alpha	Homo sapiens	114-124
24783932-7	2014	In the nitroglycerin-induced migraine group, after gavage for 7 days, rats were intraperitoneally injected nitroglycerin (10 mg/kg), and 4 h later, blood samples were collected from postcava for measuring the plasma CGRP and beta-EP levels.	Nitroglycerin	7-20	calcitonin-related polypeptide alpha	Rattus norvegicus	216-220
24555687-4	2014	Immunoblot analysis indicated a marked increase in HNE adduct formation in GTN-tolerant porcine kidney epithelial cells (PK1) and in aortae from GTN-tolerant rats and untreated Aldh2(-/-) mice.	Nitroglycerin	75-78	pyruvate kinase L/R	Rattus norvegicus	121-124
24555687-1	2014	Tolerance to nitrates such as nitroglycerin (GTN) is associated with oxidative stress, inactivation of aldehyde dehydrogenase 2 (ALDH2), and decreased GTN-induced cGMP accumulation and vasodilation.	Nitroglycerin	30-43	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	103-127
24555687-1	2014	Tolerance to nitrates such as nitroglycerin (GTN) is associated with oxidative stress, inactivation of aldehyde dehydrogenase 2 (ALDH2), and decreased GTN-induced cGMP accumulation and vasodilation.	Nitroglycerin	30-43	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	129-134
24555687-1	2014	Tolerance to nitrates such as nitroglycerin (GTN) is associated with oxidative stress, inactivation of aldehyde dehydrogenase 2 (ALDH2), and decreased GTN-induced cGMP accumulation and vasodilation.	Nitroglycerin	45-48	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	103-127
24555687-1	2014	Tolerance to nitrates such as nitroglycerin (GTN) is associated with oxidative stress, inactivation of aldehyde dehydrogenase 2 (ALDH2), and decreased GTN-induced cGMP accumulation and vasodilation.	Nitroglycerin	45-48	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	129-134
24555687-2	2014	We hypothesized that GTN-induced inactivation of ALDH2 results in increased 4-hydroxy-2-nonenal (HNE) adduct formation of key proteins involved in GTN bioactivation, and, consequently, an attenuated vasodilator response to GTN (i.e., tolerance).	Nitroglycerin	21-24	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	49-54
24555687-2	2014	We hypothesized that GTN-induced inactivation of ALDH2 results in increased 4-hydroxy-2-nonenal (HNE) adduct formation of key proteins involved in GTN bioactivation, and, consequently, an attenuated vasodilator response to GTN (i.e., tolerance).	Nitroglycerin	147-150	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	49-54
24555687-2	2014	We hypothesized that GTN-induced inactivation of ALDH2 results in increased 4-hydroxy-2-nonenal (HNE) adduct formation of key proteins involved in GTN bioactivation, and, consequently, an attenuated vasodilator response to GTN (i.e., tolerance).	Nitroglycerin	147-150	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	49-54
24555687-5	2014	Preincubation of PK1 cells with HNE resulted in a dose-dependent decrease in GTN-induced cGMP accumulation, and pretreatment of isolated rat aorta with HNE resulted in dose-dependent decreases in the vasodilator response to GTN, thus mimicking GTN-tolerance.	Nitroglycerin	77-80	pyruvate kinase L/R	Rattus norvegicus	17-20
24555687-5	2014	Preincubation of PK1 cells with HNE resulted in a dose-dependent decrease in GTN-induced cGMP accumulation, and pretreatment of isolated rat aorta with HNE resulted in dose-dependent decreases in the vasodilator response to GTN, thus mimicking GTN-tolerance.	Nitroglycerin	224-227	pyruvate kinase L/R	Rattus norvegicus	17-20
24555687-5	2014	Preincubation of PK1 cells with HNE resulted in a dose-dependent decrease in GTN-induced cGMP accumulation, and pretreatment of isolated rat aorta with HNE resulted in dose-dependent decreases in the vasodilator response to GTN, thus mimicking GTN-tolerance.	Nitroglycerin	224-227	pyruvate kinase L/R	Rattus norvegicus	17-20
24555687-6	2014	Pretreatment of aortae from Aldh2(-/-) mice with 10 muM HNE resulted in a desensitized vasodilator response to GTN.	Nitroglycerin	111-114	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	28-33
24132139-2	2014	Tilt testing with sublingual nitroglycerin (TT-TNT) provides a test with good specificity and positivity rate in young and old patients.	Nitroglycerin	29-42	chromosome 16 open reading frame 82	Homo sapiens	47-50
24412516-8	2014	Tau dysregulation, which causes a reduction in synaptic protein levels, may be responsible for the cognitive decline observed in Ntg streptozotocin-treated mice.	Nitroglycerin	129-132	microtubule associated protein tau	Homo sapiens	0-3
24636539-5	2014	In this study we evaluated the role of CB2 receptors in two animal models of pain that may be relevant for migraine: the tail flick test and the formalin test performed during NTG-induced hyperalgesia.	Nitroglycerin	176-179	cannabinoid receptor 2	Rattus norvegicus	39-42
24336068-6	2014	Using glyceryl trinitrate (GTN), an agonist of nitric oxide (NO) signaling known to block HIF-1alpha accumulation in hypoxic cells, we prevented hypoxia-induced PD-L1 expression and diminished resistance to CTL-mediated lysis.	Nitroglycerin	6-25	hypoxia inducible factor 1 subunit alpha	Homo sapiens	90-100
24529122-9	2014	In multivariate analysis, lower SBP-dip (P = 0.007) and DBP-dip (P = 0.03) were independently associated with lower GTN response.	Nitroglycerin	116-119	selenium binding protein 1	Homo sapiens	32-35
24529122-9	2014	In multivariate analysis, lower SBP-dip (P = 0.007) and DBP-dip (P = 0.03) were independently associated with lower GTN response.	Nitroglycerin	116-119	D-box binding PAR bZIP transcription factor	Homo sapiens	56-59
24000375-0	2014	Nitric oxide synthase, calcitonin gene-related peptide and NK-1 receptor mechanisms are involved in GTN-induced neuronal activation.	Nitroglycerin	100-103	calcitonin-related polypeptide alpha	Rattus norvegicus	23-54
24000375-0	2014	Nitric oxide synthase, calcitonin gene-related peptide and NK-1 receptor mechanisms are involved in GTN-induced neuronal activation.	Nitroglycerin	100-103	tachykinin receptor 1	Rattus norvegicus	59-72
24000375-2	2014	Here we analyse the effect of nitric oxide synthase (NOS) and calcitonin gene-related peptide (CGRP) systems on the GTN-induced neuronal activation in this model.	Nitroglycerin	116-119	calcitonin-related polypeptide alpha	Rattus norvegicus	62-93
24000375-2	2014	Here we analyse the effect of nitric oxide synthase (NOS) and calcitonin gene-related peptide (CGRP) systems on the GTN-induced neuronal activation in this model.	Nitroglycerin	116-119	calcitonin-related polypeptide alpha	Rattus norvegicus	95-99
24000375-6	2014	RESULTS: GTN-treated rats showed a significant increase of nNOS and CGRP in dura mater and CGRP in the trigeminal nucleus caudalis (TNC).	Nitroglycerin	9-12	nitric oxide synthase 1	Rattus norvegicus	59-63
24000375-6	2014	RESULTS: GTN-treated rats showed a significant increase of nNOS and CGRP in dura mater and CGRP in the trigeminal nucleus caudalis (TNC).	Nitroglycerin	9-12	calcitonin-related polypeptide alpha	Rattus norvegicus	68-72
24000375-6	2014	RESULTS: GTN-treated rats showed a significant increase of nNOS and CGRP in dura mater and CGRP in the trigeminal nucleus caudalis (TNC).	Nitroglycerin	9-12	calcitonin-related polypeptide alpha	Rattus norvegicus	91-95
24000375-9	2014	Pre-treatment with L-NAME and L-733060 also significantly inhibited GTN induced Fos expression.	Nitroglycerin	68-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-83
24000375-10	2014	CONCLUSION: The present study indicates that blockers of CGRP, NOS and NK-1 receptors all inhibit GTN induced Fos activation.	Nitroglycerin	98-101	calcitonin-related polypeptide alpha	Rattus norvegicus	57-61
24000375-10	2014	CONCLUSION: The present study indicates that blockers of CGRP, NOS and NK-1 receptors all inhibit GTN induced Fos activation.	Nitroglycerin	98-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-113
24336068-6	2014	Using glyceryl trinitrate (GTN), an agonist of nitric oxide (NO) signaling known to block HIF-1alpha accumulation in hypoxic cells, we prevented hypoxia-induced PD-L1 expression and diminished resistance to CTL-mediated lysis.	Nitroglycerin	6-25	CD274 molecule	Homo sapiens	161-166
24336068-6	2014	Using glyceryl trinitrate (GTN), an agonist of nitric oxide (NO) signaling known to block HIF-1alpha accumulation in hypoxic cells, we prevented hypoxia-induced PD-L1 expression and diminished resistance to CTL-mediated lysis.	Nitroglycerin	27-30	hypoxia inducible factor 1 subunit alpha	Homo sapiens	90-100
24336068-6	2014	Using glyceryl trinitrate (GTN), an agonist of nitric oxide (NO) signaling known to block HIF-1alpha accumulation in hypoxic cells, we prevented hypoxia-induced PD-L1 expression and diminished resistance to CTL-mediated lysis.	Nitroglycerin	27-30	CD274 molecule	Homo sapiens	161-166
24460523-5	2014	Glyceryl-tri-nitrate significantly reduced the expression of leukocyte Fcgamma receptor CD32 over time, compared to control.	Nitroglycerin	0-20	Fc gamma receptor IIa	Homo sapiens	88-92
23992559-3	2014	METHODS: Out of 671 consecutive subjects undergoing nitroglycerin-potentiated HUT for suspected VVS, 369 patients with normal electrocardiogram and no structural heart disease were included in our study.	Nitroglycerin	52-65	VVS	Homo sapiens	96-99
24044945-6	2014	Under this backdrop, in search of less toxic and more effective MDR reversing agents our laboratory has developed the different metal chelates of Schiff base N-(2-hydroxy acetophenone)glycinate (NG) which is structurally similar to azatyrosine [L-beta-(5-hydroxy-2-pyridyl)-alanine] that inhibits tumor formation by deactivating the c-Raf-1 kinase and c-Ha-ras signalling pathway.	Nitroglycerin	195-197	transcription factor like 5	Homo sapiens	352-356
24734241-0	2014	Peri- and postanalgesic properties of lidokain, lornoxicam, and nitroglycerine combination at intravenous regional anesthesia.	Nitroglycerin	64-78	perilipin 1	Homo sapiens	0-4
24157631-9	2014	Even so, NTG (iv) improved the neurological outcome and (v) reduced neurodegeneration, mainly in the hippocampal CA1 region.	Nitroglycerin	9-12	carbonic anhydrase 1	Rattus norvegicus	113-116
25146184-5	2014	In rat reticulocytes, GTN decreased the activity of mitochondrial MnSOD and increased the activity of CuZnSOD.	Nitroglycerin	22-25	superoxide dismutase 2	Rattus norvegicus	66-71
24164360-3	2014	Because of a recent report of aldehyde dehydrogenase 2 (ALDH2)-catalyzed glyceryl trinitrate (GTN) vasorelaxation by denitration of GTN to 1,2-glyceryl dinitrate (1,2-GDN) and nitrite, we therefore investigated a catalytic activity of ALDH2 for nitrite reduction and subsequent effect on N(omega)-nitro-l-arginine methyl ester (l-NAME)-induced hypertension in normoxic rat.	Nitroglycerin	73-92	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	30-54
24164360-3	2014	Because of a recent report of aldehyde dehydrogenase 2 (ALDH2)-catalyzed glyceryl trinitrate (GTN) vasorelaxation by denitration of GTN to 1,2-glyceryl dinitrate (1,2-GDN) and nitrite, we therefore investigated a catalytic activity of ALDH2 for nitrite reduction and subsequent effect on N(omega)-nitro-l-arginine methyl ester (l-NAME)-induced hypertension in normoxic rat.	Nitroglycerin	73-92	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	56-61
24164360-3	2014	Because of a recent report of aldehyde dehydrogenase 2 (ALDH2)-catalyzed glyceryl trinitrate (GTN) vasorelaxation by denitration of GTN to 1,2-glyceryl dinitrate (1,2-GDN) and nitrite, we therefore investigated a catalytic activity of ALDH2 for nitrite reduction and subsequent effect on N(omega)-nitro-l-arginine methyl ester (l-NAME)-induced hypertension in normoxic rat.	Nitroglycerin	73-92	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	235-240
24164360-3	2014	Because of a recent report of aldehyde dehydrogenase 2 (ALDH2)-catalyzed glyceryl trinitrate (GTN) vasorelaxation by denitration of GTN to 1,2-glyceryl dinitrate (1,2-GDN) and nitrite, we therefore investigated a catalytic activity of ALDH2 for nitrite reduction and subsequent effect on N(omega)-nitro-l-arginine methyl ester (l-NAME)-induced hypertension in normoxic rat.	Nitroglycerin	94-97	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	30-54
24164360-3	2014	Because of a recent report of aldehyde dehydrogenase 2 (ALDH2)-catalyzed glyceryl trinitrate (GTN) vasorelaxation by denitration of GTN to 1,2-glyceryl dinitrate (1,2-GDN) and nitrite, we therefore investigated a catalytic activity of ALDH2 for nitrite reduction and subsequent effect on N(omega)-nitro-l-arginine methyl ester (l-NAME)-induced hypertension in normoxic rat.	Nitroglycerin	94-97	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	56-61
24164360-3	2014	Because of a recent report of aldehyde dehydrogenase 2 (ALDH2)-catalyzed glyceryl trinitrate (GTN) vasorelaxation by denitration of GTN to 1,2-glyceryl dinitrate (1,2-GDN) and nitrite, we therefore investigated a catalytic activity of ALDH2 for nitrite reduction and subsequent effect on N(omega)-nitro-l-arginine methyl ester (l-NAME)-induced hypertension in normoxic rat.	Nitroglycerin	94-97	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	235-240
24164360-3	2014	Because of a recent report of aldehyde dehydrogenase 2 (ALDH2)-catalyzed glyceryl trinitrate (GTN) vasorelaxation by denitration of GTN to 1,2-glyceryl dinitrate (1,2-GDN) and nitrite, we therefore investigated a catalytic activity of ALDH2 for nitrite reduction and subsequent effect on N(omega)-nitro-l-arginine methyl ester (l-NAME)-induced hypertension in normoxic rat.	Nitroglycerin	132-135	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	30-54
24164360-3	2014	Because of a recent report of aldehyde dehydrogenase 2 (ALDH2)-catalyzed glyceryl trinitrate (GTN) vasorelaxation by denitration of GTN to 1,2-glyceryl dinitrate (1,2-GDN) and nitrite, we therefore investigated a catalytic activity of ALDH2 for nitrite reduction and subsequent effect on N(omega)-nitro-l-arginine methyl ester (l-NAME)-induced hypertension in normoxic rat.	Nitroglycerin	132-135	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	56-61
24164360-3	2014	Because of a recent report of aldehyde dehydrogenase 2 (ALDH2)-catalyzed glyceryl trinitrate (GTN) vasorelaxation by denitration of GTN to 1,2-glyceryl dinitrate (1,2-GDN) and nitrite, we therefore investigated a catalytic activity of ALDH2 for nitrite reduction and subsequent effect on N(omega)-nitro-l-arginine methyl ester (l-NAME)-induced hypertension in normoxic rat.	Nitroglycerin	132-135	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	235-240
24120622-8	2014	However, the G/G genotypic and G allelic distributions of the CaSR R990G polymorphism in the HTG group were higher than the NTG group (p&lt;0.001).	Nitroglycerin	124-127	calcium sensing receptor	Homo sapiens	62-66
24120622-9	2014	After stratification, in obese subjects, the homozygous (G/G) distribution of the CaSR R990G polymorphism in the HTG group was significantly higher than in the NTG group (p=0.001), and showed an increased risk of HTG at baseline [OR=2.55, 95% CI=1.65-3.92, p&lt;0.006].	Nitroglycerin	160-163	calcium sensing receptor	Homo sapiens	82-86
25146184-5	2014	In rat reticulocytes, GTN decreased the activity of mitochondrial MnSOD and increased the activity of CuZnSOD.	Nitroglycerin	22-25	superoxide dismutase 1	Rattus norvegicus	102-109
25146184-6	2014	In rat RBCs, GTN induced increase of Vit E concentration (at high doses), but decreased glutathione content and activities of all glutathione-dependent antioxidative enzymes; the OPP pathway activity significantly increased.	Nitroglycerin	13-16	vitrin	Rattus norvegicus	37-40
24126018-8	2013	ALDH3A1 was also shown to denitrate NTG, producing primarily glyceryl 1,2-dinitrate (1,2-GDN) in preference to glyceryl 1,3-dinitrate (1,3-GDN).	Nitroglycerin	36-39	aldehyde dehydrogenase family 3, subfamily A1	Mus musculus	0-7
24064205-0	2013	Catalysis of nitrite generation from nitroglycerin by glyceraldehyde-3-phosphate dehydrogenase (GAPDH).	Nitroglycerin	37-50	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	54-94
24516056-3	2013	RESULTS: The immunohistochemical expression of RASSF7 and RASSF8 was higher in PTC and MTC than in NTG (P &lt; 0.001).	Nitroglycerin	99-102	Ras association domain family member 7	Homo sapiens	47-53
24064205-0	2013	Catalysis of nitrite generation from nitroglycerin by glyceraldehyde-3-phosphate dehydrogenase (GAPDH).	Nitroglycerin	37-50	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	96-101
24064205-2	2013	We report here that glyceraldehyde-3-phosphate dehydrogenase (GAPDH) catalyzes the release of nitrite from GTN.	Nitroglycerin	107-110	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	20-60
24064205-2	2013	We report here that glyceraldehyde-3-phosphate dehydrogenase (GAPDH) catalyzes the release of nitrite from GTN.	Nitroglycerin	107-110	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	62-67
24064205-5	2013	Reductive denitration of GTN in the absence of DTT results in dose- and time-dependent inhibition of GAPDH dehydrogenase activity.	Nitroglycerin	25-28	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	101-106
24064205-6	2013	Disulfiram, a thiol-modifying drug, inhibits both the dehydrogenase and GTN reductase activity of GAPDH, while DTT or tris(2-carboxyethyl)phosphine reverse the GTN-induced inhibition.	Nitroglycerin	72-75	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	98-103
24064205-7	2013	Incubation of intact human erythrocytes or hemolysates with 2mM GTN for 60min results in 50% inhibition of GAPDH"s dehydrogenase activity, indicating that GTN is taken up by these cells and that the dehydrogenase is a target of GTN.	Nitroglycerin	64-67	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	107-112
24064205-7	2013	Incubation of intact human erythrocytes or hemolysates with 2mM GTN for 60min results in 50% inhibition of GAPDH"s dehydrogenase activity, indicating that GTN is taken up by these cells and that the dehydrogenase is a target of GTN.	Nitroglycerin	155-158	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	107-112
24064205-7	2013	Incubation of intact human erythrocytes or hemolysates with 2mM GTN for 60min results in 50% inhibition of GAPDH"s dehydrogenase activity, indicating that GTN is taken up by these cells and that the dehydrogenase is a target of GTN.	Nitroglycerin	155-158	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	107-112
24064205-8	2013	Thus, erythrocyte GAPDH may contribute to GTN bioactivation.	Nitroglycerin	42-45	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	18-23
24256609-0	2013	The calcitonin gene-related peptide receptor antagonist MK-8825 decreases spinal trigeminal activity during nitroglycerin infusion.	Nitroglycerin	108-121	calcitonin-related polypeptide alpha	Rattus norvegicus	4-35
24256609-3	2013	In animal experiments nitrovasodilators like nitroglycerin induced increases in spinal trigeminal activity, which were reversed after inhibition of CGRP receptors.	Nitroglycerin	45-58	calcitonin-related polypeptide alpha	Rattus norvegicus	148-152
24256609-4	2013	In the present study we asked if CGRP receptor inhibition can also prevent spinal trigeminal activity induced by nitroglycerin.	Nitroglycerin	113-126	calcitonin-related polypeptide alpha	Rattus norvegicus	33-37
24256609-9	2013	CONCLUSIONS: CGRP receptors may be important in an early phase of nitroglycerin-induced central trigeminal activity.	Nitroglycerin	66-79	calcitonin-related polypeptide alpha	Rattus norvegicus	13-17
24516056-3	2013	RESULTS: The immunohistochemical expression of RASSF7 and RASSF8 was higher in PTC and MTC than in NTG (P &lt; 0.001).	Nitroglycerin	99-102	Ras association domain family member 8	Homo sapiens	58-64
24516056-5	2013	CONCLUSIONS: RASSF7 and RASSF8 expression was increased in PTC and MTC compared to NTG, and this may be linked to the development and progression of thyroid carcinoma.	Nitroglycerin	83-86	Ras association domain family member 7	Homo sapiens	13-19
24516056-5	2013	CONCLUSIONS: RASSF7 and RASSF8 expression was increased in PTC and MTC compared to NTG, and this may be linked to the development and progression of thyroid carcinoma.	Nitroglycerin	83-86	Ras association domain family member 8	Homo sapiens	24-30
24693369-2	2013	The purpose of this study was to investigate the effect of BTX-A on the immunoreactive levels of calcitonin gene-related peptide (CGRP) and substance P (SP) in the jugular plasma and medulla oblongata of migraine in rats induced by nitroglycerin (NTG), and then to evaluate and compare the effectiveness of fixed (muscle)-sites and acupoint-sites injection of BTX-A for migraine therapy of patients in a randomly controlled trial extending over four months.	Nitroglycerin	232-245	calcitonin-related polypeptide alpha	Rattus norvegicus	97-128
24693369-2	2013	The purpose of this study was to investigate the effect of BTX-A on the immunoreactive levels of calcitonin gene-related peptide (CGRP) and substance P (SP) in the jugular plasma and medulla oblongata of migraine in rats induced by nitroglycerin (NTG), and then to evaluate and compare the effectiveness of fixed (muscle)-sites and acupoint-sites injection of BTX-A for migraine therapy of patients in a randomly controlled trial extending over four months.	Nitroglycerin	247-250	calcitonin-related polypeptide alpha	Rattus norvegicus	97-128
24693369-6	2013	RESULTS: Local BTX-A injection suppressed NTG-induced CGRP-LI and SP-LI levels in jugular plasma and oblongata.	Nitroglycerin	42-45	calcitonin-related polypeptide alpha	Rattus norvegicus	54-58
24693369-9	2013	CONCLUSIONS: The evidence that BTX-A decreases NTG-induced CGRP-LI and SP-LI levels in trigeminovascular system suggests that BTX-A attenuates migraine by suppression of neuropeptide release.	Nitroglycerin	47-50	calcitonin-related polypeptide alpha	Rattus norvegicus	59-63
23793290-0	2013	Potent inhibition of aldehyde dehydrogenase-2 by diphenyleneiodonium: focus on nitroglycerin bioactivation.	Nitroglycerin	79-92	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	21-45
24004534-0	2013	Changes in calcitonin gene-related peptide (CGRP) receptor component and nitric oxide receptor (sGC) immunoreactivity in rat trigeminal ganglion following glyceroltrinitrate pretreatment.	Nitroglycerin	155-173	calcitonin-related polypeptide alpha	Rattus norvegicus	11-42
24004534-0	2013	Changes in calcitonin gene-related peptide (CGRP) receptor component and nitric oxide receptor (sGC) immunoreactivity in rat trigeminal ganglion following glyceroltrinitrate pretreatment.	Nitroglycerin	155-173	guanylate cyclase 1 soluble subunit alpha 1	Rattus norvegicus	96-99
24004534-14	2013	The percentage of sGC-immunopositive neurons (51% after vehicle) was decreased after GTN infusion (48%).	Nitroglycerin	85-88	guanylate cyclase 1 soluble subunit alpha 1	Rattus norvegicus	18-21
24004534-15	2013	CONCLUSIONS: Prolonged infusion of GTN caused increased fractions of RAMP1- and decreased fractions of sGC-immunopositive neurons in the trigeminal ganglion.	Nitroglycerin	35-38	receptor activity modifying protein 1	Rattus norvegicus	69-74
24004534-15	2013	CONCLUSIONS: Prolonged infusion of GTN caused increased fractions of RAMP1- and decreased fractions of sGC-immunopositive neurons in the trigeminal ganglion.	Nitroglycerin	35-38	guanylate cyclase 1 soluble subunit alpha 1	Rattus norvegicus	103-106
23793290-1	2013	Aldehyde dehydrogenase-2 (ALDH2) catalyzes vascular bioactivation of the antianginal drug nitroglycerin (GTN) to yield nitric oxide (NO) or a related species that activates soluble guanylate cyclase (sGC), resulting in cGMP-mediated vasodilation.	Nitroglycerin	90-103	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	0-24
23793290-1	2013	Aldehyde dehydrogenase-2 (ALDH2) catalyzes vascular bioactivation of the antianginal drug nitroglycerin (GTN) to yield nitric oxide (NO) or a related species that activates soluble guanylate cyclase (sGC), resulting in cGMP-mediated vasodilation.	Nitroglycerin	90-103	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	26-31
23793290-1	2013	Aldehyde dehydrogenase-2 (ALDH2) catalyzes vascular bioactivation of the antianginal drug nitroglycerin (GTN) to yield nitric oxide (NO) or a related species that activates soluble guanylate cyclase (sGC), resulting in cGMP-mediated vasodilation.	Nitroglycerin	90-103	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	173-198
23793290-1	2013	Aldehyde dehydrogenase-2 (ALDH2) catalyzes vascular bioactivation of the antianginal drug nitroglycerin (GTN) to yield nitric oxide (NO) or a related species that activates soluble guanylate cyclase (sGC), resulting in cGMP-mediated vasodilation.	Nitroglycerin	90-103	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	200-203
23793290-1	2013	Aldehyde dehydrogenase-2 (ALDH2) catalyzes vascular bioactivation of the antianginal drug nitroglycerin (GTN) to yield nitric oxide (NO) or a related species that activates soluble guanylate cyclase (sGC), resulting in cGMP-mediated vasodilation.	Nitroglycerin	105-108	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	0-24
23793290-1	2013	Aldehyde dehydrogenase-2 (ALDH2) catalyzes vascular bioactivation of the antianginal drug nitroglycerin (GTN) to yield nitric oxide (NO) or a related species that activates soluble guanylate cyclase (sGC), resulting in cGMP-mediated vasodilation.	Nitroglycerin	105-108	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	26-31
23793290-1	2013	Aldehyde dehydrogenase-2 (ALDH2) catalyzes vascular bioactivation of the antianginal drug nitroglycerin (GTN) to yield nitric oxide (NO) or a related species that activates soluble guanylate cyclase (sGC), resulting in cGMP-mediated vasodilation.	Nitroglycerin	105-108	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	173-198
23793290-1	2013	Aldehyde dehydrogenase-2 (ALDH2) catalyzes vascular bioactivation of the antianginal drug nitroglycerin (GTN) to yield nitric oxide (NO) or a related species that activates soluble guanylate cyclase (sGC), resulting in cGMP-mediated vasodilation.	Nitroglycerin	105-108	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	200-203
23793290-2	2013	Accordingly, established ALDH2 inhibitors attenuate GTN-induced vasorelaxation in vitro and in vivo.	Nitroglycerin	52-55	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	25-30
23793290-3	2013	However, the ALDH2 hypothesis has not been reconciled with early studies demonstrating potent inhibition of the GTN response by diphenyleneiodonium (DPI), a widely used inhibitor of flavoproteins, in particular NADPH oxidases.	Nitroglycerin	112-115	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	13-18
23793290-6	2013	Denitration and bioactivation of 1-2 microM GTN, assayed as 1,2-glycerol dinitrate formation and activation of purified sGC, respectively, were inhibited by DPI with a half-maximally active concentration of about 0.2 microM in a GTN-competitive manner.	Nitroglycerin	44-47	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	120-123
23793290-8	2013	Our data identify ALDH2 as highly sensitive target of DPI and explain inhibition of GTN-induced relaxation by this drug observed previously.	Nitroglycerin	84-87	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	18-23
23387808-6	2013	The nerve fibre layer of NTG patients was thicker than that of HTG patients (mean, NTG/HTG: GDx total: 46.9/44.0 mum, p = 0.073; GDx superior: 57.2/49.9 mum, p = 0.0001; GDx inferior: 54.9/49.7 mum, p = 0.001).	Nitroglycerin	25-28	ubiquitin like 4A	Homo sapiens	129-132
23387808-6	2013	The nerve fibre layer of NTG patients was thicker than that of HTG patients (mean, NTG/HTG: GDx total: 46.9/44.0 mum, p = 0.073; GDx superior: 57.2/49.9 mum, p = 0.0001; GDx inferior: 54.9/49.7 mum, p = 0.001).	Nitroglycerin	25-28	ubiquitin like 4A	Homo sapiens	129-132
23055050-3	2013	The administration in mice of the NO donors nitroglycerin (GTN) and sodium nitroprusside (SNP) produced a delayed meningeal upregulation of interleukin-1ss and inducible NO synthase.	Nitroglycerin	44-57	nitric oxide synthase 2, inducible	Mus musculus	140-181
23230283-0	2013	Acute and chronic effects of glyceryl trinitrate therapy on insulin and glucose regulation in humans.	Nitroglycerin	29-48	insulin	Homo sapiens	60-67
23230283-1	2013	This study examined the effect of acute and sustained transdermal glyceryl trinitrate (GTN) therapy on insulin and glucose regulation.	Nitroglycerin	66-85	insulin	Homo sapiens	103-110
23230283-1	2013	This study examined the effect of acute and sustained transdermal glyceryl trinitrate (GTN) therapy on insulin and glucose regulation.	Nitroglycerin	87-90	insulin	Homo sapiens	103-110
23230283-11	2013	These observations document that GTN therapy modifies glucose metabolism causing evidence of increased insulin resistance during sustained therapy in normal humans.	Nitroglycerin	33-36	insulin	Homo sapiens	103-110
23194305-0	2013	Tolerance to nitroglycerin through proteasomal down-regulation of aldehyde dehydrogenase-2 in a genetic mouse model of ascorbate deficiency.	Nitroglycerin	13-26	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	66-90
23578992-3	2013	GTN and SNP produced a delayed meningeal inflammation, as showed by the upregulation of interleukin (IL)-1beta and inducible NO synthase (iNOS), and a prolonged cold allodynia and heat hyperalgesia with a time-course consistent with NO-induced migraine attacks.	Nitroglycerin	0-3	interleukin 1 beta	Homo sapiens	88-110
23578992-3	2013	GTN and SNP produced a delayed meningeal inflammation, as showed by the upregulation of interleukin (IL)-1beta and inducible NO synthase (iNOS), and a prolonged cold allodynia and heat hyperalgesia with a time-course consistent with NO-induced migraine attacks.	Nitroglycerin	0-3	nitric oxide synthase 2	Homo sapiens	115-136
23578992-3	2013	GTN and SNP produced a delayed meningeal inflammation, as showed by the upregulation of interleukin (IL)-1beta and inducible NO synthase (iNOS), and a prolonged cold allodynia and heat hyperalgesia with a time-course consistent with NO-induced migraine attacks.	Nitroglycerin	0-3	nitric oxide synthase 2	Homo sapiens	138-142
23447360-6	2013	NTG-evoked delayed meningeal nociceptor sensitization was associated with a robust extracellular signal-regulated kinase (ERK) phosphorylation in meningeal arteries.	Nitroglycerin	0-3	mitogen-activated protein kinase 1	Homo sapiens	83-120
23447360-6	2013	NTG-evoked delayed meningeal nociceptor sensitization was associated with a robust extracellular signal-regulated kinase (ERK) phosphorylation in meningeal arteries.	Nitroglycerin	0-3	mitogen-activated protein kinase 1	Homo sapiens	122-125
23447360-7	2013	Pharmacological blockade of meningeal ERK phosphorylation inhibited the development of NTG-evoked delayed meningeal nociceptor sensitization.	Nitroglycerin	87-90	mitogen-activated protein kinase 1	Homo sapiens	38-41
23447360-9	2013	The arterial ERK phosphorylation and its involvement in mediating the NTG-evoked delayed sensitization points to an important, yet unappreciated, role of the meningeal vasculature in the genesis of migraine pain.	Nitroglycerin	70-73	mitogen-activated protein kinase 1	Homo sapiens	13-16
23636092-4	2013	Mice engineered to carry the CKIdelta-T44A allele were more sensitive to pain after treatment with the migraine trigger nitroglycerin.	Nitroglycerin	120-133	casein kinase 1, delta	Mus musculus	29-37
23194305-10	2013	The results support the view that impaired ALDH2-catalysed metabolism of GTN contributes significantly to the development of vascular nitrate tolerance and reveal a hitherto unrecognized protective effect of ascorbate in the vasculature.	Nitroglycerin	73-76	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	43-48
23055050-3	2013	The administration in mice of the NO donors nitroglycerin (GTN) and sodium nitroprusside (SNP) produced a delayed meningeal upregulation of interleukin-1ss and inducible NO synthase.	Nitroglycerin	59-62	nitric oxide synthase 2, inducible	Mus musculus	140-181
23055050-8	2013	Furthermore, the PKC blocker, Calphostin C, prevented the GTN and SNP-induced pain hypersensitivity.	Nitroglycerin	58-61	protein kinase C, epsilon	Mus musculus	17-20
23319593-8	2013	HYD and NTG at low concentrations (1 mum), scavenged superoxide in isolated cardiomyocytes, whereas in cardiac homogenates, NTG inhibited xanthine oxidoreductase activity and scavenged NADPH oxidase-dependent superoxide more efficiently than HYD.	Nitroglycerin	124-127	xanthine dehydrogenase	Rattus norvegicus	138-161
22886025-3	2013	cGMP levels were significantly increased while AbetaPP and BACE1 protein levels were statistically lower in cerebral microvessels from nitroglycerin-treated eNOS-/- mice as compared to vehicle-treated mice.	Nitroglycerin	135-148	beta-site APP cleaving enzyme 1	Mus musculus	59-64
22994391-0	2013	Effect of overexpression of human aldehyde dehydrogenase 2 in LLC-PK1 cells on glyceryl trinitrate biotransformation and cGMP accumulation.	Nitroglycerin	79-98	aldehyde dehydrogenase 2 family member	Homo sapiens	34-58
22994391-1	2013	BACKGROUND AND PURPOSE: Recent studies suggest a primary role for aldehyde dehydrogenase 2 (ALDH2) in mediating the biotransformation of organic nitrates, such as glyceryl trinitrate (GTN), to the proximal activator of soluble guanylyl cyclase (sGC), resulting in increased cGMP accumulation and vasodilation.	Nitroglycerin	163-182	aldehyde dehydrogenase 2 family member	Homo sapiens	66-90
22994391-1	2013	BACKGROUND AND PURPOSE: Recent studies suggest a primary role for aldehyde dehydrogenase 2 (ALDH2) in mediating the biotransformation of organic nitrates, such as glyceryl trinitrate (GTN), to the proximal activator of soluble guanylyl cyclase (sGC), resulting in increased cGMP accumulation and vasodilation.	Nitroglycerin	163-182	aldehyde dehydrogenase 2 family member	Homo sapiens	92-97
22994391-1	2013	BACKGROUND AND PURPOSE: Recent studies suggest a primary role for aldehyde dehydrogenase 2 (ALDH2) in mediating the biotransformation of organic nitrates, such as glyceryl trinitrate (GTN), to the proximal activator of soluble guanylyl cyclase (sGC), resulting in increased cGMP accumulation and vasodilation.	Nitroglycerin	184-187	aldehyde dehydrogenase 2 family member	Homo sapiens	66-90
22994391-1	2013	BACKGROUND AND PURPOSE: Recent studies suggest a primary role for aldehyde dehydrogenase 2 (ALDH2) in mediating the biotransformation of organic nitrates, such as glyceryl trinitrate (GTN), to the proximal activator of soluble guanylyl cyclase (sGC), resulting in increased cGMP accumulation and vasodilation.	Nitroglycerin	184-187	aldehyde dehydrogenase 2 family member	Homo sapiens	92-97
22994391-4	2013	We used a pcDNA3.1-human ALDH2 expression vector to establish a stably transfected cell line (PK1(ALDH2)) that overexpressed ALDH2, or small interfering RNA (siRNA) to deplete endogenous ALDH2, and assessed GTN biotransformation and GTN-induced cGMP formation.	Nitroglycerin	207-210	prokineticin 1	Homo sapiens	94-97
22994391-4	2013	We used a pcDNA3.1-human ALDH2 expression vector to establish a stably transfected cell line (PK1(ALDH2)) that overexpressed ALDH2, or small interfering RNA (siRNA) to deplete endogenous ALDH2, and assessed GTN biotransformation and GTN-induced cGMP formation.	Nitroglycerin	233-236	prokineticin 1	Homo sapiens	94-97
22994391-6	2013	In PK1(ALDH2), GTN biotransformation was significantly increased as a result of increased glyceryl-1,2-dinitrate formation compared to wild-type or PK1(vector).	Nitroglycerin	15-18	prokineticin 1	Homo sapiens	3-6
22994391-6	2013	In PK1(ALDH2), GTN biotransformation was significantly increased as a result of increased glyceryl-1,2-dinitrate formation compared to wild-type or PK1(vector).	Nitroglycerin	15-18	aldehyde dehydrogenase 2 family member	Homo sapiens	7-12
22994391-6	2013	In PK1(ALDH2), GTN biotransformation was significantly increased as a result of increased glyceryl-1,2-dinitrate formation compared to wild-type or PK1(vector).	Nitroglycerin	15-18	prokineticin 1	Homo sapiens	148-151
22994391-7	2013	However, the incubation of PK1(ALDH2) with 1 or 10 muM GTN did not alter GTN-induced cGMP accumulation compared with wild-type or PK1(vector) cells.	Nitroglycerin	55-58	prokineticin 1	Homo sapiens	27-30
22994391-7	2013	However, the incubation of PK1(ALDH2) with 1 or 10 muM GTN did not alter GTN-induced cGMP accumulation compared with wild-type or PK1(vector) cells.	Nitroglycerin	55-58	aldehyde dehydrogenase 2 family member	Homo sapiens	31-36
22913654-6	2013	RESULTS: Data showed a reduced expression of NTG-induced Fos protein in the paraventricular nucleus (PVH), supraoptic nucleus (SON), and nucleus trigeminalis caudalis (SPVC) of male rats in comparison with female rats.	Nitroglycerin	45-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-60
22913654-7	2013	Furthermore, in castrated female rats, NTG-induced neuronal activation was reduced in PVH, SON, central nucleus of the amygdala (AMI), nucleus tractus solitarius (NTS), area postrema (AP), and SPVC, while in castrated male rats Fos expression was reduced uniquely in the SPVC.	Nitroglycerin	39-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	228-231
23546291-1	2013	The contribution of aldehyde dehydrogenase type 2 (ALDH2) to bioactivation of glyceryl trinitrate (GTN) and isosorbide dinitrate (ISDN) was systematically examined in excised rabbit aorta and anesthetized whole animal with cyanamide, an ALDH2 inhibitor.	Nitroglycerin	78-97	aldehyde dehydrogenase, mitochondrial	Oryctolagus cuniculus	20-49
23546291-1	2013	The contribution of aldehyde dehydrogenase type 2 (ALDH2) to bioactivation of glyceryl trinitrate (GTN) and isosorbide dinitrate (ISDN) was systematically examined in excised rabbit aorta and anesthetized whole animal with cyanamide, an ALDH2 inhibitor.	Nitroglycerin	78-97	aldehyde dehydrogenase, mitochondrial	Oryctolagus cuniculus	51-56
23546291-1	2013	The contribution of aldehyde dehydrogenase type 2 (ALDH2) to bioactivation of glyceryl trinitrate (GTN) and isosorbide dinitrate (ISDN) was systematically examined in excised rabbit aorta and anesthetized whole animal with cyanamide, an ALDH2 inhibitor.	Nitroglycerin	99-102	aldehyde dehydrogenase, mitochondrial	Oryctolagus cuniculus	20-49
23546291-1	2013	The contribution of aldehyde dehydrogenase type 2 (ALDH2) to bioactivation of glyceryl trinitrate (GTN) and isosorbide dinitrate (ISDN) was systematically examined in excised rabbit aorta and anesthetized whole animal with cyanamide, an ALDH2 inhibitor.	Nitroglycerin	99-102	aldehyde dehydrogenase, mitochondrial	Oryctolagus cuniculus	51-56
23546291-6	2013	These results indicate that the bioactivation pathway(s) of GTN is ALDH2-dependent in aortic smooth muscle, while ADLH2-independent mechanism(s) largely take place in the whole body.	Nitroglycerin	60-63	aldehyde dehydrogenase, mitochondrial	Oryctolagus cuniculus	67-72
23419531-14	2013	Cholecystokinin-induced gallbladder ejection fraction with nitroglycerin pretreatment, measured with ultrasonography can be useful to select a subgroup of patients who can benefit from sphincterotomy.	Nitroglycerin	59-72	cholecystokinin	Homo sapiens	0-15
23840259-7	2013	This in vivo effect of NG was relevant to that of granulocyte colony stimulating factor (G-CSF) that was known to improve neutropenia.	Nitroglycerin	23-25	colony stimulating factor 3 (granulocyte)	Mus musculus	50-87
23840259-7	2013	This in vivo effect of NG was relevant to that of granulocyte colony stimulating factor (G-CSF) that was known to improve neutropenia.	Nitroglycerin	23-25	colony stimulating factor 3 (granulocyte)	Mus musculus	89-94
23840259-9	2013	In addition, NG enhanced nitric oxide (NO) synthesis and secretions of cytokines including IL-6 and TNF- alpha .	Nitroglycerin	13-15	interleukin 6	Mus musculus	91-95
23840259-9	2013	In addition, NG enhanced nitric oxide (NO) synthesis and secretions of cytokines including IL-6 and TNF- alpha .	Nitroglycerin	13-15	tumor necrosis factor	Mus musculus	100-110
23840259-10	2013	Consistently, NG treatment induced phosphorylation of ERK, JNK, IKK, I kappa B alpha , and NF- kappa B in Raw264.7 cells.	Nitroglycerin	14-16	mitogen-activated protein kinase 8	Mus musculus	59-62
23840259-10	2013	Consistently, NG treatment induced phosphorylation of ERK, JNK, IKK, I kappa B alpha , and NF- kappa B in Raw264.7 cells.	Nitroglycerin	14-16	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha	Mus musculus	64-84
23840259-10	2013	Consistently, NG treatment induced phosphorylation of ERK, JNK, IKK, I kappa B alpha , and NF- kappa B in Raw264.7 cells.	Nitroglycerin	14-16	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	91-102
22886025-3	2013	cGMP levels were significantly increased while AbetaPP and BACE1 protein levels were statistically lower in cerebral microvessels from nitroglycerin-treated eNOS-/- mice as compared to vehicle-treated mice.	Nitroglycerin	135-148	nitric oxide synthase 3, endothelial cell	Mus musculus	157-161
24396568-7	2013	It is concluded that nitroglycerine comprises the protective effects of propofol against TNF-alpha stimulation in endothelial cells, primarily through PKC-beta2 dependent NADPH oxidase activation.	Nitroglycerin	21-35	tumor necrosis factor	Homo sapiens	89-98
24396568-2	2013	We determined whether chronic administration with nitroglycerine compromises the protective effects of propofol against tumor necrosis factor (TNF-) induced toxicity in endothelial cells by PKC- beta2 dependent NADPH oxidase activation.	Nitroglycerin	50-64	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	195-200
24396568-0	2013	Nitroglycerine-induced nitrate tolerance compromises propofol protection of the endothelial cells against TNF-alpha: the role of PKC-beta2 and NADPH oxidase.	Nitroglycerin	0-14	tumor necrosis factor	Homo sapiens	106-115
24396568-7	2013	It is concluded that nitroglycerine comprises the protective effects of propofol against TNF-alpha stimulation in endothelial cells, primarily through PKC-beta2 dependent NADPH oxidase activation.	Nitroglycerin	21-35	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	155-160
24396568-0	2013	Nitroglycerine-induced nitrate tolerance compromises propofol protection of the endothelial cells against TNF-alpha: the role of PKC-beta2 and NADPH oxidase.	Nitroglycerin	0-14	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	133-138
24396568-4	2013	TNF-alpha increased the levels of superoxide, Nox (nitrate and nitrite), malondialdehyde, and nitrotyrosine production, accompanied by increased protein expression of p-PKC-beta2, gP91phox, and endothelial cell apoptosis, whereas all these changes were further enhanced by nitroglycerine.	Nitroglycerin	273-287	tumor necrosis factor	Homo sapiens	0-9
24396568-2	2013	We determined whether chronic administration with nitroglycerine compromises the protective effects of propofol against tumor necrosis factor (TNF-) induced toxicity in endothelial cells by PKC- beta2 dependent NADPH oxidase activation.	Nitroglycerin	50-64	tumor necrosis factor	Homo sapiens	120-141
23001375-6	2012	RESULTS: Diabetic Ntg mice displayed diastolic dysfunction and increased cardiomyocyte size, expression of atrial and B-type natriuretic peptides (Anp, Bnp), fibrosis and apoptosis, as well as increased superoxide generation and increased protein kinase C beta2 (PKCbeta2), p22                   (                     phox                   ) and apoptosis signal-regulating kinase 1 (Ask1) expression.	Nitroglycerin	18-21	natriuretic peptide type A	Mus musculus	147-150
24396568-2	2013	We determined whether chronic administration with nitroglycerine compromises the protective effects of propofol against tumor necrosis factor (TNF-) induced toxicity in endothelial cells by PKC- beta2 dependent NADPH oxidase activation.	Nitroglycerin	50-64	tumor necrosis factor	Homo sapiens	143-147
23001375-6	2012	RESULTS: Diabetic Ntg mice displayed diastolic dysfunction and increased cardiomyocyte size, expression of atrial and B-type natriuretic peptides (Anp, Bnp), fibrosis and apoptosis, as well as increased superoxide generation and increased protein kinase C beta2 (PKCbeta2), p22                   (                     phox                   ) and apoptosis signal-regulating kinase 1 (Ask1) expression.	Nitroglycerin	18-21	natriuretic peptide type B	Mus musculus	152-155
23001375-6	2012	RESULTS: Diabetic Ntg mice displayed diastolic dysfunction and increased cardiomyocyte size, expression of atrial and B-type natriuretic peptides (Anp, Bnp), fibrosis and apoptosis, as well as increased superoxide generation and increased protein kinase C beta2 (PKCbeta2), p22                   (                     phox                   ) and apoptosis signal-regulating kinase 1 (Ask1) expression.	Nitroglycerin	18-21	dynein cytoplasmic 1 heavy chain 1	Mus musculus	274-277
23001375-6	2012	RESULTS: Diabetic Ntg mice displayed diastolic dysfunction and increased cardiomyocyte size, expression of atrial and B-type natriuretic peptides (Anp, Bnp), fibrosis and apoptosis, as well as increased superoxide generation and increased protein kinase C beta2 (PKCbeta2), p22                   (                     phox                   ) and apoptosis signal-regulating kinase 1 (Ask1) expression.	Nitroglycerin	18-21	mitogen-activated protein kinase kinase kinase 5	Mus musculus	347-383
23001375-6	2012	RESULTS: Diabetic Ntg mice displayed diastolic dysfunction and increased cardiomyocyte size, expression of atrial and B-type natriuretic peptides (Anp, Bnp), fibrosis and apoptosis, as well as increased superoxide generation and increased protein kinase C beta2 (PKCbeta2), p22                   (                     phox                   ) and apoptosis signal-regulating kinase 1 (Ask1) expression.	Nitroglycerin	18-21	mitogen-activated protein kinase kinase kinase 5	Mus musculus	385-389
23146303-5	2012	This study aimed to define whether PTEN is involved in the pathogenesis of migraine through modulating NR2B, nitric oxide synthase (NOS), and nitric oxide (NO) in the trigeminal ganglia of rats with glyceryl trinitrate-induced migraine.	Nitroglycerin	199-218	phosphatase and tensin homolog	Rattus norvegicus	35-39
22988236-6	2012	Assuming that the structures of the triple mutant and wild-type ALDH2 reflect binding of GTN to the catalytic site and the first reaction step, respectively, superposition of the two structures indicates that denitration of GTN is initiated by nucleophilic attack of Cys-302 at one of the terminal nitrate groups, resulting in formation of the observed thionitrate intermediate and release of 1,2-glyceryl dinitrate.	Nitroglycerin	89-92	aldehyde dehydrogenase 2 family member	Homo sapiens	64-69
22988236-0	2012	Vascular bioactivation of nitroglycerin by aldehyde dehydrogenase-2: reaction intermediates revealed by crystallography and mass spectrometry.	Nitroglycerin	26-39	aldehyde dehydrogenase 2 family member	Homo sapiens	43-67
22988236-6	2012	Assuming that the structures of the triple mutant and wild-type ALDH2 reflect binding of GTN to the catalytic site and the first reaction step, respectively, superposition of the two structures indicates that denitration of GTN is initiated by nucleophilic attack of Cys-302 at one of the terminal nitrate groups, resulting in formation of the observed thionitrate intermediate and release of 1,2-glyceryl dinitrate.	Nitroglycerin	224-227	aldehyde dehydrogenase 2 family member	Homo sapiens	64-69
22988236-1	2012	Aldehyde dehydrogenase-2 (ALDH2) catalyzes the bioactivation of nitroglycerin (glyceryl trinitrate, GTN) in blood vessels, resulting in vasodilation by nitric oxide (NO) or a related species.	Nitroglycerin	64-77	aldehyde dehydrogenase 2 family member	Homo sapiens	0-24
22988236-7	2012	Our results shed light on the molecular mechanism of the GTN denitration reaction and provide useful information on the structural requirements for high affinity binding of organic nitrates to the catalytic site of ALDH2.	Nitroglycerin	57-60	aldehyde dehydrogenase 2 family member	Homo sapiens	215-220
22988236-1	2012	Aldehyde dehydrogenase-2 (ALDH2) catalyzes the bioactivation of nitroglycerin (glyceryl trinitrate, GTN) in blood vessels, resulting in vasodilation by nitric oxide (NO) or a related species.	Nitroglycerin	64-77	aldehyde dehydrogenase 2 family member	Homo sapiens	26-31
22988236-1	2012	Aldehyde dehydrogenase-2 (ALDH2) catalyzes the bioactivation of nitroglycerin (glyceryl trinitrate, GTN) in blood vessels, resulting in vasodilation by nitric oxide (NO) or a related species.	Nitroglycerin	79-98	aldehyde dehydrogenase 2 family member	Homo sapiens	0-24
22820168-6	2012	Relative to the NTg controls, GET-1 mice displayed a marked decrease in pain-like behavioral responses during the second phase of formalin-induced pain (i.e., 15-20 min after injection), whereas the responses elicited in TET-1 mice were unaltered.	Nitroglycerin	16-19	activating transcription factor 7 interacting protein 2	Mus musculus	30-35
22988236-1	2012	Aldehyde dehydrogenase-2 (ALDH2) catalyzes the bioactivation of nitroglycerin (glyceryl trinitrate, GTN) in blood vessels, resulting in vasodilation by nitric oxide (NO) or a related species.	Nitroglycerin	79-98	aldehyde dehydrogenase 2 family member	Homo sapiens	26-31
22988236-1	2012	Aldehyde dehydrogenase-2 (ALDH2) catalyzes the bioactivation of nitroglycerin (glyceryl trinitrate, GTN) in blood vessels, resulting in vasodilation by nitric oxide (NO) or a related species.	Nitroglycerin	100-103	aldehyde dehydrogenase 2 family member	Homo sapiens	0-24
22988236-1	2012	Aldehyde dehydrogenase-2 (ALDH2) catalyzes the bioactivation of nitroglycerin (glyceryl trinitrate, GTN) in blood vessels, resulting in vasodilation by nitric oxide (NO) or a related species.	Nitroglycerin	100-103	aldehyde dehydrogenase 2 family member	Homo sapiens	26-31
22386348-12	2012	CONCLUSION: In this porcine model of asphyxial CA, the addition of nitroglycerin to vasopressin and epinephrine maintained elevated coronary perfusion pressure during asphyxia CA and resulted in significantly better neurologic and histopathologic outcome in comparison with epinephrine alone.	Nitroglycerin	67-80	vasopressin	Sus scrofa	84-95
22859492-0	2012	P300/CBP associated factor regulates nitroglycerin-dependent arterial relaxation by N(epsilon)-lysine acetylation of contractile proteins.	Nitroglycerin	37-50	lysine acetyltransferase 2B	Rattus norvegicus	0-26
22909898-1	2012	OBJECTIVE: The aim of this study was to investigate whether the neuropeptide calcitonin gene related peptide (CGRP) contributes to nitroglycerin (GTN) response in patients with chronic heart failure (CHF) and the association with the mitochondrial aldehyde dehydrogenase-2 (ALDH2) Glu504Lys (ALDH2*2) polymorphism.	Nitroglycerin	146-149	calcitonin related polypeptide alpha	Homo sapiens	77-108
22909898-0	2012	Influence of ALDH2 Glu504Lys polymorphism on nitroglycerin response in chronic heart failure and involvement of Calcitonin Gene Related Peptide (CGRP).	Nitroglycerin	45-58	aldehyde dehydrogenase 2 family member	Homo sapiens	13-18
22618520-1	2012	OBJECTIVES: To investigate whether the addition of nitroglycerine to transcatheter arterial (chemo)embolization (TAE/TACE) can increase the delivery and effectiveness of TAE/TACE in patients with hepatocellular carcinoma (HCC) by dual-energy CT. METHODS: HCC patients (BCLC stage A or B) were randomized to (n = 51) or not to (n = 50) receive nitroglycerine and an emulsion of Lipiodol with or without doxorubicin, followed by embolization with Gelfoam pledgets.	Nitroglycerin	51-65	ADAM metallopeptidase domain 17	Homo sapiens	117-121
22618520-1	2012	OBJECTIVES: To investigate whether the addition of nitroglycerine to transcatheter arterial (chemo)embolization (TAE/TACE) can increase the delivery and effectiveness of TAE/TACE in patients with hepatocellular carcinoma (HCC) by dual-energy CT. METHODS: HCC patients (BCLC stage A or B) were randomized to (n = 51) or not to (n = 50) receive nitroglycerine and an emulsion of Lipiodol with or without doxorubicin, followed by embolization with Gelfoam pledgets.	Nitroglycerin	51-65	ADAM metallopeptidase domain 17	Homo sapiens	174-178
22618520-6	2012	CONCLUSIONS: Nitroglycerine increased delivery of the Lipiodol emulsion via TAE/TACE to HCC tumours with significant tumour reduction.	Nitroglycerin	13-27	ADAM metallopeptidase domain 17	Homo sapiens	80-84
22909898-1	2012	OBJECTIVE: The aim of this study was to investigate whether the neuropeptide calcitonin gene related peptide (CGRP) contributes to nitroglycerin (GTN) response in patients with chronic heart failure (CHF) and the association with the mitochondrial aldehyde dehydrogenase-2 (ALDH2) Glu504Lys (ALDH2*2) polymorphism.	Nitroglycerin	131-144	calcitonin related polypeptide alpha	Homo sapiens	77-108
22909898-1	2012	OBJECTIVE: The aim of this study was to investigate whether the neuropeptide calcitonin gene related peptide (CGRP) contributes to nitroglycerin (GTN) response in patients with chronic heart failure (CHF) and the association with the mitochondrial aldehyde dehydrogenase-2 (ALDH2) Glu504Lys (ALDH2*2) polymorphism.	Nitroglycerin	146-149	calcitonin related polypeptide alpha	Homo sapiens	110-114
22909898-1	2012	OBJECTIVE: The aim of this study was to investigate whether the neuropeptide calcitonin gene related peptide (CGRP) contributes to nitroglycerin (GTN) response in patients with chronic heart failure (CHF) and the association with the mitochondrial aldehyde dehydrogenase-2 (ALDH2) Glu504Lys (ALDH2*2) polymorphism.	Nitroglycerin	131-144	calcitonin related polypeptide alpha	Homo sapiens	110-114
22909898-10	2012	At the end of GTN infusion, ALDH2*1/*1 homozygous patients showed higher degrees of both the absolute decrease in SBP (DSBP) (p &lt; 0.001) and increase in LVEF (p &lt; 0.001) than carriers of the ALDH2*2 allele.	Nitroglycerin	14-17	aldehyde dehydrogenase 2 family member	Homo sapiens	28-33
22909898-10	2012	At the end of GTN infusion, ALDH2*1/*1 homozygous patients showed higher degrees of both the absolute decrease in SBP (DSBP) (p &lt; 0.001) and increase in LVEF (p &lt; 0.001) than carriers of the ALDH2*2 allele.	Nitroglycerin	14-17	aldehyde dehydrogenase 2 family member	Homo sapiens	197-202
22909898-11	2012	Mean plasma concentration of CGRP was increased after GTN infusion (p &lt; 0.001), but not changed after saline infusion (p &gt; 0.05).	Nitroglycerin	54-57	calcitonin related polypeptide alpha	Homo sapiens	29-33
22909898-13	2012	CONCLUSIONS: ALDH2*2 polymorphism is associated with contributions of CGRP to GTN response in CHF patients.	Nitroglycerin	78-81	aldehyde dehydrogenase 2 family member	Homo sapiens	13-18
22909898-13	2012	CONCLUSIONS: ALDH2*2 polymorphism is associated with contributions of CGRP to GTN response in CHF patients.	Nitroglycerin	78-81	calcitonin related polypeptide alpha	Homo sapiens	70-74
22452408-2	2012	Our results showed that Glyceryl Monosterate-Poloxamer 188 SLNs (average diameter of 522.466 nm) showed slow drug release rates (63.18% of lamivudine and 62.37% of zidovudine were released in 12 hrs) among all the SLN formulations.	Nitroglycerin	24-32	sarcolipin	Mus musculus	59-62
23009074-9	2012	Among NTG eyes, IOPcc was greater than GAT (19.8 and 14.4 mm Hg; p &lt; 0.001) and the difference between IOPcc and GAT was greatest for this subgroup of patients with NTG (p &lt;= 0.01).	Nitroglycerin	168-171	glycine-N-acyltransferase	Homo sapiens	106-119
22824464-4	2012	Moreover, NG-induced apoptosis of HepG2 cells was characteristic of intracellular reactive oxygen species (ROS) generation, loss of mitochondrial membrane potential (Deltapsim) and enhanced Bax-to-Bcl-2 ratio.	Nitroglycerin	10-12	BCL2 associated X, apoptosis regulator	Homo sapiens	190-193
22824464-4	2012	Moreover, NG-induced apoptosis of HepG2 cells was characteristic of intracellular reactive oxygen species (ROS) generation, loss of mitochondrial membrane potential (Deltapsim) and enhanced Bax-to-Bcl-2 ratio.	Nitroglycerin	10-12	BCL2 apoptosis regulator	Homo sapiens	197-202
22552400-11	2012	These findings suggest that NO donors, such as NOC-18 and GTN, enhance the anticancer effects of PEM by increasing the RFC1 and FPGS expression and stimulating cGMP signaling pathways in cancer cells.	Nitroglycerin	58-61	solute carrier family 19 (folate transporter), member 1	Mus musculus	119-123
22936184-8	2012	CONCLUSIONS: This preliminary study indicates that the expression patterns of ERbeta1 and ERbeta2 differ between malignant PTC lesions and benign NTG tissue, and their expression might be involved in the female predominance of PTC during the reproductive years.	Nitroglycerin	146-149	ret proto-oncogene	Homo sapiens	123-126
21724624-9	2012	Isolated IMA-rings from animals subjected to MPO revealed markedly diminished relaxation in response to acetylcholine (P &lt; 0.01) and nitroglycerine as opposed to controls (P &lt; 0.001).	Nitroglycerin	136-150	myeloperoxidase	Homo sapiens	45-48
22552400-11	2012	These findings suggest that NO donors, such as NOC-18 and GTN, enhance the anticancer effects of PEM by increasing the RFC1 and FPGS expression and stimulating cGMP signaling pathways in cancer cells.	Nitroglycerin	58-61	folylpolyglutamyl synthetase	Mus musculus	128-132
22465477-5	2012	The results with allopurinol and cyanamide suggest that only mitochondrial aldehyde dehydrogenase is involved in the bioactivation of GTN, sodium nitrite, and GSNO, whereas both pathways are involved in the bioactivation of nitrite anion in the intact rat.	Nitroglycerin	134-137	aldehyde dehydrogenase 2 family member	Rattus norvegicus	61-97
22539824-9	2012	In animals pretreated intravenously with the nitric oxide donor glyceryl trinitrate (GTN, 250 mug/kg) the mechanically evoked activity decreased after injection of CGRP and increased after injection of olcegepant.	Nitroglycerin	64-83	calcitonin related polypeptide alpha	Homo sapiens	164-168
22539824-9	2012	In animals pretreated intravenously with the nitric oxide donor glyceryl trinitrate (GTN, 250 mug/kg) the mechanically evoked activity decreased after injection of CGRP and increased after injection of olcegepant.	Nitroglycerin	85-88	calcitonin related polypeptide alpha	Homo sapiens	164-168
22539824-11	2012	CGRP receptors in the trigeminal ganglion may influence neuronal activity evoked by mechanical stimulation of meningeal afferents only after pretreatment with GTN.	Nitroglycerin	159-162	calcitonin-related polypeptide alpha	Rattus norvegicus	0-4
22207712-0	2012	Vascular bioactivation of nitroglycerin is catalyzed by cytosolic aldehyde dehydrogenase-2.	Nitroglycerin	26-39	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	66-90
22546019-1	2012	BACKGROUND: Asymmetric NG,NG-dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase, is regulated by the enzymatic participants of synthetic and metabolic processes, i.e., type I protein N-arginine methyltransferase (PRMT) and dimethylarginine dimethylaminohydrolase (DDAH).	Nitroglycerin	23-25	dimethylarginine dimethylaminohydrolase 1	Homo sapiens	246-285
22546019-1	2012	BACKGROUND: Asymmetric NG,NG-dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase, is regulated by the enzymatic participants of synthetic and metabolic processes, i.e., type I protein N-arginine methyltransferase (PRMT) and dimethylarginine dimethylaminohydrolase (DDAH).	Nitroglycerin	23-25	dimethylarginine dimethylaminohydrolase 1	Homo sapiens	287-291
22266491-1	2012	Recent studies demonstrate that alpha lipoic acid can prevent nitroglycerin tolerance by restoring aldehyde dehydrogenase 2 (ALDH2) activity and ALDH2-mediated detoxification of aldehydes is thought as an endogenous mechanism against ischemia-reperfusion injury.	Nitroglycerin	62-75	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	125-130
22266491-1	2012	Recent studies demonstrate that alpha lipoic acid can prevent nitroglycerin tolerance by restoring aldehyde dehydrogenase 2 (ALDH2) activity and ALDH2-mediated detoxification of aldehydes is thought as an endogenous mechanism against ischemia-reperfusion injury.	Nitroglycerin	62-75	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	145-150
22207712-1	2012	RATIONALE: According to general view, aldehyde dehydrogenase-2 (ALDH2) catalyzes the high-affinity pathway of vascular nitroglycerin (GTN) bioactivation in smooth muscle mitochondria.	Nitroglycerin	119-132	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	38-62
22207712-1	2012	RATIONALE: According to general view, aldehyde dehydrogenase-2 (ALDH2) catalyzes the high-affinity pathway of vascular nitroglycerin (GTN) bioactivation in smooth muscle mitochondria.	Nitroglycerin	119-132	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	64-69
22207712-1	2012	RATIONALE: According to general view, aldehyde dehydrogenase-2 (ALDH2) catalyzes the high-affinity pathway of vascular nitroglycerin (GTN) bioactivation in smooth muscle mitochondria.	Nitroglycerin	134-137	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	38-62
22207712-1	2012	RATIONALE: According to general view, aldehyde dehydrogenase-2 (ALDH2) catalyzes the high-affinity pathway of vascular nitroglycerin (GTN) bioactivation in smooth muscle mitochondria.	Nitroglycerin	134-137	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	64-69
22207712-3	2012	OBJECTIVE: In the present study, we investigated whether bioactivation of GTN is affected by the subcellular localization of ALDH2 using immortalized ALDH2-deficient aortic smooth muscle cells and mouse aortas with selective overexpression of the enzyme in either cytosol or mitochondria.	Nitroglycerin	74-77	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	125-130
22207712-6	2012	Cytosolic overexpression of ALDH2 restored GTN-induced relaxation and GTN denitration to wild-type levels, whereas overexpression in mitochondria (6-fold vs wild-type) had no effect on relaxation.	Nitroglycerin	43-46	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	28-33
22207712-6	2012	Cytosolic overexpression of ALDH2 restored GTN-induced relaxation and GTN denitration to wild-type levels, whereas overexpression in mitochondria (6-fold vs wild-type) had no effect on relaxation.	Nitroglycerin	70-73	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	28-33
22207712-7	2012	Overexpression of ALDH2 in the cytosol of ALDH2-deficient aortic smooth muscle cells led to a significant increase in GTN denitration and cyclic GMP accumulation, whereas mitochondrial overexpression had no effect.	Nitroglycerin	118-121	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	18-23
22207712-8	2012	CONCLUSIONS: The data indicate that vascular bioactivation of GTN is catalyzed by cytosolic ALDH2.	Nitroglycerin	62-65	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	92-97
22179079-6	2012	RESULTS: Nitroglycerin decreased aortic and finger blood pressure, radial DBP, vascular resistance, augmentation index and pulse wave velocity, and increased heart rate, cardiac index, stroke index and aortic reflection time (P &lt; 0.030 for all).	Nitroglycerin	9-22	D-box binding PAR bZIP transcription factor	Homo sapiens	74-77
22037515-4	2012	Here, we demonstrate that at such concentrations the pharmacologic effects of nitroglycerin are largely dependent on the phosphatidylinositol 3-kinase, Akt/PKB, and phosphatase and tensin homolog deleted on chromosome 10 (PTEN) signal transduction axis.	Nitroglycerin	78-91	AKT serine/threonine kinase 1	Homo sapiens	152-176
22245521-9	2012	PACAP-38-LI in the plasma, SC and TRG remained unchanged after CS, but it was increased significantly in the TNC 90 and 180 min after NTG injection.	Nitroglycerin	134-137	adenylate cyclase activating polypeptide 1	Rattus norvegicus	0-5
22037515-4	2012	Here, we demonstrate that at such concentrations the pharmacologic effects of nitroglycerin are largely dependent on the phosphatidylinositol 3-kinase, Akt/PKB, and phosphatase and tensin homolog deleted on chromosome 10 (PTEN) signal transduction axis.	Nitroglycerin	78-91	phosphatase and tensin homolog	Homo sapiens	222-226
22037515-5	2012	Furthermore, we demonstrate that nitroglycerin-dependent accumulation of 3,4,5-InsP(3), probably because of inhibition of PTEN, is important for eNOS activation, conferring a mechanistic basis for GTN pharmacological action at pharmacologically relevant doses.	Nitroglycerin	33-46	phosphatase and tensin homolog	Homo sapiens	122-126
22037515-5	2012	Furthermore, we demonstrate that nitroglycerin-dependent accumulation of 3,4,5-InsP(3), probably because of inhibition of PTEN, is important for eNOS activation, conferring a mechanistic basis for GTN pharmacological action at pharmacologically relevant doses.	Nitroglycerin	197-200	phosphatase and tensin homolog	Homo sapiens	122-126
22174360-4	2012	Anaesthesia and low blood pressure caused by high GTN doses both can affect the expression of nociceptive marker c-fos.	Nitroglycerin	50-53	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	113-118
23244123-8	2012	Using annexin V/PI double staining it could be shown that GTN induces early apoptosis on HeLa cells after 24, 48 and 72 h. It could be concluded that goniothalamin showing a promising cytotoxicity effect against several cancer cell lines including cervical cancer cells (HeLa) with apoptosis as the mode of cell death induced on HeLa cells by Goniothalamin was.	Nitroglycerin	58-61	annexin A5	Homo sapiens	6-15
22174360-9	2012	RESULTS: A significant upregulation of c-fos mRNA was observed in the trigeminal nucleus caudalis at 30 min and 2 h that was followed by an upregulation of Fos protein in the trigeminal nucleus caudalis at 2 h and 4 h after GTN infusion.	Nitroglycerin	224-227	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	39-44
22174360-9	2012	RESULTS: A significant upregulation of c-fos mRNA was observed in the trigeminal nucleus caudalis at 30 min and 2 h that was followed by an upregulation of Fos protein in the trigeminal nucleus caudalis at 2 h and 4 h after GTN infusion.	Nitroglycerin	224-227	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	156-159
22040938-5	2012	Nitroglycerin tolerance is caused, at least in part, by inactivation of aldehyde dehydrogenase 2 (ALDH2), an enzyme that converts GTN to the vasodilator, NO.	Nitroglycerin	0-13	aldehyde dehydrogenase 2 family member	Homo sapiens	72-96
22040938-5	2012	Nitroglycerin tolerance is caused, at least in part, by inactivation of aldehyde dehydrogenase 2 (ALDH2), an enzyme that converts GTN to the vasodilator, NO.	Nitroglycerin	0-13	aldehyde dehydrogenase 2 family member	Homo sapiens	98-103
22040938-5	2012	Nitroglycerin tolerance is caused, at least in part, by inactivation of aldehyde dehydrogenase 2 (ALDH2), an enzyme that converts GTN to the vasodilator, NO.	Nitroglycerin	130-133	aldehyde dehydrogenase 2 family member	Homo sapiens	72-96
22040938-5	2012	Nitroglycerin tolerance is caused, at least in part, by inactivation of aldehyde dehydrogenase 2 (ALDH2), an enzyme that converts GTN to the vasodilator, NO.	Nitroglycerin	130-133	aldehyde dehydrogenase 2 family member	Homo sapiens	98-103
22040938-7	2012	Coadministration of Alda-1, an activator of ALDH2, with GTN improves metabolism of reactive aldehyde adducts and prevents the GTN-induced increase in cardiac dysfunction following MI.	Nitroglycerin	56-59	aldehyde dehydrogenase 2 family member	Homo sapiens	44-49
22040938-7	2012	Coadministration of Alda-1, an activator of ALDH2, with GTN improves metabolism of reactive aldehyde adducts and prevents the GTN-induced increase in cardiac dysfunction following MI.	Nitroglycerin	126-129	aldehyde dehydrogenase 2 family member	Homo sapiens	44-49
22033344-7	2012	NTG-induced photophobia both in the early (0-30 min) and late phases (90-120 min) due to direct vasodilation and trigeminal sensitization, respectively, was significantly reduced in PACAP(-/-) mice.	Nitroglycerin	0-3	adenylate cyclase activating polypeptide 1	Mus musculus	182-187
22506100-8	2012	With the present paper, we present and discuss our recent and previous findings on the role of HO-1 for the prevention of nitroglycerin-induced nitrate tolerance and for the beneficial effects of PETN therapy.	Nitroglycerin	122-135	heme oxygenase 1	Homo sapiens	95-99
22033344-0	2012	Pituitary adenylate cyclase-activating polypeptide plays a key role in nitroglycerol-induced trigeminovascular activation in mice.	Nitroglycerin	71-84	adenylate cyclase activating polypeptide 1	Mus musculus	0-50
22033344-9	2012	The number of c-Fos expressing cells referring to neuronal activation in the trigeminal ganglia and nucleus caudalis significantly increased 4h after NTG in PACAP(+/+), but not in PACAP(-/-) animals.	Nitroglycerin	150-153	FBJ osteosarcoma oncogene	Mus musculus	14-19
22033344-3	2012	Nitroglycerol (NTG)-induced pathophysiological changes were investigated in this study in PACAP gene-deleted (PACAP(-/-)) and wildtype (PACAP(+/+)) mice.	Nitroglycerin	0-13	adenylate cyclase activating polypeptide 1	Mus musculus	90-95
22033344-9	2012	The number of c-Fos expressing cells referring to neuronal activation in the trigeminal ganglia and nucleus caudalis significantly increased 4h after NTG in PACAP(+/+), but not in PACAP(-/-) animals.	Nitroglycerin	150-153	adenylate cyclase activating polypeptide 1	Mus musculus	157-162
21818694-2	2011	Mitochondrial aldehyde dehydrogenase (ALDH2) is the principal enzyme responsible for NO liberation from nitroglycerin (NTG), but lacks activity towards other ORN.	Nitroglycerin	104-117	aldehyde dehydrogenase 2 family member	Homo sapiens	38-43
21818694-2	2011	Mitochondrial aldehyde dehydrogenase (ALDH2) is the principal enzyme responsible for NO liberation from nitroglycerin (NTG), but lacks activity towards other ORN.	Nitroglycerin	119-122	aldehyde dehydrogenase 2 family member	Homo sapiens	38-43
21818694-3	2011	Cytosolic aldehyde dehydrogenase (ALDH1a1) can produce NO from NTG, but its activity towards other ORN is unknown.	Nitroglycerin	63-66	aldehyde dehydrogenase 1 family member A1	Homo sapiens	34-41
21818694-5	2011	Following a 10-min incubation with purified enzyme, 0.1 mM NTG and 1 mM ISDN potently inactivated ALDH1a1 (to 21.9% +- 11.1% and 0.44% +- 1.04% of control activity, respectively) and ALDH2 (no activity remaining and 4.57% +- 7.92% of control activity, respectively), while 1 mM IS-5-MN exerted only modest inactivation of ALDH1a1 (reduced to 89% +- 4.3% of control).	Nitroglycerin	59-62	aldehyde dehydrogenase 1 family member A1	Homo sapiens	98-105
21818694-5	2011	Following a 10-min incubation with purified enzyme, 0.1 mM NTG and 1 mM ISDN potently inactivated ALDH1a1 (to 21.9% +- 11.1% and 0.44% +- 1.04% of control activity, respectively) and ALDH2 (no activity remaining and 4.57% +- 7.92% of control activity, respectively), while 1 mM IS-5-MN exerted only modest inactivation of ALDH1a1 (reduced to 89% +- 4.3% of control).	Nitroglycerin	59-62	aldehyde dehydrogenase 2 family member	Homo sapiens	183-188
21818694-5	2011	Following a 10-min incubation with purified enzyme, 0.1 mM NTG and 1 mM ISDN potently inactivated ALDH1a1 (to 21.9% +- 11.1% and 0.44% +- 1.04% of control activity, respectively) and ALDH2 (no activity remaining and 4.57% +- 7.92% of control activity, respectively), while 1 mM IS-5-MN exerted only modest inactivation of ALDH1a1 (reduced to 89% +- 4.3% of control).	Nitroglycerin	59-62	aldehyde dehydrogenase 1 family member A1	Homo sapiens	322-329
22049071-0	2011	ALDH2 activator inhibits increased myocardial infarction injury by nitroglycerin tolerance.	Nitroglycerin	67-80	aldehyde dehydrogenase 2 family member	Homo sapiens	0-5
22049071-3	2011	Nitroglycerin tolerance is a result of inactivation of aldehyde dehydrogenase 2 (ALDH2), an enzyme essential for cardioprotection in animals subjected to myocardial infarction.	Nitroglycerin	0-13	aldehyde dehydrogenase 2 family member	Homo sapiens	55-79
22049071-3	2011	Nitroglycerin tolerance is a result of inactivation of aldehyde dehydrogenase 2 (ALDH2), an enzyme essential for cardioprotection in animals subjected to myocardial infarction.	Nitroglycerin	0-13	aldehyde dehydrogenase 2 family member	Homo sapiens	81-86
22049071-7	2011	Nitroglycerin inhibited ALDH2 activity in vitro, an effect that was blocked by Alda-1, an activator of ALDH2.	Nitroglycerin	0-13	aldehyde dehydrogenase 2 family member	Homo sapiens	24-29
22049071-7	2011	Nitroglycerin inhibited ALDH2 activity in vitro, an effect that was blocked by Alda-1, an activator of ALDH2.	Nitroglycerin	0-13	aldehyde dehydrogenase 2 family member	Homo sapiens	103-108
22049071-9	2011	If our animal studies showing that nitroglycerin tolerance increases cardiac injury upon ischemic insult are corroborated in humans, activators of ALDH2 such as Alda-1 may help to protect patients with myocardial infarction from this nitroglycerin-induced increase in cardiac injury while maintaining the cardiac benefits of the increased nitric oxide concentrations produced by nitroglycerin.	Nitroglycerin	35-48	aldehyde dehydrogenase 2 family member	Homo sapiens	147-152
22049071-9	2011	If our animal studies showing that nitroglycerin tolerance increases cardiac injury upon ischemic insult are corroborated in humans, activators of ALDH2 such as Alda-1 may help to protect patients with myocardial infarction from this nitroglycerin-induced increase in cardiac injury while maintaining the cardiac benefits of the increased nitric oxide concentrations produced by nitroglycerin.	Nitroglycerin	234-247	aldehyde dehydrogenase 2 family member	Homo sapiens	147-152
22049071-9	2011	If our animal studies showing that nitroglycerin tolerance increases cardiac injury upon ischemic insult are corroborated in humans, activators of ALDH2 such as Alda-1 may help to protect patients with myocardial infarction from this nitroglycerin-induced increase in cardiac injury while maintaining the cardiac benefits of the increased nitric oxide concentrations produced by nitroglycerin.	Nitroglycerin	234-247	aldehyde dehydrogenase 2 family member	Homo sapiens	147-152
20716121-6	2011	HO-1 related carbon monoxide (CO) production was detected in NTg, HO-1 Tg and HO-1 Tg + SnPPIX treated groups, and a substantial increase in CO production was observed in the HO-1 Tg hearts subjected to ischemia/reperfusion.	Nitroglycerin	61-64	heme oxygenase 1	Mus musculus	0-4
21757654-0	2011	Nitroglycerin-induced endothelial dysfunction and tolerance involve adverse phosphorylation and S-Glutathionylation of endothelial nitric oxide synthase: beneficial effects of therapy with the AT1 receptor blocker telmisartan.	Nitroglycerin	0-13	nitric oxide synthase 3	Rattus norvegicus	119-152
21757654-1	2011	OBJECTIVE: Continuous administration of nitroglycerin (GTN) causes tolerance and endothelial dysfunction by inducing reactive oxygen species (ROS) production from various enzymatic sources, such as mitochondria, NADPH oxidase, and an uncoupled endothelial nitric oxide synthase (eNOS).	Nitroglycerin	40-53	nitric oxide synthase 3	Rattus norvegicus	244-277
21757654-1	2011	OBJECTIVE: Continuous administration of nitroglycerin (GTN) causes tolerance and endothelial dysfunction by inducing reactive oxygen species (ROS) production from various enzymatic sources, such as mitochondria, NADPH oxidase, and an uncoupled endothelial nitric oxide synthase (eNOS).	Nitroglycerin	40-53	nitric oxide synthase 3	Rattus norvegicus	279-283
21757654-1	2011	OBJECTIVE: Continuous administration of nitroglycerin (GTN) causes tolerance and endothelial dysfunction by inducing reactive oxygen species (ROS) production from various enzymatic sources, such as mitochondria, NADPH oxidase, and an uncoupled endothelial nitric oxide synthase (eNOS).	Nitroglycerin	55-58	nitric oxide synthase 3	Rattus norvegicus	244-277
21757654-1	2011	OBJECTIVE: Continuous administration of nitroglycerin (GTN) causes tolerance and endothelial dysfunction by inducing reactive oxygen species (ROS) production from various enzymatic sources, such as mitochondria, NADPH oxidase, and an uncoupled endothelial nitric oxide synthase (eNOS).	Nitroglycerin	55-58	nitric oxide synthase 3	Rattus norvegicus	279-283
21757654-9	2011	GTN-induced decrease in Ser1177, increase in Thr495 phosphorylation or S-glutathionylation of eNOS, and decrease in mitochondrial aldehyde dehydrogenase expression were normalized by telmisartan.	Nitroglycerin	0-3	nitric oxide synthase 3	Rattus norvegicus	94-98
21757654-9	2011	GTN-induced decrease in Ser1177, increase in Thr495 phosphorylation or S-glutathionylation of eNOS, and decrease in mitochondrial aldehyde dehydrogenase expression were normalized by telmisartan.	Nitroglycerin	0-3	aldehyde dehydrogenase 2 family member	Rattus norvegicus	116-152
21757654-10	2011	CONCLUSIONS: These data identify modification of eNOS phosphorylation as an important component of GTN-induced endothelial dysfunction.	Nitroglycerin	99-102	nitric oxide synthase 3	Rattus norvegicus	49-53
21799398-9	2011	ATIII administration increases heparin sensitivity and decreases heparin requirements compared with FFP in patients undergoing CABGS with peroperative NTG infusion.	Nitroglycerin	151-154	serpin family C member 1	Homo sapiens	0-5
21799398-10	2011	ATIII may be preferred to FFP in patients with heparin resistance due to NTG infusion undergoing CABGS.	Nitroglycerin	73-76	serpin family C member 1	Homo sapiens	0-5
21506955-6	2011	CONCLUSIONS AND IMPLICATIONS: The dissociation of reduced ALDH activity and ALDH2 expression from the duration of the impaired vasodilator and biotransformation responses to GTN in nitrate-tolerant blood vessels, suggests that factors other than changes in ALDH2-mediated GTN bioactivation contribute to nitrate tolerance.	Nitroglycerin	174-177	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	58-62
21506955-6	2011	CONCLUSIONS AND IMPLICATIONS: The dissociation of reduced ALDH activity and ALDH2 expression from the duration of the impaired vasodilator and biotransformation responses to GTN in nitrate-tolerant blood vessels, suggests that factors other than changes in ALDH2-mediated GTN bioactivation contribute to nitrate tolerance.	Nitroglycerin	174-177	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	76-81
21523859-1	2011	It is commonly accepted that the major effect of nitroglycerin (NG) is realized through the release of nitric oxide (NO) catalyzed by aldehyde dehydrogenase-2 (ALDH2).	Nitroglycerin	49-62	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	134-158
21523859-1	2011	It is commonly accepted that the major effect of nitroglycerin (NG) is realized through the release of nitric oxide (NO) catalyzed by aldehyde dehydrogenase-2 (ALDH2).	Nitroglycerin	49-62	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	160-165
21523859-1	2011	It is commonly accepted that the major effect of nitroglycerin (NG) is realized through the release of nitric oxide (NO) catalyzed by aldehyde dehydrogenase-2 (ALDH2).	Nitroglycerin	64-66	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	134-158
21523859-1	2011	It is commonly accepted that the major effect of nitroglycerin (NG) is realized through the release of nitric oxide (NO) catalyzed by aldehyde dehydrogenase-2 (ALDH2).	Nitroglycerin	64-66	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	160-165
21765367-6	2011	A 7-day period of treatment with patches releasing 0.07 mg of nitroglycerin per hour yielded nitrate tolerance and a state of insulin resistance and no increase in insulin sensitivity in response to food.	Nitroglycerin	62-75	insulin	Oryctolagus cuniculus	126-133
21799398-0	2011	Peroperative effects of fresh frozen plasma and antithrombin III on heparin sensitivity and coagulation during nitroglycerine infusion in coronary artery bypass surgery.	Nitroglycerin	111-125	serpin family C member 1	Homo sapiens	48-64
21506955-0	2011	Changes in aldehyde dehydrogenase 2 expression in rat blood vessels during glyceryl trinitrate tolerance development and reversal.	Nitroglycerin	75-94	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	11-35
21506955-1	2011	BACKGROUND AND PURPOSE: Recent studies have suggested an essential role for aldehyde dehydrogenase 2 (ALDH2) in the bioactivation of organic nitrates such as glyceryl trinitrate (GTN).	Nitroglycerin	158-177	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	76-100
21506955-1	2011	BACKGROUND AND PURPOSE: Recent studies have suggested an essential role for aldehyde dehydrogenase 2 (ALDH2) in the bioactivation of organic nitrates such as glyceryl trinitrate (GTN).	Nitroglycerin	158-177	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	102-107
21506955-1	2011	BACKGROUND AND PURPOSE: Recent studies have suggested an essential role for aldehyde dehydrogenase 2 (ALDH2) in the bioactivation of organic nitrates such as glyceryl trinitrate (GTN).	Nitroglycerin	179-182	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	76-100
21506955-1	2011	BACKGROUND AND PURPOSE: Recent studies have suggested an essential role for aldehyde dehydrogenase 2 (ALDH2) in the bioactivation of organic nitrates such as glyceryl trinitrate (GTN).	Nitroglycerin	179-182	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	102-107
21506955-4	2011	KEY RESULTS: A decrease was observed in both ALDH2 protein expression (80% in tolerant veins and 30% in tolerant arteries after 48 h exposure to GTN) and aortic ALDH activity, concomitant with decreased vasodilator responses to GTN and decreased aortic GTN biotransformation.	Nitroglycerin	145-148	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	45-50
21506955-4	2011	KEY RESULTS: A decrease was observed in both ALDH2 protein expression (80% in tolerant veins and 30% in tolerant arteries after 48 h exposure to GTN) and aortic ALDH activity, concomitant with decreased vasodilator responses to GTN and decreased aortic GTN biotransformation.	Nitroglycerin	145-148	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	45-49
21506955-4	2011	KEY RESULTS: A decrease was observed in both ALDH2 protein expression (80% in tolerant veins and 30% in tolerant arteries after 48 h exposure to GTN) and aortic ALDH activity, concomitant with decreased vasodilator responses to GTN and decreased aortic GTN biotransformation.	Nitroglycerin	228-231	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	45-50
21506955-4	2011	KEY RESULTS: A decrease was observed in both ALDH2 protein expression (80% in tolerant veins and 30% in tolerant arteries after 48 h exposure to GTN) and aortic ALDH activity, concomitant with decreased vasodilator responses to GTN and decreased aortic GTN biotransformation.	Nitroglycerin	228-231	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	45-50
21506955-5	2011	However, after a 24 h drug-free period following 48 h of GTN exposure, vasodilator responses to GTN and aortic GTN biotransformation activity had returned to control values, whereas vascular ALDH2 expression and aortic ALDH activity were still significantly depressed, and remained so for 3-5 days following cessation of GTN exposure.	Nitroglycerin	57-60	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	191-195
20716121-4	2011	Significant post-ischemic recovery in coronary flow (CF), aortic flow (AF), aortic pressure (AOP) and first derivative of AOP (AOPdp/dt) were detected in the HO-1 Tg group compared to the NTg values.	Nitroglycerin	188-191	heme oxygenase 1	Mus musculus	158-162
20716121-10	2011	Immunohistochemical staining of HO-1 was intensified in HO-1 Tg compared to the NTg myocardium.	Nitroglycerin	80-83	heme oxygenase 1	Mus musculus	32-36
21536753-1	2011	To elucidate the mechanism underlying reduction of nitroglycerin (GTN) to nitric oxide (NO) by mitochondrial aldehyde dehydrogenase (ALDH2), we generated mutants of the enzyme lacking the cysteines adjacent to reactive Cys302 (C301S and C303S), the glutamate that participates as a general base in aldehyde oxidation (E268Q) or combinations of these residues.	Nitroglycerin	51-64	aldehyde dehydrogenase 2 family member	Homo sapiens	133-138
21766372-0	2011	Identification of nitroglycerin-induced cysteine modifications of pro-matrix metalloproteinase-9.	Nitroglycerin	18-31	matrix metallopeptidase 9	Homo sapiens	70-96
21766372-1	2011	Nitroglycerin (NTG), an important cardiovascular agent, has been shown recently to activate matrix metalloproteinase-9 (MMP-9) in biological systems, possibly leading to destabilization of atherosclerotic plaques.	Nitroglycerin	0-13	matrix metallopeptidase 9	Homo sapiens	92-118
21766372-1	2011	Nitroglycerin (NTG), an important cardiovascular agent, has been shown recently to activate matrix metalloproteinase-9 (MMP-9) in biological systems, possibly leading to destabilization of atherosclerotic plaques.	Nitroglycerin	0-13	matrix metallopeptidase 9	Homo sapiens	120-125
21766372-1	2011	Nitroglycerin (NTG), an important cardiovascular agent, has been shown recently to activate matrix metalloproteinase-9 (MMP-9) in biological systems, possibly leading to destabilization of atherosclerotic plaques.	Nitroglycerin	15-18	matrix metallopeptidase 9	Homo sapiens	92-118
21766372-1	2011	Nitroglycerin (NTG), an important cardiovascular agent, has been shown recently to activate matrix metalloproteinase-9 (MMP-9) in biological systems, possibly leading to destabilization of atherosclerotic plaques.	Nitroglycerin	15-18	matrix metallopeptidase 9	Homo sapiens	120-125
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.	Nitroglycerin	56-59	urotensin 2	Homo sapiens	113-118
21704284-9	2011	Calcium antagonists and GTN relax the contraction caused by hU-II with different potencies.	Nitroglycerin	24-27	urotensin 2	Homo sapiens	60-65
21704284-10	2011	However, calcium antagonists are more effective than GTN in preventing the contraction induced by hU-II.	Nitroglycerin	53-56	urotensin 2	Homo sapiens	98-103
21536753-0	2011	Site-directed mutagenesis of aldehyde dehydrogenase-2 suggests three distinct pathways of nitroglycerin biotransformation.	Nitroglycerin	90-103	aldehyde dehydrogenase 2 family member	Homo sapiens	29-53
21536753-1	2011	To elucidate the mechanism underlying reduction of nitroglycerin (GTN) to nitric oxide (NO) by mitochondrial aldehyde dehydrogenase (ALDH2), we generated mutants of the enzyme lacking the cysteines adjacent to reactive Cys302 (C301S and C303S), the glutamate that participates as a general base in aldehyde oxidation (E268Q) or combinations of these residues.	Nitroglycerin	66-69	aldehyde dehydrogenase 2 family member	Homo sapiens	133-138
21536753-5	2011	These results suggest three alternative pathways for the reaction of ALDH2 with GTN, all involving formation of a thionitrate/sulfenyl nitrite intermediate at Cys302 as the initial step.	Nitroglycerin	80-83	aldehyde dehydrogenase 2 family member	Homo sapiens	69-74
21536753-9	2011	Although the latter reaction accounts for less than 10% of total turnover of GTN metabolism catalyzed by wild-type ALDH2, it is most likely essential for vascular GTN bioactivation.	Nitroglycerin	77-80	aldehyde dehydrogenase 2 family member	Homo sapiens	115-120
21536753-9	2011	Although the latter reaction accounts for less than 10% of total turnover of GTN metabolism catalyzed by wild-type ALDH2, it is most likely essential for vascular GTN bioactivation.	Nitroglycerin	163-166	aldehyde dehydrogenase 2 family member	Homo sapiens	115-120
21480950-1	2011	AIMS: To assess the effect of the calcitonin gene-related peptide (CGRP) receptor antagonist, telcagepant, on the haemodynamic response to sublingual nitroglycerin (NTG).	Nitroglycerin	150-163	calcitonin related polypeptide alpha	Homo sapiens	34-65
21331665-7	2011	Heat coagulation of middle meningeal artery may ameliorate sufferings of rat induced by NTG and play an important role in restraining the release of CGRP as well as the activation of neurons in trigeminal nucleus caudalis in rats following NTG infusion.	Nitroglycerin	240-243	calcitonin-related polypeptide alpha	Rattus norvegicus	149-153
22021773-1	2011	OBJECTIVES: To determine whether polymorphisms at codon 487 (*1, GAA=Glu; *2, AAA=Lys) of mitochondrial aldehyde dehydrogenase 2 (ALDH2) influence nitroglycerine (glyceryl trinitrate (GTN))-induced vasodilation, and whether GTN or isosorbide dinitrate (ISDN) is a more effective antianginal agent in each ALDH2 genotype.	Nitroglycerin	147-161	aldehyde dehydrogenase 2 family member	Homo sapiens	130-135
22021773-1	2011	OBJECTIVES: To determine whether polymorphisms at codon 487 (*1, GAA=Glu; *2, AAA=Lys) of mitochondrial aldehyde dehydrogenase 2 (ALDH2) influence nitroglycerine (glyceryl trinitrate (GTN))-induced vasodilation, and whether GTN or isosorbide dinitrate (ISDN) is a more effective antianginal agent in each ALDH2 genotype.	Nitroglycerin	163-182	aldehyde dehydrogenase 2 family member	Homo sapiens	130-135
22021773-1	2011	OBJECTIVES: To determine whether polymorphisms at codon 487 (*1, GAA=Glu; *2, AAA=Lys) of mitochondrial aldehyde dehydrogenase 2 (ALDH2) influence nitroglycerine (glyceryl trinitrate (GTN))-induced vasodilation, and whether GTN or isosorbide dinitrate (ISDN) is a more effective antianginal agent in each ALDH2 genotype.	Nitroglycerin	184-187	aldehyde dehydrogenase 2 family member	Homo sapiens	130-135
22021773-1	2011	OBJECTIVES: To determine whether polymorphisms at codon 487 (*1, GAA=Glu; *2, AAA=Lys) of mitochondrial aldehyde dehydrogenase 2 (ALDH2) influence nitroglycerine (glyceryl trinitrate (GTN))-induced vasodilation, and whether GTN or isosorbide dinitrate (ISDN) is a more effective antianginal agent in each ALDH2 genotype.	Nitroglycerin	224-227	aldehyde dehydrogenase 2 family member	Homo sapiens	130-135
21576282-5	2011	In NES compared with NTG groups, lower cystatin-C (1449 versus 2739 ng/mL, P&lt;0.05) and IL-6 (25 versus 50 pg/mL, P&lt;0.05) were observed.	Nitroglycerin	21-24	cystatin C	Homo sapiens	39-49
21331665-0	2011	Effects of heating coagulation of middle meningeal artery on plasma CGRP level and c-fos expression in migraine rat triggered by nitroglycerin.	Nitroglycerin	129-142	calcitonin-related polypeptide alpha	Rattus norvegicus	68-72
21331665-0	2011	Effects of heating coagulation of middle meningeal artery on plasma CGRP level and c-fos expression in migraine rat triggered by nitroglycerin.	Nitroglycerin	129-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
21331665-5	2011	We found that NTG led to markedly increase in plasma CGRP level and c-fos expression in trigeminal nucleus caudalis compared with the isotonic saline-treated group (P &lt; 0.05).	Nitroglycerin	14-17	calcitonin-related polypeptide alpha	Rattus norvegicus	53-57
21331665-5	2011	We found that NTG led to markedly increase in plasma CGRP level and c-fos expression in trigeminal nucleus caudalis compared with the isotonic saline-treated group (P &lt; 0.05).	Nitroglycerin	14-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
21550392-9	2011	The extravasation produced by topical GTN due to expression of iNOS in dural macrophages was also reduced to 1.555+-0.03384 and 1.425+-0.01204 by preventive treatment with ANE at the dose of 250 and 500 mg/kg, orally, respectively.	Nitroglycerin	38-41	nitric oxide synthase 2	Rattus norvegicus	63-67
21641407-0	2011	Glyceryl trinitrate inhibits hypoxia-induced release of soluble fms-like tyrosine kinase-1 and endoglin from placental tissues.	Nitroglycerin	0-19	endoglin	Homo sapiens	95-103
21641407-6	2011	Treatment of explants with GTN also prevented the hypoxia-induced accumulation of hypoxia-inducible factor-1alpha, a key mediator of cellular adaptations to hypoxia.	Nitroglycerin	27-30	hypoxia inducible factor 1 subunit alpha	Homo sapiens	82-113
21480950-1	2011	AIMS: To assess the effect of the calcitonin gene-related peptide (CGRP) receptor antagonist, telcagepant, on the haemodynamic response to sublingual nitroglycerin (NTG).	Nitroglycerin	150-163	calcitonin related polypeptide alpha	Homo sapiens	67-71
21480950-1	2011	AIMS: To assess the effect of the calcitonin gene-related peptide (CGRP) receptor antagonist, telcagepant, on the haemodynamic response to sublingual nitroglycerin (NTG).	Nitroglycerin	165-168	calcitonin related polypeptide alpha	Homo sapiens	34-65
21331757-5	2011	In addition, the effect of AEA (administered 30 min before NTG injection) was investigated on NTG-induced Fos expression and evaluated 4 h following NTG injection.	Nitroglycerin	94-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
21809559-0	2011	[Heat coagulation of middle meningeal artery affects plasma CGRP and substance P levels in migraine rat triggered by nitroglycerin].	Nitroglycerin	117-130	calcitonin-related polypeptide alpha	Rattus norvegicus	60-64
21809559-1	2011	OBJECTIVE: To detect the influence of heat coagulation of middle meningeal artery (MMA) on plasma CGRP and SP levels in migraine rat triggered by nitroglycerin (NTG).	Nitroglycerin	146-159	calcitonin-related polypeptide alpha	Rattus norvegicus	98-102
21809559-1	2011	OBJECTIVE: To detect the influence of heat coagulation of middle meningeal artery (MMA) on plasma CGRP and SP levels in migraine rat triggered by nitroglycerin (NTG).	Nitroglycerin	161-164	calcitonin-related polypeptide alpha	Rattus norvegicus	98-102
21809559-10	2011	CONCLUSION: Heat coagulation of MMA may relieve symptoms of rats following nitroglycerin infusion, possibly by inhibiting the release of CGRP and SP.	Nitroglycerin	75-88	calcitonin-related polypeptide alpha	Rattus norvegicus	137-141
21331757-5	2011	In addition, the effect of AEA (administered 30 min before NTG injection) was investigated on NTG-induced Fos expression and evaluated 4 h following NTG injection.	Nitroglycerin	94-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
21331757-7	2011	Pre-treatment with AEA significantly reduced the NTG-induced neuronal activation in nucleus trigeminalis caudalis, confirming the results obtained in our previous study, and in area postrema, while the same treatment induced an increase of Fos expression in paraventricular and supraoptic nuclei of the hypothalamus, parabrachial nucleus, and periaqueductal grey.	Nitroglycerin	49-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	240-243
21223993-7	2011	Additionally, using redox proteomics analyses we identified two oxidatively-modified proteins: phosphatidylethanolamine-binding protein 1 and Pin-1 with decreased levels of protein 3-nitrotyrosine in J20 Tg mice relative to NTg.	Nitroglycerin	224-227	peptidyl-prolyl cis/trans isomerase, NIMA-interacting 1	Mus musculus	142-147
21252222-8	2011	In the presence of glyceryl trinitrate and to a lesser extent pentaerythritol tetranitrate, ALDH-2 may be switched to a peroxynitrite synthase.	Nitroglycerin	19-38	aldehyde dehydrogenase 2 family member	Homo sapiens	92-98
21059625-0	2011	Comments on "Calcitonin gene-related peptide (CGRP) levels during glyceryl trinitrate (GTN)-induced headache in healthy volunteers".	Nitroglycerin	66-85	calcitonin related polypeptide alpha	Homo sapiens	46-50
21156214-6	2011	NTG exposure significantly up-regulated NF-kappaB DNA nuclear binding activity and MMP-9 protein expression, and reduced tissue inhibitor of metalloproteinase-1 (TIMP-1) expression; these effects were abrogated in the presence of the NF-kappaB inhibitor parthenolide (a chemical inhibitor derived from the feverfew plant).	Nitroglycerin	0-3	matrix metallopeptidase 9	Homo sapiens	83-88
21156214-6	2011	NTG exposure significantly up-regulated NF-kappaB DNA nuclear binding activity and MMP-9 protein expression, and reduced tissue inhibitor of metalloproteinase-1 (TIMP-1) expression; these effects were abrogated in the presence of the NF-kappaB inhibitor parthenolide (a chemical inhibitor derived from the feverfew plant).	Nitroglycerin	0-3	TIMP metallopeptidase inhibitor 1	Homo sapiens	162-168
21156214-8	2011	Sprague-Dawley rats exposed continuously to NTG subcutaneously for 8 days via mini-osmotic pumps showed significant induction of plasma MMP-9 dimer concentrations and the expression of a complex of MMP-9 with lipocalin-2 or neutrophil gelatinase associated lipocalin (NGAL).	Nitroglycerin	44-47	matrix metallopeptidase 9	Rattus norvegicus	136-141
21156214-8	2011	Sprague-Dawley rats exposed continuously to NTG subcutaneously for 8 days via mini-osmotic pumps showed significant induction of plasma MMP-9 dimer concentrations and the expression of a complex of MMP-9 with lipocalin-2 or neutrophil gelatinase associated lipocalin (NGAL).	Nitroglycerin	44-47	matrix metallopeptidase 9	Rattus norvegicus	198-203
21156214-8	2011	Sprague-Dawley rats exposed continuously to NTG subcutaneously for 8 days via mini-osmotic pumps showed significant induction of plasma MMP-9 dimer concentrations and the expression of a complex of MMP-9 with lipocalin-2 or neutrophil gelatinase associated lipocalin (NGAL).	Nitroglycerin	44-47	lipocalin 2	Rattus norvegicus	209-220
21156214-8	2011	Sprague-Dawley rats exposed continuously to NTG subcutaneously for 8 days via mini-osmotic pumps showed significant induction of plasma MMP-9 dimer concentrations and the expression of a complex of MMP-9 with lipocalin-2 or neutrophil gelatinase associated lipocalin (NGAL).	Nitroglycerin	44-47	lipocalin 2	Rattus norvegicus	224-266
21156214-8	2011	Sprague-Dawley rats exposed continuously to NTG subcutaneously for 8 days via mini-osmotic pumps showed significant induction of plasma MMP-9 dimer concentrations and the expression of a complex of MMP-9 with lipocalin-2 or neutrophil gelatinase associated lipocalin (NGAL).	Nitroglycerin	44-47	lipocalin 2	Rattus norvegicus	268-272
21156214-10	2011	Plasma TIMP-1 protein was down-regulated significantly by day 2 and days 4-7 in the NTG-treated rats.	Nitroglycerin	84-87	TIMP metallopeptidase inhibitor 1	Rattus norvegicus	7-13
21156214-12	2011	Our studies indicate that clinically relevant concentrations of NTG not only altered ECM matrix by changing the expression of multiple genes that govern cellular integrity, affecting cellular MMP-9/TIMP-1 balance in THP-1 human macrophages possibly via NF-kappaB activation, but also led to systemic changes in MMP-9/TIMP-1 expression and gelatinase activity in rats.	Nitroglycerin	64-67	matrix metallopeptidase 9	Homo sapiens	192-197
21156214-12	2011	Our studies indicate that clinically relevant concentrations of NTG not only altered ECM matrix by changing the expression of multiple genes that govern cellular integrity, affecting cellular MMP-9/TIMP-1 balance in THP-1 human macrophages possibly via NF-kappaB activation, but also led to systemic changes in MMP-9/TIMP-1 expression and gelatinase activity in rats.	Nitroglycerin	64-67	TIMP metallopeptidase inhibitor 1	Homo sapiens	198-204
21156214-12	2011	Our studies indicate that clinically relevant concentrations of NTG not only altered ECM matrix by changing the expression of multiple genes that govern cellular integrity, affecting cellular MMP-9/TIMP-1 balance in THP-1 human macrophages possibly via NF-kappaB activation, but also led to systemic changes in MMP-9/TIMP-1 expression and gelatinase activity in rats.	Nitroglycerin	64-67	matrix metallopeptidase 9	Homo sapiens	311-316
21156214-12	2011	Our studies indicate that clinically relevant concentrations of NTG not only altered ECM matrix by changing the expression of multiple genes that govern cellular integrity, affecting cellular MMP-9/TIMP-1 balance in THP-1 human macrophages possibly via NF-kappaB activation, but also led to systemic changes in MMP-9/TIMP-1 expression and gelatinase activity in rats.	Nitroglycerin	64-67	TIMP metallopeptidase inhibitor 1	Homo sapiens	317-323
21156756-1	2011	Mitochondrial aldehyde dehydrogenase (ALDH2) contributes to vascular bioactivation of the antianginal drugs nitroglycerin (GTN) and pentaerythrityl tetranitrate (PETN), resulting in cGMP-mediated vasodilation.	Nitroglycerin	108-121	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	38-43
21156756-1	2011	Mitochondrial aldehyde dehydrogenase (ALDH2) contributes to vascular bioactivation of the antianginal drugs nitroglycerin (GTN) and pentaerythrityl tetranitrate (PETN), resulting in cGMP-mediated vasodilation.	Nitroglycerin	123-126	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	38-43
21156756-2	2011	Although continuous treatment with GTN results in the loss of efficacy that is presumably caused by inactivation of ALDH2, PETN does not induce vascular tolerance.	Nitroglycerin	35-38	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	116-121
21156756-4	2011	Pharmacological inhibition or gene deletion of ALDH2 attenuated vasodilation to both GTN and PETN to virtually the same degree as long-term treatment with GTN, whereas treatment with PETN did not cause tolerance.	Nitroglycerin	85-88	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	47-52
21059625-0	2011	Comments on "Calcitonin gene-related peptide (CGRP) levels during glyceryl trinitrate (GTN)-induced headache in healthy volunteers".	Nitroglycerin	87-90	calcitonin related polypeptide alpha	Homo sapiens	46-50
21185507-2	2011	BACKGROUND: Animal studies have demonstrated that administration of 3-hydroxy-3 methylglutaryl coenzyme A reductase inhibitors can protect against GTN-induced endothelial dysfunction and tolerance, likely through an antioxidant mechanism.	Nitroglycerin	147-150	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	68-115
20959429-2	2010	We tested the hypothesis that NO releases CGRP to cause the delayed migraine attack after GTN.	Nitroglycerin	90-93	calcitonin related polypeptide alpha	Homo sapiens	42-46
20974582-1	2011	BACKGROUND: Nitrovasodilators, such as glyceroltrinitrate (GTN), which produce nitric oxide (NO) in the organism, are known to cause delayed headaches in migraineurs, accompanied by increased plasma levels of calcitonin gene-related peptide (CGRP) in the cranial venous outflow.	Nitroglycerin	39-57	calcitonin-related polypeptide alpha	Rattus norvegicus	209-240
20974582-1	2011	BACKGROUND: Nitrovasodilators, such as glyceroltrinitrate (GTN), which produce nitric oxide (NO) in the organism, are known to cause delayed headaches in migraineurs, accompanied by increased plasma levels of calcitonin gene-related peptide (CGRP) in the cranial venous outflow.	Nitroglycerin	39-57	calcitonin-related polypeptide alpha	Rattus norvegicus	242-246
20974582-1	2011	BACKGROUND: Nitrovasodilators, such as glyceroltrinitrate (GTN), which produce nitric oxide (NO) in the organism, are known to cause delayed headaches in migraineurs, accompanied by increased plasma levels of calcitonin gene-related peptide (CGRP) in the cranial venous outflow.	Nitroglycerin	59-62	calcitonin-related polypeptide alpha	Rattus norvegicus	209-240
20974582-1	2011	BACKGROUND: Nitrovasodilators, such as glyceroltrinitrate (GTN), which produce nitric oxide (NO) in the organism, are known to cause delayed headaches in migraineurs, accompanied by increased plasma levels of calcitonin gene-related peptide (CGRP) in the cranial venous outflow.	Nitroglycerin	59-62	calcitonin-related polypeptide alpha	Rattus norvegicus	242-246
20974582-7	2011	RESULTS: The proportions of CGRP- and nNOS- as well as double-immunopositive neurons were increased after GTN infusion compared to saline treatment in all parts of the trigeminal ganglion (CGRP) or restricted to the ophthalmic region (nNOS).	Nitroglycerin	106-109	calcitonin-related polypeptide alpha	Rattus norvegicus	28-32
20974582-7	2011	RESULTS: The proportions of CGRP- and nNOS- as well as double-immunopositive neurons were increased after GTN infusion compared to saline treatment in all parts of the trigeminal ganglion (CGRP) or restricted to the ophthalmic region (nNOS).	Nitroglycerin	106-109	nitric oxide synthase 1	Rattus norvegicus	38-42
20974582-7	2011	RESULTS: The proportions of CGRP- and nNOS- as well as double-immunopositive neurons were increased after GTN infusion compared to saline treatment in all parts of the trigeminal ganglion (CGRP) or restricted to the ophthalmic region (nNOS).	Nitroglycerin	106-109	calcitonin-related polypeptide alpha	Rattus norvegicus	189-193
20974582-7	2011	RESULTS: The proportions of CGRP- and nNOS- as well as double-immunopositive neurons were increased after GTN infusion compared to saline treatment in all parts of the trigeminal ganglion (CGRP) or restricted to the ophthalmic region (nNOS).	Nitroglycerin	106-109	nitric oxide synthase 1	Rattus norvegicus	235-239
22256559-12	2011	Following the cold-pressor test the mean NPY concentration was significantly decreased in the NTG group, but remained virtually unchanged in the HTG group and controls.	Nitroglycerin	94-97	neuropeptide Y	Homo sapiens	41-44
22256559-13	2011	In the NTG patients, significant increase in the mean ET-1 concentration and decrease in the mean NPY concentration seen after the cold-pressor test were accompanied by a significant decrease in the mean MS (mean retinal sensitivity) value in the second eye examined after the cold-pressor test, but no correlation was found between changes in the MS values and changes in the ET-1 and NPY concentrations.	Nitroglycerin	7-10	endothelin 1	Homo sapiens	54-58
22256559-13	2011	In the NTG patients, significant increase in the mean ET-1 concentration and decrease in the mean NPY concentration seen after the cold-pressor test were accompanied by a significant decrease in the mean MS (mean retinal sensitivity) value in the second eye examined after the cold-pressor test, but no correlation was found between changes in the MS values and changes in the ET-1 and NPY concentrations.	Nitroglycerin	7-10	neuropeptide Y	Homo sapiens	98-101
22256559-13	2011	In the NTG patients, significant increase in the mean ET-1 concentration and decrease in the mean NPY concentration seen after the cold-pressor test were accompanied by a significant decrease in the mean MS (mean retinal sensitivity) value in the second eye examined after the cold-pressor test, but no correlation was found between changes in the MS values and changes in the ET-1 and NPY concentrations.	Nitroglycerin	7-10	endothelin 1	Homo sapiens	377-389
22256559-15	2011	CONCLUSIONS: Our findings suggest abnormal neuro-endothelial mechanisms of vascular tone control in NTG patients, related to the effects of ET-1 and NPY, secondary to endothelial dysfunction and to dysregulation of the autonomic nervous system.	Nitroglycerin	100-103	endothelin 1	Homo sapiens	140-152
20854827-7	2010	Serca2a protein expression was significantly increased in NTG and TG hearts injected with Ad.Ser for up to 6 weeks.	Nitroglycerin	58-61	ATPase, Ca++ transporting, cardiac muscle, slow twitch 2	Mus musculus	0-7
21076717-1	2010	INTRODUCTION: Continuous treatment with nitroglycerin (GTN) causes tolerance and endothelial dysfunction, both of which may involve endothelial nitric oxide synthase (eNOS) dysfunction.	Nitroglycerin	40-53	nitric oxide synthase 3	Homo sapiens	132-165
21076717-1	2010	INTRODUCTION: Continuous treatment with nitroglycerin (GTN) causes tolerance and endothelial dysfunction, both of which may involve endothelial nitric oxide synthase (eNOS) dysfunction.	Nitroglycerin	55-58	nitric oxide synthase 3	Homo sapiens	132-165
20543077-8	2010	These results suggest that ALDH2 plays an important role in the bioactivation of GTN and nitrite in the pulmonary and systemic vascular beds and that the reduction of nitrite to vasoactive NO does not play an important role in mediating vasodilator responses to GTN in the intact chest rat.	Nitroglycerin	81-84	aldehyde dehydrogenase 2 family member	Rattus norvegicus	27-32
20613714-2	2010	To investigate the relationship between circulating FGF-23 levels and the response of forearm blood flow to ischemia (flow-mediated vasodilatation, FMD) and nitroglycerin, we tested 183 patients with stage 3-4 chronic kidney disease (CKD).	Nitroglycerin	157-170	fibroblast growth factor 23	Homo sapiens	52-58
20487350-7	2010	CONCLUSIONS: The rate of VVS induced by nitroglycerine-potentiated HUT is similar in elderly and younger patients.	Nitroglycerin	40-54	VVS	Homo sapiens	25-28
20543077-0	2010	Mitochondrial aldehyde dehydrogenase mediates vasodilator responses of glyceryl trinitrate and sodium nitrite in the pulmonary vascular bed of the rat.	Nitroglycerin	71-90	aldehyde dehydrogenase 2 family member	Rattus norvegicus	0-36
20543077-1	2010	It has been reported that mitochondrial aldehyde dehydrogenase (ALDH2) catalyzes the formation of glyceryl dinitrate and inorganic nitrite from glyceryl trinitrate (GTN), leading to an increase in cGMP and vasodilation in the coronary and systemic vascular beds.	Nitroglycerin	144-163	aldehyde dehydrogenase 2 family member	Rattus norvegicus	26-62
20543077-1	2010	It has been reported that mitochondrial aldehyde dehydrogenase (ALDH2) catalyzes the formation of glyceryl dinitrate and inorganic nitrite from glyceryl trinitrate (GTN), leading to an increase in cGMP and vasodilation in the coronary and systemic vascular beds.	Nitroglycerin	144-163	aldehyde dehydrogenase 2 family member	Rattus norvegicus	64-69
20122895-8	2010	Finally, a cross-talk between mitochondria and NADPH oxidases (Nox2) was shown in nitroglycerin-induced tolerance involving the mitochondrial permeability transition pore and ATP-sensitive potassium channels.	Nitroglycerin	82-95	cytochrome b-245 beta chain	Homo sapiens	63-67
20543077-1	2010	It has been reported that mitochondrial aldehyde dehydrogenase (ALDH2) catalyzes the formation of glyceryl dinitrate and inorganic nitrite from glyceryl trinitrate (GTN), leading to an increase in cGMP and vasodilation in the coronary and systemic vascular beds.	Nitroglycerin	165-168	aldehyde dehydrogenase 2 family member	Rattus norvegicus	26-62
20543077-1	2010	It has been reported that mitochondrial aldehyde dehydrogenase (ALDH2) catalyzes the formation of glyceryl dinitrate and inorganic nitrite from glyceryl trinitrate (GTN), leading to an increase in cGMP and vasodilation in the coronary and systemic vascular beds.	Nitroglycerin	165-168	aldehyde dehydrogenase 2 family member	Rattus norvegicus	64-69
20931854-7	2010	Compared to NG group, the levels of SGK1 and FN mRNA and protein were increased in HG group after stimulating for 24 hours (P &lt; 0.01).	Nitroglycerin	12-14	serum/glucocorticoid regulated kinase 1	Homo sapiens	36-40
20931854-7	2010	Compared to NG group, the levels of SGK1 and FN mRNA and protein were increased in HG group after stimulating for 24 hours (P &lt; 0.01).	Nitroglycerin	12-14	fibronectin 1	Homo sapiens	45-47
20574135-7	2010	When NTG alone was continuously administered, vascular superoxide was produced, there was a decrease in the cardiac CYP1A1/1A2 level, and depletion of P-VASP.	Nitroglycerin	5-8	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	116-122
19925620-0	2010	Kynurenate derivative attenuates the nitroglycerin-induced CamKIIalpha and CGRP expression changes.	Nitroglycerin	37-50	calcitonin-related polypeptide alpha	Rattus norvegicus	75-79
20215428-10	2010	Akt phosphorylation was elevated approximately 15-fold in IGF-1R nondiabetic mice compared with Ntg, and this was maintained in a setting of diabetes.	Nitroglycerin	96-99	thymoma viral proto-oncogene 1	Mus musculus	0-3
19925620-1	2010	OBJECTIVE: To examine the efficacy of L-kynurenine and a novel kynurenic acid derivative on the nitroglycerin-induced calmodulin-dependent protein kinase II alpha (CamKIIalpha) and calcitonin gene-related peptide (CGRP) expression changes in the rat caudal trigeminal nucleus.	Nitroglycerin	96-109	calcitonin-related polypeptide alpha	Rattus norvegicus	181-212
19925620-1	2010	OBJECTIVE: To examine the efficacy of L-kynurenine and a novel kynurenic acid derivative on the nitroglycerin-induced calmodulin-dependent protein kinase II alpha (CamKIIalpha) and calcitonin gene-related peptide (CGRP) expression changes in the rat caudal trigeminal nucleus.	Nitroglycerin	96-109	calcitonin-related polypeptide alpha	Rattus norvegicus	214-218
19925620-3	2010	In the rat, nitroglycerin activates second-order neurons in the caudal trigeminal nucleus, and increases expression of the CamKIIalpha and decreases that of the CGRP there.	Nitroglycerin	12-25	calcitonin-related polypeptide alpha	Rattus norvegicus	161-165
19925620-9	2010	Results.- L-kynurenine and 2-(2-N,N-dimethylaminoethylamine-1-carbonyl)-1H-quinolin-4-one hydrochloride pretreatment attenuated the nitroglycerin-induced changes in CamKIIalpha and CGRP immunoreactivity in the rat caudal trigeminal nucleus.	Nitroglycerin	132-145	calcitonin-related polypeptide alpha	Rattus norvegicus	181-185
19673898-0	2010	Calcitonin gene-related peptide (CGRP) levels during glyceryl trinitrate (GTN)-induced headache in healthy volunteers.	Nitroglycerin	53-72	calcitonin related polypeptide alpha	Homo sapiens	0-31
20079349-9	2010	Our results indicate that glyceryl trinitrate and sildenafil reduce tactile allodynia in diabetic rats suggesting that nitric oxide and cyclic GMP supply is an important step in their mechanism of action of these drugs in diabetic animals.	Nitroglycerin	26-45	5'-nucleotidase, cytosolic II	Homo sapiens	143-146
19819065-4	2010	Our results show that: (1) all three genes are stably expressed in Huh-7/NTG cells, (2) I-125 and H3-PCV uptake were markedly increased in the Huh-7/NTG cells in vitro, (3) cellular survival and tumor growth of Huh-7/NTG was inhibited by I-131 or GCV both in vitro and in vivo, and was much prominent with combination therapy, (4) in vivo imaging with I-124 and F-18 FHBG revealed increased uptake in the Huh-7/NTG tumor.	Nitroglycerin	73-76	MIR7-3 host gene	Homo sapiens	67-72
19819065-4	2010	Our results show that: (1) all three genes are stably expressed in Huh-7/NTG cells, (2) I-125 and H3-PCV uptake were markedly increased in the Huh-7/NTG cells in vitro, (3) cellular survival and tumor growth of Huh-7/NTG was inhibited by I-131 or GCV both in vitro and in vivo, and was much prominent with combination therapy, (4) in vivo imaging with I-124 and F-18 FHBG revealed increased uptake in the Huh-7/NTG tumor.	Nitroglycerin	73-76	MIR7-3 host gene	Homo sapiens	143-148
19819065-4	2010	Our results show that: (1) all three genes are stably expressed in Huh-7/NTG cells, (2) I-125 and H3-PCV uptake were markedly increased in the Huh-7/NTG cells in vitro, (3) cellular survival and tumor growth of Huh-7/NTG was inhibited by I-131 or GCV both in vitro and in vivo, and was much prominent with combination therapy, (4) in vivo imaging with I-124 and F-18 FHBG revealed increased uptake in the Huh-7/NTG tumor.	Nitroglycerin	73-76	MIR7-3 host gene	Homo sapiens	143-148
19819065-4	2010	Our results show that: (1) all three genes are stably expressed in Huh-7/NTG cells, (2) I-125 and H3-PCV uptake were markedly increased in the Huh-7/NTG cells in vitro, (3) cellular survival and tumor growth of Huh-7/NTG was inhibited by I-131 or GCV both in vitro and in vivo, and was much prominent with combination therapy, (4) in vivo imaging with I-124 and F-18 FHBG revealed increased uptake in the Huh-7/NTG tumor.	Nitroglycerin	73-76	MIR7-3 host gene	Homo sapiens	143-148
19819065-4	2010	Our results show that: (1) all three genes are stably expressed in Huh-7/NTG cells, (2) I-125 and H3-PCV uptake were markedly increased in the Huh-7/NTG cells in vitro, (3) cellular survival and tumor growth of Huh-7/NTG was inhibited by I-131 or GCV both in vitro and in vivo, and was much prominent with combination therapy, (4) in vivo imaging with I-124 and F-18 FHBG revealed increased uptake in the Huh-7/NTG tumor.	Nitroglycerin	149-152	MIR7-3 host gene	Homo sapiens	67-72
19819065-4	2010	Our results show that: (1) all three genes are stably expressed in Huh-7/NTG cells, (2) I-125 and H3-PCV uptake were markedly increased in the Huh-7/NTG cells in vitro, (3) cellular survival and tumor growth of Huh-7/NTG was inhibited by I-131 or GCV both in vitro and in vivo, and was much prominent with combination therapy, (4) in vivo imaging with I-124 and F-18 FHBG revealed increased uptake in the Huh-7/NTG tumor.	Nitroglycerin	149-152	MIR7-3 host gene	Homo sapiens	143-148
19673898-0	2010	Calcitonin gene-related peptide (CGRP) levels during glyceryl trinitrate (GTN)-induced headache in healthy volunteers.	Nitroglycerin	53-72	calcitonin related polypeptide alpha	Homo sapiens	33-37
19819065-4	2010	Our results show that: (1) all three genes are stably expressed in Huh-7/NTG cells, (2) I-125 and H3-PCV uptake were markedly increased in the Huh-7/NTG cells in vitro, (3) cellular survival and tumor growth of Huh-7/NTG was inhibited by I-131 or GCV both in vitro and in vivo, and was much prominent with combination therapy, (4) in vivo imaging with I-124 and F-18 FHBG revealed increased uptake in the Huh-7/NTG tumor.	Nitroglycerin	149-152	MIR7-3 host gene	Homo sapiens	143-148
19819065-4	2010	Our results show that: (1) all three genes are stably expressed in Huh-7/NTG cells, (2) I-125 and H3-PCV uptake were markedly increased in the Huh-7/NTG cells in vitro, (3) cellular survival and tumor growth of Huh-7/NTG was inhibited by I-131 or GCV both in vitro and in vivo, and was much prominent with combination therapy, (4) in vivo imaging with I-124 and F-18 FHBG revealed increased uptake in the Huh-7/NTG tumor.	Nitroglycerin	149-152	MIR7-3 host gene	Homo sapiens	143-148
19673898-0	2010	Calcitonin gene-related peptide (CGRP) levels during glyceryl trinitrate (GTN)-induced headache in healthy volunteers.	Nitroglycerin	74-77	calcitonin related polypeptide alpha	Homo sapiens	0-31
19819065-4	2010	Our results show that: (1) all three genes are stably expressed in Huh-7/NTG cells, (2) I-125 and H3-PCV uptake were markedly increased in the Huh-7/NTG cells in vitro, (3) cellular survival and tumor growth of Huh-7/NTG was inhibited by I-131 or GCV both in vitro and in vivo, and was much prominent with combination therapy, (4) in vivo imaging with I-124 and F-18 FHBG revealed increased uptake in the Huh-7/NTG tumor.	Nitroglycerin	149-152	MIR7-3 host gene	Homo sapiens	67-72
19819065-4	2010	Our results show that: (1) all three genes are stably expressed in Huh-7/NTG cells, (2) I-125 and H3-PCV uptake were markedly increased in the Huh-7/NTG cells in vitro, (3) cellular survival and tumor growth of Huh-7/NTG was inhibited by I-131 or GCV both in vitro and in vivo, and was much prominent with combination therapy, (4) in vivo imaging with I-124 and F-18 FHBG revealed increased uptake in the Huh-7/NTG tumor.	Nitroglycerin	149-152	MIR7-3 host gene	Homo sapiens	143-148
19819065-4	2010	Our results show that: (1) all three genes are stably expressed in Huh-7/NTG cells, (2) I-125 and H3-PCV uptake were markedly increased in the Huh-7/NTG cells in vitro, (3) cellular survival and tumor growth of Huh-7/NTG was inhibited by I-131 or GCV both in vitro and in vivo, and was much prominent with combination therapy, (4) in vivo imaging with I-124 and F-18 FHBG revealed increased uptake in the Huh-7/NTG tumor.	Nitroglycerin	149-152	MIR7-3 host gene	Homo sapiens	143-148
19819065-4	2010	Our results show that: (1) all three genes are stably expressed in Huh-7/NTG cells, (2) I-125 and H3-PCV uptake were markedly increased in the Huh-7/NTG cells in vitro, (3) cellular survival and tumor growth of Huh-7/NTG was inhibited by I-131 or GCV both in vitro and in vivo, and was much prominent with combination therapy, (4) in vivo imaging with I-124 and F-18 FHBG revealed increased uptake in the Huh-7/NTG tumor.	Nitroglycerin	149-152	MIR7-3 host gene	Homo sapiens	143-148
19673898-0	2010	Calcitonin gene-related peptide (CGRP) levels during glyceryl trinitrate (GTN)-induced headache in healthy volunteers.	Nitroglycerin	74-77	calcitonin related polypeptide alpha	Homo sapiens	33-37
19673898-2	2010	We hypothesized that GTN-induced headache may activate the trigeminovascular system and be associated with increased levels of sensory neuropeptides, including calcitonin gene-related peptide (CGRP).	Nitroglycerin	21-24	calcitonin related polypeptide alpha	Homo sapiens	160-191
19673898-2	2010	We hypothesized that GTN-induced headache may activate the trigeminovascular system and be associated with increased levels of sensory neuropeptides, including calcitonin gene-related peptide (CGRP).	Nitroglycerin	21-24	calcitonin related polypeptide alpha	Homo sapiens	193-197
19673898-7	2010	After a 20-min intravenous infusion of GTN 0.12 microg kg(-1) min(-1), median peak headache intensity was 4 (range 2-6) (P &lt; 0.05), while jugular CGRP-LI levels were unchanged (19.0 +- 2.8 pmol/l; P &gt; 0.05).	Nitroglycerin	39-42	calcitonin related polypeptide alpha	Homo sapiens	149-153
19489890-4	2010	NTG administration also induced Fos expression, an anatomical marker of neuronal activity in neurons of the trigeminal nucleus caudalis and cervical spinal cord dorsal horn, suggesting that enhanced nociceptive processing within the spinal cord contributes to the increased nociceptive behaviour.	Nitroglycerin	0-3	FBJ osteosarcoma oncogene	Mus musculus	32-35
19606374-9	2010	In obesity, adiponectin related to GTN (beta = 0.46, p &lt; 0.001), RCF (beta = 0.4, p = 0.001) and LDL cholesterol (beta = 0.33, p = 0.004).	Nitroglycerin	35-38	adiponectin, C1Q and collagen domain containing	Homo sapiens	12-23
19515121-8	2010	Anandamide also proved effective in preventing nitroglycerin-induced activation (c-Fos) of neurons in the nucleus trigeminalis caudalis.	Nitroglycerin	47-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
19906643-1	2010	The East Asian variant of mitochondrial aldehyde dehydrogenase (ALDH2) exhibits significantly reduced dehydrogenase, esterase, and nitroglycerin (GTN) denitrating activities.	Nitroglycerin	131-144	aldehyde dehydrogenase 2 family member	Homo sapiens	64-69
19906643-0	2010	Characterization of the East Asian variant of aldehyde dehydrogenase-2: bioactivation of nitroglycerin and effects of Alda-1.	Nitroglycerin	89-102	aldehyde dehydrogenase 2 family member	Homo sapiens	46-70
19906643-1	2010	The East Asian variant of mitochondrial aldehyde dehydrogenase (ALDH2) exhibits significantly reduced dehydrogenase, esterase, and nitroglycerin (GTN) denitrating activities.	Nitroglycerin	146-149	aldehyde dehydrogenase 2 family member	Homo sapiens	64-69
19906643-3	2010	In the present study we compared the wild type enzyme (ALDH2*1) with the Asian variant (ALDH2*2) regarding GTN bioactivation and the effects of Alda-1.	Nitroglycerin	107-110	aldehyde dehydrogenase 2 family member	Homo sapiens	55-60
19906643-3	2010	In the present study we compared the wild type enzyme (ALDH2*1) with the Asian variant (ALDH2*2) regarding GTN bioactivation and the effects of Alda-1.	Nitroglycerin	107-110	aldehyde dehydrogenase 2 family member	Homo sapiens	88-93
19906643-7	2010	Although ALDH2*2 exhibited 7-fold lower GTN denitrating activity and GTN affinity than ALDH2*1, the rate of nitric oxide formation was only reduced 2-fold, and soluble guanylate cyclase (sGC) activation was more pronounced than with wild type ALDH2 at saturating GTN.	Nitroglycerin	40-43	aldehyde dehydrogenase 2 family member	Homo sapiens	9-14
19906643-7	2010	Although ALDH2*2 exhibited 7-fold lower GTN denitrating activity and GTN affinity than ALDH2*1, the rate of nitric oxide formation was only reduced 2-fold, and soluble guanylate cyclase (sGC) activation was more pronounced than with wild type ALDH2 at saturating GTN.	Nitroglycerin	69-72	aldehyde dehydrogenase 2 family member	Homo sapiens	9-14
19906643-7	2010	Although ALDH2*2 exhibited 7-fold lower GTN denitrating activity and GTN affinity than ALDH2*1, the rate of nitric oxide formation was only reduced 2-fold, and soluble guanylate cyclase (sGC) activation was more pronounced than with wild type ALDH2 at saturating GTN.	Nitroglycerin	69-72	aldehyde dehydrogenase 2 family member	Homo sapiens	9-14
19906643-8	2010	Alda-1 caused slight inhibition of GTN denitration and did not increase GTN-induced sGC activation in the presence of either variant.	Nitroglycerin	35-38	aldolase, fructose-bisphosphate A	Homo sapiens	0-4
19906643-10	2010	In addition, our data revealed an unexpected discrepancy between GTN reductase activity and sGC activation, suggesting that GTN denitration and bioactivation may reflect independent pathways of ALDH2-catalyzed GTN biotransformation.	Nitroglycerin	65-68	aldehyde dehydrogenase 2 family member	Homo sapiens	194-199
19906643-10	2010	In addition, our data revealed an unexpected discrepancy between GTN reductase activity and sGC activation, suggesting that GTN denitration and bioactivation may reflect independent pathways of ALDH2-catalyzed GTN biotransformation.	Nitroglycerin	124-127	aldehyde dehydrogenase 2 family member	Homo sapiens	194-199
19160042-1	2010	The objective of this research paper is to evaluate the effect of prophylactic nitroglycerin in the prevention of post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis (PEP) by performing a meta-analysis of randomized controlled trials (RCTs).	Nitroglycerin	79-92	progestagen associated endometrial protein	Homo sapiens	187-190
21081219-3	2010	The formation of reactive oxygen and nitrogen species in the mitochondria and the subsequent inhibition of the nitrate-bioactivating enzyme mitochondrial aldehyde dehydrogenase (ALDH-2) appear to play a central role, at least for GTN, that is, bioactivated by ALDH-2.	Nitroglycerin	230-233	aldehyde dehydrogenase 2 family member	Homo sapiens	178-184
19160042-5	2010	Meta-analysis of these trials indicated a significant association between the use of nitroglycerin and the reduction of PEP (RR 0.60; 95%CI: 0.39-0.92; P = 0.02).	Nitroglycerin	85-98	progestagen associated endometrial protein	Homo sapiens	120-123
19160042-6	2010	However, subsequent sensitive analysis failed to confirm that nitroglycerin was statistically superior to a placebo in reducing PEP (RR 0.68; 95%CI: 0.41-1.11; P = 0.12).	Nitroglycerin	62-75	progestagen associated endometrial protein	Homo sapiens	128-131
19160042-8	2010	Further clinical trials are required to confirm the effect of nitroglycerin in the prevention of PEP.	Nitroglycerin	62-75	progestagen associated endometrial protein	Homo sapiens	97-100
19836459-2	2010	The possibility has been raised that NTG may increase the activity of matrix metalloproteinases (MMP), which could lead to disruption and dislodging of atherosclerotic plaques.	Nitroglycerin	37-40	matrix metallopeptidase 9	Homo sapiens	97-100
20072908-4	2010	During bioconversion of nitroglycerin, and also in the presence of reactive oxygen and nitrogen species, the active site thiols of ALDH-2 are oxidized and the enzyme looses its activity.	Nitroglycerin	24-37	aldehyde dehydrogenase 2 family member	Homo sapiens	131-137
19836459-3	2010	This study examined the broad effects of acute NTG exposure on the expression and activity of genes encoding MMP-9, as well as an array of ECM and adhesion molecules in THP-1 human macrophages.	Nitroglycerin	47-50	matrix metallopeptidase 9	Homo sapiens	109-114
19836459-7	2010	NTG exposure, caused a significant increase in total MMP-9 protein expression (1.96-fold) and active MMP-9 (3.7-fold) concentrations.	Nitroglycerin	0-3	matrix metallopeptidase 9	Homo sapiens	53-58
19836459-7	2010	NTG exposure, caused a significant increase in total MMP-9 protein expression (1.96-fold) and active MMP-9 (3.7-fold) concentrations.	Nitroglycerin	0-3	matrix metallopeptidase 9	Homo sapiens	101-106
19836459-8	2010	Recombinant MMP-9 was significantly activated by NTG and its dinitrate metabolites, indicating post-translation modification of this protein by organic nitrates.	Nitroglycerin	49-52	matrix metallopeptidase 9	Homo sapiens	12-17
19836459-9	2010	These results indicate that NTG exposure could broadly affect the gene expression and activity of proteases that govern the ECM cascade, thereby potentially altering atherosclerotic plaque stability.	Nitroglycerin	28-31	multimerin 1	Homo sapiens	124-127
19864020-0	2009	Glyceroltrinitrate facilitates stimulated CGRP release but not gene expression of CGRP or its receptor components in rat trigeminal ganglia.	Nitroglycerin	0-18	calcitonin-related polypeptide alpha	Rattus norvegicus	42-46
20131116-6	2010	RESULTS: After injection of 50 microg and 100 microg nitroglycerin, BP significantly decreased both in HTX (systolic (s) BP p = 0.0001; diastolic (d) BP p = 0.0001) and in controls (sBP p = 0.006; dBP p = 0.05).	Nitroglycerin	53-66	selenium binding protein 1	Homo sapiens	182-185
20131116-8	2010	Following analysis of the data in relation to its individual baseline, a significantly higher reduction of the BP induced by 100 microg nitroglycerin was observed in the HTX group compared to the HT group (p = 0.02 for sBP and p = 0.03 for dBP).	Nitroglycerin	136-149	selenium binding protein 1	Homo sapiens	219-222
20131116-10	2010	The reduction in sBP was correlated to cyclosporine A levels (p = 0.04 after 50microg nitroglycerin; p = 0.05 after 100 microg nitroglycerin).	Nitroglycerin	86-99	selenium binding protein 1	Homo sapiens	17-20
20131116-10	2010	The reduction in sBP was correlated to cyclosporine A levels (p = 0.04 after 50microg nitroglycerin; p = 0.05 after 100 microg nitroglycerin).	Nitroglycerin	127-140	selenium binding protein 1	Homo sapiens	17-20
20131116-11	2010	CONCLUSION: After application of nitroglycerin, sBP is reduced immediately in HTX with uncontrolled cyclosporine-induced hypertension.	Nitroglycerin	33-46	selenium binding protein 1	Homo sapiens	48-51
19793083-8	2009	We also demonstrated that NG enhanced tumor delivery with another macromolecular drug candidate, PZP, i.e. polyethylene glycol-conjugated zinc protoporphyrin IX, which inhibits heme oxygenase-1.	Nitroglycerin	26-28	PZP, alpha-2-macroglobulin like	Mus musculus	97-100
19793083-8	2009	We also demonstrated that NG enhanced tumor delivery with another macromolecular drug candidate, PZP, i.e. polyethylene glycol-conjugated zinc protoporphyrin IX, which inhibits heme oxygenase-1.	Nitroglycerin	26-28	heme oxygenase 1	Mus musculus	177-193
19795347-6	2009	In contrast, the glutathione reductase concentrations did not decrease during the first phase of reperfusion and were directly correlated with those of antioxidants, endothelin levels increased less than in the untreated groups and, in the case of nitroglycerin, the nitrite concentration was significantly greater than in the remaining groups.	Nitroglycerin	248-261	glutathione-disulfide reductase	Homo sapiens	17-38
19864020-6	2009	After a two hour infusion of the NO donor glyceroltrinitrate (250microg/kg/h), however, inflammatory mediators-induced CGRP release was 80% higher compared to control animals.	Nitroglycerin	42-60	calcitonin related polypeptide alpha	Homo sapiens	119-123
19733216-5	2009	A significant increase in nuclear content of p65, an indicator of NF-kappaB activation, was detected in trigeminal nucleus caudalis in rats following injection with nitroglycerin.	Nitroglycerin	165-178	synaptotagmin 1	Rattus norvegicus	45-48
19911129-3	2009	Furthermore, ALDH2 catalyzes nitroglycerin to nitrate and 1, 2-glyceryldinitrate during therapy for angina pectoris, myocardial infarction, and heart failure.	Nitroglycerin	29-42	aldehyde dehydrogenase 2 family member	Homo sapiens	13-18
19533580-0	2009	Demethylbellidifolin prevents nitroglycerin tolerance via improved aldehyde dehydrogenase 2 activity.	Nitroglycerin	30-43	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	67-91
19533580-8	2009	In cultured human umbilical vein endothelial cells (HUVECs), incubation of NTG for 16 h increased reactive oxygen species (ROS) production, attenuated cyclic guanosine monophosphate (cGMP) levels and decreased the activity of aldehyde dehydrogenase 2 (ALDH-2), the main enzyme responsible for NTG bioactivation.	Nitroglycerin	75-78	aldehyde dehydrogenase 2 family member	Homo sapiens	226-250
19533580-8	2009	In cultured human umbilical vein endothelial cells (HUVECs), incubation of NTG for 16 h increased reactive oxygen species (ROS) production, attenuated cyclic guanosine monophosphate (cGMP) levels and decreased the activity of aldehyde dehydrogenase 2 (ALDH-2), the main enzyme responsible for NTG bioactivation.	Nitroglycerin	75-78	aldehyde dehydrogenase 2 family member	Homo sapiens	252-258
19533580-10	2009	In conclusion, DMB prevents NTG tolerance via increasing ALDH-2 activity through decreasing ROS production.	Nitroglycerin	28-31	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	57-63
19744475-1	2009	Four hours after systemic administration of the nitric oxide donor nitroglycerin (10 mg/kg bodyweight, s.c.), the neurons of the rat caudal trigeminal nucleus are activated, the area covered by calcitonin gene-related peptide (CGRP)-immunoreactive fibres is decreased and the neuronal nitric oxide synthase (nNOS)- and the calmodulin-dependent protein kinase II alpha (CamKIIalpha)-immunopositive neurons in the same area are increased.	Nitroglycerin	67-80	calcitonin-related polypeptide alpha	Rattus norvegicus	194-225
19744475-1	2009	Four hours after systemic administration of the nitric oxide donor nitroglycerin (10 mg/kg bodyweight, s.c.), the neurons of the rat caudal trigeminal nucleus are activated, the area covered by calcitonin gene-related peptide (CGRP)-immunoreactive fibres is decreased and the neuronal nitric oxide synthase (nNOS)- and the calmodulin-dependent protein kinase II alpha (CamKIIalpha)-immunopositive neurons in the same area are increased.	Nitroglycerin	67-80	calcitonin-related polypeptide alpha	Rattus norvegicus	227-231
19744475-1	2009	Four hours after systemic administration of the nitric oxide donor nitroglycerin (10 mg/kg bodyweight, s.c.), the neurons of the rat caudal trigeminal nucleus are activated, the area covered by calcitonin gene-related peptide (CGRP)-immunoreactive fibres is decreased and the neuronal nitric oxide synthase (nNOS)- and the calmodulin-dependent protein kinase II alpha (CamKIIalpha)-immunopositive neurons in the same area are increased.	Nitroglycerin	67-80	nitric oxide synthase 1	Rattus norvegicus	276-306
19744475-1	2009	Four hours after systemic administration of the nitric oxide donor nitroglycerin (10 mg/kg bodyweight, s.c.), the neurons of the rat caudal trigeminal nucleus are activated, the area covered by calcitonin gene-related peptide (CGRP)-immunoreactive fibres is decreased and the neuronal nitric oxide synthase (nNOS)- and the calmodulin-dependent protein kinase II alpha (CamKIIalpha)-immunopositive neurons in the same area are increased.	Nitroglycerin	67-80	nitric oxide synthase 1	Rattus norvegicus	308-312
19744475-3	2009	Accordingly, the aim of the present experiments was to examine the effects of probenecid administration on the nitroglycerin-induced expressions of nNOS, CamKIIalpha and CGRP in the rat caudal trigeminal nucleus.	Nitroglycerin	111-124	nitric oxide synthase 1	Rattus norvegicus	148-152
19744475-3	2009	Accordingly, the aim of the present experiments was to examine the effects of probenecid administration on the nitroglycerin-induced expressions of nNOS, CamKIIalpha and CGRP in the rat caudal trigeminal nucleus.	Nitroglycerin	111-124	calcitonin-related polypeptide alpha	Rattus norvegicus	170-174
19744475-6	2009	The data suggest that the changes caused by nitroglycerin in the expressions of CGRP, nNOS and CamKIIalpha can be influenced by probenecid modulating the inflammatory functions in the nervous system.	Nitroglycerin	44-57	calcitonin-related polypeptide alpha	Rattus norvegicus	80-84
19744475-6	2009	The data suggest that the changes caused by nitroglycerin in the expressions of CGRP, nNOS and CamKIIalpha can be influenced by probenecid modulating the inflammatory functions in the nervous system.	Nitroglycerin	44-57	nitric oxide synthase 1	Rattus norvegicus	86-90
19563531-2	2009	The side effects and potency of nitroglycerine depend on mitochondrial aldehyde dehydrogenase (ALDH-2).	Nitroglycerin	32-46	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	95-101
19617408-5	2009	The expression of phospho-p38 MAPK and phospho-MAPK-activated protein kinase 2 levels were significantly suppressed in TG mice heart than in NTG mice after diabetes induction.	Nitroglycerin	141-144	mitogen-activated protein kinase 14	Mus musculus	26-29
19346443-5	2009	In contrast to PETN, acute GTN treatment resulted in a 60% decrease in WBC ALDH-2 activity (high-performance liquid chromatography), 30% reduction of nitrate bioactivation, and 25% decrease in serum antioxidant capacity (fluorescence assay), which all were prevented by pretreatment with LA.	Nitroglycerin	27-30	aldehyde dehydrogenase 2 family member	Homo sapiens	75-81
19808370-10	2009	Judged against the response to nitroglycerin, ET-1 accounted for 53.2% of coronary tone in advanced TCA but only 12.9% without advanced TCA.	Nitroglycerin	31-44	endothelin 1	Homo sapiens	46-50
19506075-0	2009	Role of the general base Glu-268 in nitroglycerin bioactivation and superoxide formation by aldehyde dehydrogenase-2.	Nitroglycerin	36-49	aldehyde dehydrogenase 2 family member	Homo sapiens	92-116
19506075-1	2009	Mitochondrial aldehyde dehydrogenase-2 (ALDH2) plays an essential role in nitroglycerin (GTN) bioactivation, resulting in formation of NO or a related activator of soluble guanylate cyclase.	Nitroglycerin	74-87	aldehyde dehydrogenase 2 family member	Homo sapiens	14-38
19506075-1	2009	Mitochondrial aldehyde dehydrogenase-2 (ALDH2) plays an essential role in nitroglycerin (GTN) bioactivation, resulting in formation of NO or a related activator of soluble guanylate cyclase.	Nitroglycerin	74-87	aldehyde dehydrogenase 2 family member	Homo sapiens	40-45
19506075-1	2009	Mitochondrial aldehyde dehydrogenase-2 (ALDH2) plays an essential role in nitroglycerin (GTN) bioactivation, resulting in formation of NO or a related activator of soluble guanylate cyclase.	Nitroglycerin	89-92	aldehyde dehydrogenase 2 family member	Homo sapiens	14-38
19506075-1	2009	Mitochondrial aldehyde dehydrogenase-2 (ALDH2) plays an essential role in nitroglycerin (GTN) bioactivation, resulting in formation of NO or a related activator of soluble guanylate cyclase.	Nitroglycerin	89-92	aldehyde dehydrogenase 2 family member	Homo sapiens	40-45
19506075-2	2009	ALDH2 denitrates GTN to 1,2-glyceryl dinitrate and nitrite but also catalyzes reduction of GTN to NO.	Nitroglycerin	17-20	aldehyde dehydrogenase 2 family member	Homo sapiens	0-5
19506075-2	2009	ALDH2 denitrates GTN to 1,2-glyceryl dinitrate and nitrite but also catalyzes reduction of GTN to NO.	Nitroglycerin	91-94	aldehyde dehydrogenase 2 family member	Homo sapiens	0-5
19506075-3	2009	To elucidate the relationship between ALDH2-catalyzed GTN bioconversion and established ALDH2 activities (dehydrogenase, esterase), we compared the function of the wild type (WT) enzyme with mutants lacking either the reactive Cys-302 (C302S) or the general base Glu-268 (E268Q).	Nitroglycerin	54-57	aldehyde dehydrogenase 2 family member	Homo sapiens	38-43
19506075-6	2009	GTN bioactivation measured as activation of purified soluble guanylate cyclase or release of NO in the presence of WT- or E268Q-ALDH2 was markedly potentiated by superoxide dismutase, suggesting that bioavailability of GTN-derived NO is limited by co-generation of superoxide.	Nitroglycerin	0-3	aldehyde dehydrogenase 2 family member	Homo sapiens	128-133
19506075-10	2009	ALDH2-catalyzed superoxide formation may essentially contribute to oxidative stress in GTN-exposed blood vessels.	Nitroglycerin	87-90	aldehyde dehydrogenase 2 family member	Homo sapiens	0-5
19576883-0	2009	Comparing the role of glutathione-S-transferase and mitochondrial aldehyde dehydrogenase in nitroglycerin biotransformation and the correlation with calcitonin gene-related peptide.	Nitroglycerin	92-105	hematopoietic prostaglandin D synthase	Rattus norvegicus	22-47
19576883-0	2009	Comparing the role of glutathione-S-transferase and mitochondrial aldehyde dehydrogenase in nitroglycerin biotransformation and the correlation with calcitonin gene-related peptide.	Nitroglycerin	92-105	aldehyde dehydrogenase 2 family member	Rattus norvegicus	52-88
19576883-1	2009	Both glutathione-S-transferase (GST) and mitochondrial aldehyde dehydrogenase (ALDH-2) have been reported to participate in the biotransformation of nitroglycerin.	Nitroglycerin	149-162	hematopoietic prostaglandin D synthase	Rattus norvegicus	5-30
19576883-1	2009	Both glutathione-S-transferase (GST) and mitochondrial aldehyde dehydrogenase (ALDH-2) have been reported to participate in the biotransformation of nitroglycerin.	Nitroglycerin	149-162	hematopoietic prostaglandin D synthase	Rattus norvegicus	32-35
19576883-1	2009	Both glutathione-S-transferase (GST) and mitochondrial aldehyde dehydrogenase (ALDH-2) have been reported to participate in the biotransformation of nitroglycerin.	Nitroglycerin	149-162	aldehyde dehydrogenase 2 family member	Rattus norvegicus	41-77
19576883-1	2009	Both glutathione-S-transferase (GST) and mitochondrial aldehyde dehydrogenase (ALDH-2) have been reported to participate in the biotransformation of nitroglycerin.	Nitroglycerin	149-162	aldehyde dehydrogenase 2 family member	Rattus norvegicus	79-85
19576883-9	2009	The change of plasma CGRP level positively correlated with the change of nitroglycerin-induced hypotensive effects.	Nitroglycerin	73-86	calcitonin-related polypeptide alpha	Rattus norvegicus	21-25
19576883-12	2009	The change of CGRP release from the rings positively correlated with the nitroglycerin-induced vasodilator responses.	Nitroglycerin	73-86	calcitonin-related polypeptide alpha	Rattus norvegicus	14-18
19576883-13	2009	The present results suggest that both GST and ALDH-2 are involved in nitroglycerin action while ALDH-2 plays a major role, and the change of CGRP contents closely correlates with the biotransformation of nitroglycerin.	Nitroglycerin	69-82	hematopoietic prostaglandin D synthase	Rattus norvegicus	38-41
19576883-13	2009	The present results suggest that both GST and ALDH-2 are involved in nitroglycerin action while ALDH-2 plays a major role, and the change of CGRP contents closely correlates with the biotransformation of nitroglycerin.	Nitroglycerin	69-82	aldehyde dehydrogenase 2 family member	Rattus norvegicus	46-52
19576883-13	2009	The present results suggest that both GST and ALDH-2 are involved in nitroglycerin action while ALDH-2 plays a major role, and the change of CGRP contents closely correlates with the biotransformation of nitroglycerin.	Nitroglycerin	69-82	calcitonin-related polypeptide alpha	Rattus norvegicus	141-145
19576883-13	2009	The present results suggest that both GST and ALDH-2 are involved in nitroglycerin action while ALDH-2 plays a major role, and the change of CGRP contents closely correlates with the biotransformation of nitroglycerin.	Nitroglycerin	204-217	hematopoietic prostaglandin D synthase	Rattus norvegicus	38-41
19576883-13	2009	The present results suggest that both GST and ALDH-2 are involved in nitroglycerin action while ALDH-2 plays a major role, and the change of CGRP contents closely correlates with the biotransformation of nitroglycerin.	Nitroglycerin	204-217	calcitonin-related polypeptide alpha	Rattus norvegicus	141-145
19580819-0	2009	l-kynurenine combined with probenecid and the novel synthetic kynurenic acid derivative attenuate nitroglycerin-induced nNOS in the rat caudal trigeminal nucleus.	Nitroglycerin	98-111	nitric oxide synthase 1	Rattus norvegicus	120-124
19580819-2	2009	In rats, 4 h after the systemic administration of NTG (10 mg/kg bw, s.c.), the neurons of the caudal trigeminal nucleus (TNC) are activated and the expression of neuronal NO synthase (nNOS) in the same area is increased suggesting a self-amplifying process in the trigeminal system, which seems to be crucial in migraine pathogenesis.	Nitroglycerin	50-53	nitric oxide synthase 1	Rattus norvegicus	184-188
19580819-8	2009	attenuated the NTG-induced nNOS expression in the rat TNC.	Nitroglycerin	15-18	nitric oxide synthase 1	Rattus norvegicus	27-31
19580819-9	2009	Our data suggest that the stimulating effect of NTG, and thus of NO, on the expression of nNOS might be modulated by increasing the KYNA level in the brain, probably through the NMDA receptors.	Nitroglycerin	48-51	nitric oxide synthase 1	Rattus norvegicus	90-94
19346443-7	2009	Treatment with GTN, but not PETN, acutely inhibits ALDH-2 activity and nitrate bioactivation in healthy volunteers.	Nitroglycerin	15-18	aldehyde dehydrogenase 2 family member	Homo sapiens	51-57
19346443-9	2009	Assessment of WBC ALDH-2 activity could be used as an easily accessible marker for the detection of nitroglycerin-induced tachyphylaxis in humans and may be of high clinical interest because recent data suggest that ALDH-2 activity correlates with protection from ischemic heart damage in infarct models.	Nitroglycerin	100-113	aldehyde dehydrogenase 2 family member	Homo sapiens	18-24
19346443-9	2009	Assessment of WBC ALDH-2 activity could be used as an easily accessible marker for the detection of nitroglycerin-induced tachyphylaxis in humans and may be of high clinical interest because recent data suggest that ALDH-2 activity correlates with protection from ischemic heart damage in infarct models.	Nitroglycerin	100-113	aldehyde dehydrogenase 2 family member	Homo sapiens	216-222
19428324-2	2009	We reported previously that purified microsomal glutathione transferase 1 (MGST1) mediates the denitration of GTN.	Nitroglycerin	110-113	microsomal glutathione S-transferase 1	Sus scrofa	75-80
20005475-2	2009	ALDH2 mediates both the detoxification of reactive aldehydes such as acetaldehyde and 4-hydroxy-2-nonenal and the bioactivation of nitroglycerin to nitric oxide.	Nitroglycerin	131-144	aldehyde dehydrogenase 2 family member	Homo sapiens	0-5
18584896-0	2009	Delayed anti-arrhythmic effect of nitroglycerin in anesthetized rats: involvement of CGRP, PKC and mK ATP channels.	Nitroglycerin	34-47	calcitonin-related polypeptide alpha	Rattus norvegicus	85-89
18584896-8	2009	These results show that a low dose of NTG has a delayed anti-arrhythmic effect and this effect may share a common mechanism with anti-infarct effects of this drug, involving CGRP release and PKC and mK(ATP) activation.	Nitroglycerin	38-41	calcitonin-related polypeptide alpha	Rattus norvegicus	174-178
19428324-6	2009	Although incubation of these cells with GTN resulted in a 3-4-fold increase in GTN biotransformation, attributed primarily to an increase in formation of the 1,3-glyceryl dinitrate metabolite, GTN-induced cGMP accumulation in cells overexpressing MGST1 was not different than that observed in wild type cells or in cells stably transfected with empty vector.	Nitroglycerin	40-43	microsomal glutathione S-transferase 1	Sus scrofa	247-252
19428324-7	2009	To determine whether overexpression of NADPH cytochrome P450 reductase might act in concert with MGST1 to generate activators of sGC, we assessed GTN-induced cGMP accumulation in MGST1-overexpressing cells that had been transiently transfected with CPR.	Nitroglycerin	146-149	cytochrome p450 oxidoreductase	Sus scrofa	39-70
19428324-7	2009	To determine whether overexpression of NADPH cytochrome P450 reductase might act in concert with MGST1 to generate activators of sGC, we assessed GTN-induced cGMP accumulation in MGST1-overexpressing cells that had been transiently transfected with CPR.	Nitroglycerin	146-149	microsomal glutathione S-transferase 1	Sus scrofa	179-184
19428324-9	2009	We conclude that although MGST1 mediates the biotransformation of GTN in intact cells, this biotransformation does not contribute to the formation of activators of sGC.	Nitroglycerin	66-69	microsomal glutathione S-transferase 1	Sus scrofa	26-31
19121366-0	2009	Selective inhibition of cyclooxygenase-2 attenuates nitroglycerin-induced calmodulin-dependent protein kinase II alpha in rat trigeminal nucleus caudalis.	Nitroglycerin	52-65	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	24-40
19223666-3	2009	Cells overexpressing GRX exhibited reduced cellular protein S-glutathionylation (PSSG) and absence of NTG tolerance, whereas those with silenced GRX showed increased extent of NTG-induced tolerance.	Nitroglycerin	102-105	glutaredoxin-1	Sus scrofa	21-24
19223666-3	2009	Cells overexpressing GRX exhibited reduced cellular protein S-glutathionylation (PSSG) and absence of NTG tolerance, whereas those with silenced GRX showed increased extent of NTG-induced tolerance.	Nitroglycerin	176-179	glutaredoxin-1	Sus scrofa	145-148
19223666-7	2009	These results indicate that the hallmark events of NTG tolerance, such as reduced bioactivation and redox signaling, are associated with GRX-dependent protein deglutathionylation.	Nitroglycerin	51-54	glutaredoxin-1	Sus scrofa	137-140
19002537-0	2009	Nitroglycerin protects small intestine from ischemia-reperfusion injury via NO-cGMP pathway and upregulation of alpha-CGRP.	Nitroglycerin	0-13	calcitonin-related polypeptide alpha	Rattus norvegicus	118-122
19002537-5	2009	The effects of nitric oxide (NO), cGMP, and alpha-calcitonin gene-related peptide (CGRP) synthesis on the effects of NTG were analyzed.	Nitroglycerin	117-120	calcitonin-related polypeptide alpha	Rattus norvegicus	83-87
19002537-10	2009	Reverse-transcription polymerase chain reaction analysis showed that NTG upregulates the expression of alpha-CGRP messenger RNA (mRNA), but not beta-CGRP mRNA in lumbar dorsal root ganglia.	Nitroglycerin	69-72	calcitonin-related polypeptide alpha	Rattus norvegicus	109-113
19223666-0	2009	Role of glutaredoxin-mediated protein S-glutathionylation in cellular nitroglycerin tolerance.	Nitroglycerin	70-83	glutaredoxin-1	Sus scrofa	8-20
19254277-1	2009	BACKGROUND AND PURPOSE: Vascular tolerance to nitroglycerin (GTN) may be caused by impaired GTN bioactivation due to inactivation of mitochondrial aldehyde dehydrogenase (ALDH2).	Nitroglycerin	46-59	aldehyde dehydrogenase, mitochondrial	Cavia porcellus	171-176
19254277-1	2009	BACKGROUND AND PURPOSE: Vascular tolerance to nitroglycerin (GTN) may be caused by impaired GTN bioactivation due to inactivation of mitochondrial aldehyde dehydrogenase (ALDH2).	Nitroglycerin	61-64	aldehyde dehydrogenase, mitochondrial	Cavia porcellus	171-176
19305337-8	2009	However, after nitroglycerin challenge, the time to the onset of the reflected wave (dependent on pulse wave velocity) was 9.5% longer (P=.014), and the time to the first systolic peak (dependent on the rapid phase of ventricular ejection) was 13.9% longer (P=.025) in women with severe hot flushes as compared with asymptomatic women.	Nitroglycerin	15-28	alcohol dehydrogenase iron containing 1	Homo sapiens	287-290
19305337-9	2009	CONCLUSION: Women with severe vasomotor hot flushes show greater vascular responsiveness to nitroglycerin than women without hot flushes.	Nitroglycerin	92-105	alcohol dehydrogenase iron containing 1	Homo sapiens	40-43
18834868-0	2009	Mitochondrial aldehyde dehydrogenase (ALDH-2)--maker of and marker for nitrate tolerance in response to nitroglycerin treatment.	Nitroglycerin	104-117	aldehyde dehydrogenase 2 family member	Homo sapiens	38-44
18834868-4	2009	Recent experimental work has defined new tolerance mechanisms, including inhibition of the enzyme that bioactivates GTN (e.g. mitochondrial aldehyde dehydrogenase [ALDH-2]) and mitochondria as potential sources of reactive oxygen species (ROS).	Nitroglycerin	116-119	aldehyde dehydrogenase 2 family member	Homo sapiens	164-170
18834868-5	2009	GTN-induced ROS inhibit the bioactivation of GTN by ALDH-2.	Nitroglycerin	0-3	aldehyde dehydrogenase 2 family member	Homo sapiens	52-58
18834868-5	2009	GTN-induced ROS inhibit the bioactivation of GTN by ALDH-2.	Nitroglycerin	45-48	aldehyde dehydrogenase 2 family member	Homo sapiens	52-58
18834868-6	2009	Both mechanisms impair GTN bioactivation, and now converge at the level of ALDH-2 to support a new theory for GTN tolerance and GTN-induced endothelial dysfunction.	Nitroglycerin	110-113	aldehyde dehydrogenase 2 family member	Homo sapiens	75-81
18834868-6	2009	Both mechanisms impair GTN bioactivation, and now converge at the level of ALDH-2 to support a new theory for GTN tolerance and GTN-induced endothelial dysfunction.	Nitroglycerin	110-113	aldehyde dehydrogenase 2 family member	Homo sapiens	75-81
18834868-9	2009	Finally, we will address the question whether ALDH-2 inactivation by nitroglycerin could be a useful marker for clinical nitrate tolerance and discuss the redox-regulation of this enzyme by oxidative stress and dihydrolipoic acid.	Nitroglycerin	69-82	aldehyde dehydrogenase 2 family member	Homo sapiens	46-52
19121366-5	2009	In our experiments, we demonstrated that pretreatment with NS398, the selective COX-2 inhibitor attenuated the NTG-induced CamKIIalpha expression in the TNC at doses of 3 and 5mg/kg.	Nitroglycerin	111-114	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	80-85
19121366-7	2009	These findings suggest that COX-2, but not COX-1 derived metabolites are important factors in the NTG-induced CamKIIalpha expression.	Nitroglycerin	98-101	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	28-33
18951990-1	2009	Reduction of nitrite to nitric oxide (NO) by components of the mitochondrial respiratory chain may link nitroglycerin biotransformation by mitochondrial aldehyde dehydrogenase (ALDH2) to activation of soluble guanylate cyclase (sGC).	Nitroglycerin	104-117	aldehyde dehydrogenase 2 family member	Homo sapiens	177-182
18951990-5	2009	Mitochondrial biotransformation of nitroglycerin was sensitive to ALDH2 inhibitors and coupled to sGC activation but not affected by respiratory substrates or inhibitors.	Nitroglycerin	35-48	aldehyde dehydrogenase 2 family member	Homo sapiens	66-71
18786921-1	2008	Mitochondrial aldehyde dehydrogenase (ALDH2) may be involved in the biotransformation of glyceryl trinitrate (GTN), and the inactivation of ALDH2 by GTN may contribute to the phenomenon of nitrate tolerance.	Nitroglycerin	89-108	aldehyde dehydrogenase 2 family member	Homo sapiens	38-43
19128906-2	2009	The double stage extraction method developed in the previous study for recovery of NG and 2,4 DNT in gunpowder residues sampled by double-sided adhesive coated stubs, was found to be applicable also for TNT, RDX and PETN.	Nitroglycerin	83-85	chromosome 16 open reading frame 82	Homo sapiens	203-206
19121572-7	2009	Besides, for the nitroglycerin-induced headache rats, the c-fos gene expression in the brain stem and hypothalamus was remarkably inhibited and the level of plasma CGRP was reduced significantly after CXVO administration at both doses 90.0 and 135.0 microg/kg.	Nitroglycerin	17-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
19121572-7	2009	Besides, for the nitroglycerin-induced headache rats, the c-fos gene expression in the brain stem and hypothalamus was remarkably inhibited and the level of plasma CGRP was reduced significantly after CXVO administration at both doses 90.0 and 135.0 microg/kg.	Nitroglycerin	17-30	calcitonin-related polypeptide alpha	Rattus norvegicus	164-168
19307691-7	2009	The present review focus first on the role of oxidative stress and second on the role of ALDH-2 in organic nitrate bioactivation leading to the development of tolerance and cross-tolerance (endothelial dysfunction) in response to nitroglycerin treatment.	Nitroglycerin	230-243	aldehyde dehydrogenase 2 family member	Homo sapiens	89-95
18786921-1	2008	Mitochondrial aldehyde dehydrogenase (ALDH2) may be involved in the biotransformation of glyceryl trinitrate (GTN), and the inactivation of ALDH2 by GTN may contribute to the phenomenon of nitrate tolerance.	Nitroglycerin	89-108	aldehyde dehydrogenase 2 family member	Homo sapiens	140-145
18786921-1	2008	Mitochondrial aldehyde dehydrogenase (ALDH2) may be involved in the biotransformation of glyceryl trinitrate (GTN), and the inactivation of ALDH2 by GTN may contribute to the phenomenon of nitrate tolerance.	Nitroglycerin	110-113	aldehyde dehydrogenase 2 family member	Homo sapiens	38-43
18786921-1	2008	Mitochondrial aldehyde dehydrogenase (ALDH2) may be involved in the biotransformation of glyceryl trinitrate (GTN), and the inactivation of ALDH2 by GTN may contribute to the phenomenon of nitrate tolerance.	Nitroglycerin	110-113	aldehyde dehydrogenase 2 family member	Homo sapiens	140-145
18786921-1	2008	Mitochondrial aldehyde dehydrogenase (ALDH2) may be involved in the biotransformation of glyceryl trinitrate (GTN), and the inactivation of ALDH2 by GTN may contribute to the phenomenon of nitrate tolerance.	Nitroglycerin	149-152	aldehyde dehydrogenase 2 family member	Homo sapiens	38-43
18786921-1	2008	Mitochondrial aldehyde dehydrogenase (ALDH2) may be involved in the biotransformation of glyceryl trinitrate (GTN), and the inactivation of ALDH2 by GTN may contribute to the phenomenon of nitrate tolerance.	Nitroglycerin	149-152	aldehyde dehydrogenase 2 family member	Homo sapiens	140-145
18786921-2	2008	We studied the GTN-induced inactivation of ALDH2 by UV/visible absorption spectroscopy.	Nitroglycerin	15-18	aldehyde dehydrogenase 2 family member	Homo sapiens	43-48
18678507-12	2008	Vasopressin-induced contraction was also reduced by high levels of glyceryl trinitrate (220 microM; 50 microg/ml) or 10 microM Y27632.	Nitroglycerin	67-86	arginine vasopressin	Homo sapiens	0-11
18727644-3	2008	COX-2 and TNF-alpha expression and MMP-9 activity were increased after continuous intravenous infusion of glyceryl trinitrate (GTN), a NO donor.	Nitroglycerin	106-125	prostaglandin-endoperoxide synthase 2	Homo sapiens	0-5
18727644-3	2008	COX-2 and TNF-alpha expression and MMP-9 activity were increased after continuous intravenous infusion of glyceryl trinitrate (GTN), a NO donor.	Nitroglycerin	106-125	tumor necrosis factor	Homo sapiens	10-19
18727644-3	2008	COX-2 and TNF-alpha expression and MMP-9 activity were increased after continuous intravenous infusion of glyceryl trinitrate (GTN), a NO donor.	Nitroglycerin	106-125	matrix metallopeptidase 9	Homo sapiens	35-40
18727644-3	2008	COX-2 and TNF-alpha expression and MMP-9 activity were increased after continuous intravenous infusion of glyceryl trinitrate (GTN), a NO donor.	Nitroglycerin	127-130	prostaglandin-endoperoxide synthase 2	Homo sapiens	0-5
18727644-3	2008	COX-2 and TNF-alpha expression and MMP-9 activity were increased after continuous intravenous infusion of glyceryl trinitrate (GTN), a NO donor.	Nitroglycerin	127-130	tumor necrosis factor	Homo sapiens	10-19
18727644-3	2008	COX-2 and TNF-alpha expression and MMP-9 activity were increased after continuous intravenous infusion of glyceryl trinitrate (GTN), a NO donor.	Nitroglycerin	127-130	matrix metallopeptidase 9	Homo sapiens	35-40
18761334-3	2008	Delayed Fos expression in response to nitroglycerin (NTG) administration is a procedure used to identify the neuroanatomical substrates of the migraine condition.	Nitroglycerin	38-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	8-11
18761334-3	2008	Delayed Fos expression in response to nitroglycerin (NTG) administration is a procedure used to identify the neuroanatomical substrates of the migraine condition.	Nitroglycerin	53-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	8-11
18946854-3	2008	Recent research has demonstrated that highly reactive nitrates, such as nitroglycerin (or glyceryl trinitrate) and pentaerthrityl tetranitrate (PETN) are bioactivated by aldehyde dehydrogenase 2 (ALDH-2), an enzyme located in mitochondria.	Nitroglycerin	72-85	aldehyde dehydrogenase 2 family member	Homo sapiens	170-194
18946854-3	2008	Recent research has demonstrated that highly reactive nitrates, such as nitroglycerin (or glyceryl trinitrate) and pentaerthrityl tetranitrate (PETN) are bioactivated by aldehyde dehydrogenase 2 (ALDH-2), an enzyme located in mitochondria.	Nitroglycerin	72-85	aldehyde dehydrogenase 2 family member	Homo sapiens	196-202
18946854-3	2008	Recent research has demonstrated that highly reactive nitrates, such as nitroglycerin (or glyceryl trinitrate) and pentaerthrityl tetranitrate (PETN) are bioactivated by aldehyde dehydrogenase 2 (ALDH-2), an enzyme located in mitochondria.	Nitroglycerin	90-109	aldehyde dehydrogenase 2 family member	Homo sapiens	170-194
18946854-3	2008	Recent research has demonstrated that highly reactive nitrates, such as nitroglycerin (or glyceryl trinitrate) and pentaerthrityl tetranitrate (PETN) are bioactivated by aldehyde dehydrogenase 2 (ALDH-2), an enzyme located in mitochondria.	Nitroglycerin	90-109	aldehyde dehydrogenase 2 family member	Homo sapiens	196-202
18574453-3	2008	In the first part of this article, we give an overview on the molecular mechanisms of GTN biotransformation resulting in vascular cyclic GMP accumulation and vasodilation with focus on the role of mitochondrial aldehyde dehydrogenase (ALDH2) and the link between the ALDH2 reaction and activation of vascular soluble guanylate cyclase (sGC).	Nitroglycerin	86-89	aldehyde dehydrogenase 2 family member	Homo sapiens	235-240
18772068-0	2008	Evidence for involvement of calcitonin gene-related peptide in nitroglycerin response and association with mitochondrial aldehyde dehydrogenase-2 (ALDH2) Glu504Lys polymorphism.	Nitroglycerin	63-76	calcitonin related polypeptide alpha	Homo sapiens	28-59
18772068-1	2008	OBJECTIVES: This study sought to determine whether calcitonin gene-related peptide (CGRP) is involved in glyceryl trinitrate (GTN) response in humans, and its association with mitochondrial aldehyde dehydrogenase-2 (ALDH2) Glu504Lys (ALDH2*2) polymorphism.	Nitroglycerin	105-124	calcitonin related polypeptide alpha	Homo sapiens	51-82
18772068-1	2008	OBJECTIVES: This study sought to determine whether calcitonin gene-related peptide (CGRP) is involved in glyceryl trinitrate (GTN) response in humans, and its association with mitochondrial aldehyde dehydrogenase-2 (ALDH2) Glu504Lys (ALDH2*2) polymorphism.	Nitroglycerin	105-124	calcitonin related polypeptide alpha	Homo sapiens	84-88
18772068-1	2008	OBJECTIVES: This study sought to determine whether calcitonin gene-related peptide (CGRP) is involved in glyceryl trinitrate (GTN) response in humans, and its association with mitochondrial aldehyde dehydrogenase-2 (ALDH2) Glu504Lys (ALDH2*2) polymorphism.	Nitroglycerin	126-129	calcitonin related polypeptide alpha	Homo sapiens	51-82
18772068-1	2008	OBJECTIVES: This study sought to determine whether calcitonin gene-related peptide (CGRP) is involved in glyceryl trinitrate (GTN) response in humans, and its association with mitochondrial aldehyde dehydrogenase-2 (ALDH2) Glu504Lys (ALDH2*2) polymorphism.	Nitroglycerin	126-129	calcitonin related polypeptide alpha	Homo sapiens	84-88
18772068-2	2008	BACKGROUND: In animal models, CGRP contributes to the cardiovascular effects of GTN.	Nitroglycerin	80-83	calcitonin related polypeptide alpha	Homo sapiens	30-34
18772068-3	2008	The enzyme principally responsible for GTN bioactivation is ALDH2.	Nitroglycerin	39-42	aldehyde dehydrogenase 2 family member	Homo sapiens	60-65
18772068-4	2008	The common ALDH2*2 polymorphism is associated with a lack of GTN efficacy.	Nitroglycerin	61-64	aldehyde dehydrogenase 2 family member	Homo sapiens	11-16
18772068-5	2008	METHODS: In 18 ALDH2*2-genotyped Chinese volunteers, we observed the changes in plasma concentrations of CGRP after sublingual GTN administration and its correlation with GTN response, and assessed the expression of CGRP messenger ribonucleic acid (mRNA) in cultured peripheral blood mononuclear cells (PBMCs) pre-treated with 10(-5) mol/l GTN.	Nitroglycerin	127-130	calcitonin related polypeptide alpha	Homo sapiens	105-109
18772068-5	2008	METHODS: In 18 ALDH2*2-genotyped Chinese volunteers, we observed the changes in plasma concentrations of CGRP after sublingual GTN administration and its correlation with GTN response, and assessed the expression of CGRP messenger ribonucleic acid (mRNA) in cultured peripheral blood mononuclear cells (PBMCs) pre-treated with 10(-5) mol/l GTN.	Nitroglycerin	171-174	calcitonin related polypeptide alpha	Homo sapiens	105-109
18772068-5	2008	METHODS: In 18 ALDH2*2-genotyped Chinese volunteers, we observed the changes in plasma concentrations of CGRP after sublingual GTN administration and its correlation with GTN response, and assessed the expression of CGRP messenger ribonucleic acid (mRNA) in cultured peripheral blood mononuclear cells (PBMCs) pre-treated with 10(-5) mol/l GTN.	Nitroglycerin	171-174	calcitonin related polypeptide alpha	Homo sapiens	105-109
18772068-6	2008	RESULTS: In contrast to carriers of the ALDH2*2 allele, ALDH2*1/*1 homozygotes showed a significantly higher extent of absolute changes in both systolic blood pressure (DeltaSBP) and HR (DeltaHR) at several time points after GTN administration.	Nitroglycerin	225-228	aldehyde dehydrogenase 2 family member	Homo sapiens	56-61
18772068-7	2008	Plasma concentrations of CGRP were increased significantly 12 min after GTN administration, the percentage increase in plasma concentrations of CGRP correlated positively with both DeltaSBP and DeltaHR, and percentage increase in plasma concentrations of CGRP was significantly higher in ALDH2*1/*1 homozygotes.	Nitroglycerin	72-75	calcitonin related polypeptide alpha	Homo sapiens	25-29
18772068-7	2008	Plasma concentrations of CGRP were increased significantly 12 min after GTN administration, the percentage increase in plasma concentrations of CGRP correlated positively with both DeltaSBP and DeltaHR, and percentage increase in plasma concentrations of CGRP was significantly higher in ALDH2*1/*1 homozygotes.	Nitroglycerin	72-75	aldehyde dehydrogenase 2 family member	Homo sapiens	288-293
18772068-8	2008	In addition, PBMCs from ALDH2*1/*1 homozygotes showed a higher-fold increase in both CGRP I and CGRP II mRNA after GTN stimulation, and the GTN-induced increase in CGRP mRNA expression in PBMCs from ALDH2*1/*1 homozygotes was inhibited by the ALDH2 inhibitor chloral hydrate.	Nitroglycerin	115-118	aldehyde dehydrogenase 2 family member	Homo sapiens	24-29
18772068-8	2008	In addition, PBMCs from ALDH2*1/*1 homozygotes showed a higher-fold increase in both CGRP I and CGRP II mRNA after GTN stimulation, and the GTN-induced increase in CGRP mRNA expression in PBMCs from ALDH2*1/*1 homozygotes was inhibited by the ALDH2 inhibitor chloral hydrate.	Nitroglycerin	115-118	calcitonin related polypeptide alpha	Homo sapiens	85-91
18772068-8	2008	In addition, PBMCs from ALDH2*1/*1 homozygotes showed a higher-fold increase in both CGRP I and CGRP II mRNA after GTN stimulation, and the GTN-induced increase in CGRP mRNA expression in PBMCs from ALDH2*1/*1 homozygotes was inhibited by the ALDH2 inhibitor chloral hydrate.	Nitroglycerin	115-118	calcitonin related polypeptide beta	Homo sapiens	96-103
18772068-8	2008	In addition, PBMCs from ALDH2*1/*1 homozygotes showed a higher-fold increase in both CGRP I and CGRP II mRNA after GTN stimulation, and the GTN-induced increase in CGRP mRNA expression in PBMCs from ALDH2*1/*1 homozygotes was inhibited by the ALDH2 inhibitor chloral hydrate.	Nitroglycerin	115-118	calcitonin related polypeptide alpha	Homo sapiens	85-89
18772068-8	2008	In addition, PBMCs from ALDH2*1/*1 homozygotes showed a higher-fold increase in both CGRP I and CGRP II mRNA after GTN stimulation, and the GTN-induced increase in CGRP mRNA expression in PBMCs from ALDH2*1/*1 homozygotes was inhibited by the ALDH2 inhibitor chloral hydrate.	Nitroglycerin	140-143	aldehyde dehydrogenase 2 family member	Homo sapiens	24-29
18772068-8	2008	In addition, PBMCs from ALDH2*1/*1 homozygotes showed a higher-fold increase in both CGRP I and CGRP II mRNA after GTN stimulation, and the GTN-induced increase in CGRP mRNA expression in PBMCs from ALDH2*1/*1 homozygotes was inhibited by the ALDH2 inhibitor chloral hydrate.	Nitroglycerin	140-143	aldehyde dehydrogenase 2 family member	Homo sapiens	199-204
18772068-8	2008	In addition, PBMCs from ALDH2*1/*1 homozygotes showed a higher-fold increase in both CGRP I and CGRP II mRNA after GTN stimulation, and the GTN-induced increase in CGRP mRNA expression in PBMCs from ALDH2*1/*1 homozygotes was inhibited by the ALDH2 inhibitor chloral hydrate.	Nitroglycerin	140-143	aldehyde dehydrogenase 2 family member	Homo sapiens	199-204
18772068-9	2008	CONCLUSIONS: We found that CGRP is associated with the cardiovascular effect of GTN through an ALDH2-dependent pathway in humans.	Nitroglycerin	80-83	calcitonin related polypeptide alpha	Homo sapiens	27-31
18772068-9	2008	CONCLUSIONS: We found that CGRP is associated with the cardiovascular effect of GTN through an ALDH2-dependent pathway in humans.	Nitroglycerin	80-83	aldehyde dehydrogenase 2 family member	Homo sapiens	95-100
18574453-4	2008	In particular, we address the identity of the bioactive species that activates sGC and the potential involvement of nitrite as an intermediate, describe our recent findings suggesting that ALDH2 catalyses direct 3-electron reduction of GTN to NO and discuss possible reaction mechanisms.	Nitroglycerin	236-239	aldehyde dehydrogenase 2 family member	Homo sapiens	189-194
18653825-3	2008	O(2)(*-) stimulated by NTG was reduced by oxypurinol (100 microM), a xanthine oxidase inhibitor.	Nitroglycerin	23-26	xanthine dehydrogenase	Mus musculus	69-85
18653825-8	2008	In vitro aorta O(2)(*-) production was enhanced by NTG incubation in both p47(phox) null and WT mice.	Nitroglycerin	51-54	NSFL1 (p97) cofactor (p47)	Mus musculus	74-77
18653825-8	2008	In vitro aorta O(2)(*-) production was enhanced by NTG incubation in both p47(phox) null and WT mice.	Nitroglycerin	51-54	NSFL1 (p97) cofactor (p47)	Mus musculus	78-82
18574453-3	2008	In the first part of this article, we give an overview on the molecular mechanisms of GTN biotransformation resulting in vascular cyclic GMP accumulation and vasodilation with focus on the role of mitochondrial aldehyde dehydrogenase (ALDH2) and the link between the ALDH2 reaction and activation of vascular soluble guanylate cyclase (sGC).	Nitroglycerin	86-89	aldehyde dehydrogenase 2 family member	Homo sapiens	267-272
18695513-0	2008	Nitroglycerin facilitates calcitonin gene-related peptide-induced behavior.	Nitroglycerin	0-13	calcitonin-related polypeptide alpha	Rattus norvegicus	26-57
18647185-6	2008	We hypothesized that vasodilatation induced by CGRP and the NO donor glyceryltrinitrate (GTN) is mediated via K(ATP) channels.	Nitroglycerin	89-92	calcitonin related polypeptide alpha	Homo sapiens	47-51
18647185-12	2008	In anesthetized rats glibenclamide significantly attenuated CGRP induced dural and TES induced dural/pial artery dilatation (P = .001; P = .001; P = .005), but had no effect on dural/pial vasodilatation induced by GTN.	Nitroglycerin	214-217	calcitonin-related polypeptide alpha	Rattus norvegicus	60-64
18312299-4	2008	METHODS: DNA of 99 patients that underwent complete surgical resection of OSCC was analyzed for GTn-repeat polymorphism in the HMOX-1 promoter by polymerase chain reaction, capillary electrophoresis and DNA sequencing.	Nitroglycerin	96-99	heme oxygenase 1	Homo sapiens	127-133
18695513-3	2008	CGRP was not significantly different from normal saline in inducing face-grooming behavior but NTG facilitated the effect of CGRP.	Nitroglycerin	95-98	calcitonin-related polypeptide alpha	Rattus norvegicus	125-129
18695513-2	2008	The aim of this study was to test whether systemic administration of nitroglycerin (NTG) influences the CGRP-induced behavior in awake rats and whether sumatriptan, a 5-HT1B/1D receptor agonist, can block the effects of NTG.	Nitroglycerin	69-82	calcitonin-related polypeptide alpha	Rattus norvegicus	104-108
18695513-2	2008	The aim of this study was to test whether systemic administration of nitroglycerin (NTG) influences the CGRP-induced behavior in awake rats and whether sumatriptan, a 5-HT1B/1D receptor agonist, can block the effects of NTG.	Nitroglycerin	84-87	calcitonin-related polypeptide alpha	Rattus norvegicus	104-108
18541319-0	2008	The kynurenate analog SZR-72 prevents the nitroglycerol-induced increase of c-fos immunoreactivity in the rat caudal trigeminal nucleus: comparative studies of the effects of SZR-72 and kynurenic acid.	Nitroglycerin	42-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
18554583-0	2008	Prevention of nitroglycerin tolerance in vitro by T0156, a selective phosphodiesterase type 5 inhibitor.	Nitroglycerin	14-27	phosphodiesterase 5A	Rattus norvegicus	69-93
18554583-2	2008	The present study aims to examine whether T0156, a newly developed potent and selective inhibitor of phosphodiesterase type 5 (PDE5), could attenuate the tolerance to nitroglycerin on rat aortas.	Nitroglycerin	167-180	phosphodiesterase 5A	Rattus norvegicus	127-131
18554583-10	2008	The present results suggest that nitroglycerin tolerance may involve an increased activity of PDE5 but not PDE3 or PDE4 isoforms in vascular smooth muscle cells since T0156 prevents the development of tolerance.	Nitroglycerin	33-46	phosphodiesterase 5A	Rattus norvegicus	94-98
18248324-3	2008	We have reported previously that beta2-TG mice (transgenic mice with cardiac-restricted overexpression of beta2-adrenergic receptors) had a lower incidence of rupture compared with NTG (non-transgenic) littermates.	Nitroglycerin	181-184	hemoglobin, beta adult minor chain	Mus musculus	33-38
18541319-1	2008	Administration of nitroglycerol in a migraine model results in an increased number of c-fos-expressing secondary sensory neurons in the caudal trigeminal nucleus.	Nitroglycerin	18-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
18541319-3	2008	Systemic treatment of rats with SZR-72, a newly synthetized kynurenic acid analog, diminished the nitroglycerol-induced increase of c-fos immunoreactivity in the brain stem highly significantly, while treatment with kynurenic acid resulted in a significantly smaller decrease, proving that SZR-72 is much more effective than kynurenic acid.	Nitroglycerin	98-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-137
18450747-1	2008	Metabolism of nitroglycerin (GTN) to 1,2-glycerol dinitrate (GDN) and nitrite by mitochondrial aldehyde dehydrogenase (ALDH2) is essentially involved in GTN bioactivation resulting in cyclic GMP-mediated vascular relaxation.	Nitroglycerin	14-27	aldehyde dehydrogenase 2 family member	Homo sapiens	119-124
18450747-3	2008	To test the hypothesis that the ALDH2 reaction is sufficient for GTN bioactivation, we measured GTN-induced formation of cGMP by purified sGC in the presence of purified ALDH2 and used a Clark-type electrode to probe for nitric oxide (NO) formation.	Nitroglycerin	96-99	aldehyde dehydrogenase 2 family member	Homo sapiens	32-37
18450747-4	2008	In addition, we studied whether GTN bioactivation is a specific feature of ALDH2 or is also catalyzed by the cytosolic isoform (ALDH1).	Nitroglycerin	32-35	aldehyde dehydrogenase 2 family member	Homo sapiens	75-80
18450747-5	2008	Purified ALDH1 and ALDH2 metabolized GTN to 1,2- and 1,3-GDN with predominant formation of the 1,2-isomer that was inhibited by chloral hydrate (ALDH1 and ALDH2) and daidzin (ALDH2).	Nitroglycerin	37-40	aldehyde dehydrogenase 1 family member A1	Homo sapiens	9-14
18450747-5	2008	Purified ALDH1 and ALDH2 metabolized GTN to 1,2- and 1,3-GDN with predominant formation of the 1,2-isomer that was inhibited by chloral hydrate (ALDH1 and ALDH2) and daidzin (ALDH2).	Nitroglycerin	37-40	aldehyde dehydrogenase 2 family member	Homo sapiens	19-24
18450747-5	2008	Purified ALDH1 and ALDH2 metabolized GTN to 1,2- and 1,3-GDN with predominant formation of the 1,2-isomer that was inhibited by chloral hydrate (ALDH1 and ALDH2) and daidzin (ALDH2).	Nitroglycerin	37-40	aldehyde dehydrogenase 1 family member A1	Homo sapiens	145-150
18450747-6	2008	GTN had no effect on sGC activity in the presence of bovine serum albumin but caused pronounced cGMP accumulation in the presence of ALDH1 or ALDH2.	Nitroglycerin	0-3	aldehyde dehydrogenase 1 family member A1	Homo sapiens	133-138
18272654-1	2008	Recent studies suggest that the mitochondrial aldehyde dehydrogenase (ALDH)2 is involved in vascular bioactivation of nitroglycerin (GTN).	Nitroglycerin	118-131	aldehyde dehydrogenase 2 family member	Homo sapiens	70-74
18272654-1	2008	Recent studies suggest that the mitochondrial aldehyde dehydrogenase (ALDH)2 is involved in vascular bioactivation of nitroglycerin (GTN).	Nitroglycerin	133-136	aldehyde dehydrogenase 2 family member	Homo sapiens	70-74
18272654-9	2008	In clear contrast, the ALDH inhibitors significantly reduced the potency of nitroglycerin by approximately 1 order of magnitude (P &lt; or = 0.01).	Nitroglycerin	76-89	aldehyde dehydrogenase 2 family member	Homo sapiens	23-27
18272654-11	2008	In human capacitance vessels, ALDH2 is a key enzyme in the biotransformation of the frequently used antianginal drug nitroglycerin.	Nitroglycerin	117-130	aldehyde dehydrogenase 2 family member	Homo sapiens	30-35
18450747-1	2008	Metabolism of nitroglycerin (GTN) to 1,2-glycerol dinitrate (GDN) and nitrite by mitochondrial aldehyde dehydrogenase (ALDH2) is essentially involved in GTN bioactivation resulting in cyclic GMP-mediated vascular relaxation.	Nitroglycerin	14-27	5'-nucleotidase, cytosolic II	Homo sapiens	191-194
18450747-1	2008	Metabolism of nitroglycerin (GTN) to 1,2-glycerol dinitrate (GDN) and nitrite by mitochondrial aldehyde dehydrogenase (ALDH2) is essentially involved in GTN bioactivation resulting in cyclic GMP-mediated vascular relaxation.	Nitroglycerin	29-32	aldehyde dehydrogenase 2 family member	Homo sapiens	119-124
18450747-1	2008	Metabolism of nitroglycerin (GTN) to 1,2-glycerol dinitrate (GDN) and nitrite by mitochondrial aldehyde dehydrogenase (ALDH2) is essentially involved in GTN bioactivation resulting in cyclic GMP-mediated vascular relaxation.	Nitroglycerin	29-32	5'-nucleotidase, cytosolic II	Homo sapiens	191-194
18450747-6	2008	GTN had no effect on sGC activity in the presence of bovine serum albumin but caused pronounced cGMP accumulation in the presence of ALDH1 or ALDH2.	Nitroglycerin	0-3	aldehyde dehydrogenase 2 family member	Homo sapiens	142-147
18450747-1	2008	Metabolism of nitroglycerin (GTN) to 1,2-glycerol dinitrate (GDN) and nitrite by mitochondrial aldehyde dehydrogenase (ALDH2) is essentially involved in GTN bioactivation resulting in cyclic GMP-mediated vascular relaxation.	Nitroglycerin	153-156	aldehyde dehydrogenase 2 family member	Homo sapiens	119-124
18450747-8	2008	GTN caused biphasic sGC activation with apparent EC(50) values of 42 +/- 2.9 and 3.1 +/- 0.4 microm in the presence of ALDH1 and ALDH2, respectively.	Nitroglycerin	0-3	aldehyde dehydrogenase 1 family member A1	Homo sapiens	119-124
18450747-1	2008	Metabolism of nitroglycerin (GTN) to 1,2-glycerol dinitrate (GDN) and nitrite by mitochondrial aldehyde dehydrogenase (ALDH2) is essentially involved in GTN bioactivation resulting in cyclic GMP-mediated vascular relaxation.	Nitroglycerin	153-156	5'-nucleotidase, cytosolic II	Homo sapiens	191-194
18450747-8	2008	GTN caused biphasic sGC activation with apparent EC(50) values of 42 +/- 2.9 and 3.1 +/- 0.4 microm in the presence of ALDH1 and ALDH2, respectively.	Nitroglycerin	0-3	aldehyde dehydrogenase 2 family member	Homo sapiens	129-134
18450747-3	2008	To test the hypothesis that the ALDH2 reaction is sufficient for GTN bioactivation, we measured GTN-induced formation of cGMP by purified sGC in the presence of purified ALDH2 and used a Clark-type electrode to probe for nitric oxide (NO) formation.	Nitroglycerin	65-68	aldehyde dehydrogenase 2 family member	Homo sapiens	32-37
18450747-9	2008	Incubation of ALDH1 or ALDH2 with GTN resulted in sustained, chloral hydrate-sensitive formation of NO.	Nitroglycerin	34-37	aldehyde dehydrogenase 1 family member A1	Homo sapiens	14-19
18450747-9	2008	Incubation of ALDH1 or ALDH2 with GTN resulted in sustained, chloral hydrate-sensitive formation of NO.	Nitroglycerin	34-37	aldehyde dehydrogenase 2 family member	Homo sapiens	23-28
18480669-8	2008	0.2 mg NTG provoked a long-lasting and significant decrease in coronary flow volume (from 140.2+/-34.2 to 91.2+/-21.8 ml/min, P&lt;0.002), a marked increase in coronary vascular resistance (from 0.62 to 0.92 mmHG x ml/min(-1), P&lt;0.002) and an inadequate increase in coronary flow volume under cardiac pacing.	Nitroglycerin	7-10	CD59 molecule (CD59 blood group)	Homo sapiens	218-224
18450747-10	2008	These data may explain the coupling of ALDH2-catalyzed GTN metabolism to sGC activation in vascular smooth muscle.	Nitroglycerin	55-58	aldehyde dehydrogenase 2 family member	Homo sapiens	39-44
18503229-1	2008	BACKGROUND: We examined whether nitroglycerin (NTG)-induced impairment of nitric oxide (NO) bioavailability could be modified by a peroxisome proliferator-activated receptor (PPAR) gammaagonist.	Nitroglycerin	32-45	PPARA	Oryctolagus cuniculus	131-173
18503229-1	2008	BACKGROUND: We examined whether nitroglycerin (NTG)-induced impairment of nitric oxide (NO) bioavailability could be modified by a peroxisome proliferator-activated receptor (PPAR) gammaagonist.	Nitroglycerin	32-45	PPARA	Oryctolagus cuniculus	175-179
18503229-1	2008	BACKGROUND: We examined whether nitroglycerin (NTG)-induced impairment of nitric oxide (NO) bioavailability could be modified by a peroxisome proliferator-activated receptor (PPAR) gammaagonist.	Nitroglycerin	47-50	PPARA	Oryctolagus cuniculus	175-179
18503229-8	2008	CONCLUSIONS: NTG-induced impairment of basal and ACh-stimulated NO production might be prevented by the co-treatment with a PPAR gamma agonist, pioglitazone through suppressions of nitrosative stress.	Nitroglycerin	13-16	peroxisome proliferator-activated receptor gamma	Oryctolagus cuniculus	124-134
18367169-0	2008	New insights into nitroglycerin effects and tolerance: role of calcitonin gene-related peptide.	Nitroglycerin	18-31	calcitonin related polypeptide alpha	Homo sapiens	63-73
18367169-2	2008	CGRP is a potent vasodilator and plays an important role in mediation of nitroglycerin-induced vascular relaxation.	Nitroglycerin	73-86	calcitonin related polypeptide alpha	Homo sapiens	0-4
18367169-3	2008	Recently, calcitonin gene-relate peptide is emerging as a potential player in nitroglycerin tolerance.	Nitroglycerin	78-91	calcitonin related polypeptide alpha	Homo sapiens	10-20
18367169-4	2008	There is increasing evidence that the decreased depressor effect of nitroglycerin in tolerant states is closely related to a decrease in calcitonin gene-relate peptide release.	Nitroglycerin	68-81	calcitonin related polypeptide alpha	Homo sapiens	137-147
18367169-5	2008	The reduced release of calcitonin gene-relate peptide in nitroglycerin tolerance is associated with the decreased nitroglycerin biotransformation due to the mitochondrial dysfunction.	Nitroglycerin	57-70	calcitonin related polypeptide alpha	Homo sapiens	23-33
18367169-5	2008	The reduced release of calcitonin gene-relate peptide in nitroglycerin tolerance is associated with the decreased nitroglycerin biotransformation due to the mitochondrial dysfunction.	Nitroglycerin	114-127	calcitonin related polypeptide alpha	Homo sapiens	23-33
18367169-6	2008	Recent work has been shown that the inhibited activity of mitochondrial isoform of aldehyde dehydrogenase and the upregulation of phosphodiesterase 1A1 are the key factors that lead to the decreased nitroglycerin biotransformation in nitroglycerin tolerance, with a subsequently reduced release of calcitonin gene-relate peptide.	Nitroglycerin	199-212	calcitonin related polypeptide alpha	Homo sapiens	298-308
18367169-6	2008	Recent work has been shown that the inhibited activity of mitochondrial isoform of aldehyde dehydrogenase and the upregulation of phosphodiesterase 1A1 are the key factors that lead to the decreased nitroglycerin biotransformation in nitroglycerin tolerance, with a subsequently reduced release of calcitonin gene-relate peptide.	Nitroglycerin	234-247	calcitonin related polypeptide alpha	Homo sapiens	298-308
18430366-8	2008	The release of NO by NTG resulted in increased cell proliferation and osteoblastic differentiation of HBMSC, as evidenced by the increment of the BrdU incorporation, the induction of ALP activity in the early stage, and the calcium deposition in the latter stage.	Nitroglycerin	21-24	alkaline phosphatase, placental	Homo sapiens	183-186
17804099-1	2008	Previous studies have shown that the development of tolerance to nitroglycerin is related to reduction of endogenous calcitonin gene-related peptide (CGRP) release.	Nitroglycerin	65-78	calcitonin-related polypeptide alpha	Rattus norvegicus	117-148
17804099-1	2008	Previous studies have shown that the development of tolerance to nitroglycerin is related to reduction of endogenous calcitonin gene-related peptide (CGRP) release.	Nitroglycerin	65-78	calcitonin-related polypeptide alpha	Rattus norvegicus	150-154
17804099-2	2008	In the present study, Nitroglycerin caused a concentration-dependent relaxation concomitantly with a significant increase in the release of CGRP in the isolated rat thoracic aorta, an effect that was reduced by preincubation with capsaicin.	Nitroglycerin	22-35	calcitonin-related polypeptide alpha	Rattus norvegicus	140-144
17804099-3	2008	Pretreatment with nitroglycerin significantly decreased its vasodilation and depressor effect and the release of CGRP, which was restored in the presence of vinpocetine, an inhibitor of phosphodiesterase.	Nitroglycerin	18-31	calcitonin-related polypeptide alpha	Rattus norvegicus	113-117
17804099-4	2008	The present results suggest that reversal of tolerance to nitroglycerin with vinpocetine is related to the increased release of CGRP in the rat.	Nitroglycerin	58-71	calcitonin-related polypeptide alpha	Rattus norvegicus	128-132
18386218-2	2008	METHODS: We examined the reactivity of cerebral arterioles in adult and aged Fisher-344 rats to endothelial nitric oxide synthase (eNOS)-dependent (acetylcholine and adenosine diphosphate [ADP]) and-independent (nitroglycerin) agonists before and during application of tempol, apocynin, and diphenyleneiodonium chloride (DPI).	Nitroglycerin	212-225	nitric oxide synthase 3	Rattus norvegicus	131-135
18289604-0	2008	Involvement of the endothelial DDAH/ADMA pathway in nitroglycerin tolerance: the role of ALDH-2.	Nitroglycerin	52-65	dimethylarginine dimethylaminohydrolase 1	Homo sapiens	31-35
18289604-1	2008	Previous studies have shown that nitroglycerin (GTN) tolerance is closely related to an oxidative stress-induced decrease in activity of mitochondrial isoforms of aldehyde dehydrogenase (ALDH-2), and prolonged GTN treatment causes endothelial dysfunction.	Nitroglycerin	33-46	aldehyde dehydrogenase 2 family member	Homo sapiens	187-193
18289604-1	2008	Previous studies have shown that nitroglycerin (GTN) tolerance is closely related to an oxidative stress-induced decrease in activity of mitochondrial isoforms of aldehyde dehydrogenase (ALDH-2), and prolonged GTN treatment causes endothelial dysfunction.	Nitroglycerin	48-51	aldehyde dehydrogenase 2 family member	Homo sapiens	187-193
18289604-4	2008	The aim of the present study was to determine whether the DDAH/ADMA pathway is involved in the development of GTN tolerance in endothelial cells.	Nitroglycerin	110-113	dimethylarginine dimethylaminohydrolase 1	Homo sapiens	58-62
18289604-5	2008	Tolerance, reflected by the decrease in cyclic GMP (cGMP) production, was induced by exposure of human umbilical vein endothelial cells (HUVECs) to GTN (10 microM) for 16 h. While the treatment increased reactive oxygen species (ROS) production/malondialdehyde (MDA) concentration and decreased ALDH-2 activity as well as cGMP production, it markedly increased the level of ADMA in culture medium and decreased DDAH activity in endothelial cells.	Nitroglycerin	148-151	aldehyde dehydrogenase 2 family member	Homo sapiens	295-301
18289604-5	2008	Tolerance, reflected by the decrease in cyclic GMP (cGMP) production, was induced by exposure of human umbilical vein endothelial cells (HUVECs) to GTN (10 microM) for 16 h. While the treatment increased reactive oxygen species (ROS) production/malondialdehyde (MDA) concentration and decreased ALDH-2 activity as well as cGMP production, it markedly increased the level of ADMA in culture medium and decreased DDAH activity in endothelial cells.	Nitroglycerin	148-151	dimethylarginine dimethylaminohydrolase 1	Homo sapiens	411-415
18289604-6	2008	Exogenous ADMA significantly enhanced ROS production/MDA concentration and inhibited ALDH-2 activity, and overexpression of DDAH2 could significantly suppress GTN-induced oxidative stress and inhibition of ALDH-2 activity, which is also attenuated by L-arginine.	Nitroglycerin	159-162	dimethylarginine dimethylaminohydrolase 2	Homo sapiens	124-129
18289604-7	2008	Therefore, our results suggest for the first time that the endothelial DDAH/ADMA pathway plays an important role in the development/maintenance of GTN tolerance.	Nitroglycerin	147-150	dimethylarginine dimethylaminohydrolase 1	Homo sapiens	71-75
18178728-16	2008	iNOS was higher in AT2TG-AS than in NTG-AS mice but not significantly different.	Nitroglycerin	36-39	nitric oxide synthase 2, inducible	Mus musculus	0-4
18157936-1	2008	Mitochondrial aldehyde dehydrogenase (ALDH-2) reduces reactive oxygen species (ROS) formation related to toxic aldehydes; additionally, it provides a bioactivating pathway for nitroglycerin.	Nitroglycerin	176-189	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	38-44
18276782-6	2008	Expression of proinflammatory genes such as Egr-1, VCAM-1, and ICAM was significantly increased in tg mice relative to ntg controls.	Nitroglycerin	119-122	early growth response 1	Mus musculus	44-49
18418439-6	2008	In addition, chronic hyperglycemia also increased the activity of catalase and superoxide dismutase in the hearts of NTG and Gsalpha diabetic mice.	Nitroglycerin	117-120	catalase	Mus musculus	66-74
18418439-7	2008	Hearts of NTG diabetic mice, but not Gsalpha mice, showed increased expression of proapoptosis Bax, downregulation in Bcl2, and an increase in the Bax/Bcl2 ratio.	Nitroglycerin	10-13	BCL2-associated X protein	Mus musculus	95-98
18418439-7	2008	Hearts of NTG diabetic mice, but not Gsalpha mice, showed increased expression of proapoptosis Bax, downregulation in Bcl2, and an increase in the Bax/Bcl2 ratio.	Nitroglycerin	10-13	B cell leukemia/lymphoma 2	Mus musculus	118-122
18418439-7	2008	Hearts of NTG diabetic mice, but not Gsalpha mice, showed increased expression of proapoptosis Bax, downregulation in Bcl2, and an increase in the Bax/Bcl2 ratio.	Nitroglycerin	10-13	BCL2-associated X protein	Mus musculus	147-150
18418439-7	2008	Hearts of NTG diabetic mice, but not Gsalpha mice, showed increased expression of proapoptosis Bax, downregulation in Bcl2, and an increase in the Bax/Bcl2 ratio.	Nitroglycerin	10-13	B cell leukemia/lymphoma 2	Mus musculus	151-155
18157936-4	2008	Maximal nitroglycerin dose applied in vivo lead to a "super-desensitized" nitroglycerin response in isolated ALDH-2(-/-) aortas, inaccessible in C57Bl6 mice.	Nitroglycerin	8-21	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	109-115
18157936-4	2008	Maximal nitroglycerin dose applied in vivo lead to a "super-desensitized" nitroglycerin response in isolated ALDH-2(-/-) aortas, inaccessible in C57Bl6 mice.	Nitroglycerin	74-87	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	109-115
18037907-6	2008	KEY RESULTS: A 24 h incubation with NTG attenuated relaxation of coronary arteries to NTG, which was associated with decreased PKG activity.	Nitroglycerin	36-39	protein kinase cGMP-dependent 1	Homo sapiens	127-130
18037907-8	2008	PKG protein and mRNA were down-regulated by a 24 h incubation with NTG at 10(-5) M but not at 10(-7) M. Acute exposure to exogenous superoxide inhibited PKG activity stimulated by NTG at 10(-7) M but not at 10(-5) M. Superoxide had no effect on PKG activity stimulated with exogenous cGMP.	Nitroglycerin	67-70	protein kinase cGMP-dependent 1	Homo sapiens	0-3
18037907-9	2008	CONCLUSIONS AND IMPLICATIONS: Nitrate tolerance induced by NTG at low concentrations may result from an increased production of reactive oxygen species acting on sites upstream of PKG.	Nitroglycerin	59-62	protein kinase cGMP-dependent 1	Homo sapiens	180-183
18037907-8	2008	PKG protein and mRNA were down-regulated by a 24 h incubation with NTG at 10(-5) M but not at 10(-7) M. Acute exposure to exogenous superoxide inhibited PKG activity stimulated by NTG at 10(-7) M but not at 10(-5) M. Superoxide had no effect on PKG activity stimulated with exogenous cGMP.	Nitroglycerin	67-70	protein kinase cGMP-dependent 1	Homo sapiens	153-156
18037907-10	2008	The tolerance induced by NTG at higher concentrations may be in part due to suppression of PKG expression resulting from sustained activation of the enzyme.	Nitroglycerin	25-28	protein kinase cGMP-dependent 1	Homo sapiens	91-94
18037907-8	2008	PKG protein and mRNA were down-regulated by a 24 h incubation with NTG at 10(-5) M but not at 10(-7) M. Acute exposure to exogenous superoxide inhibited PKG activity stimulated by NTG at 10(-7) M but not at 10(-5) M. Superoxide had no effect on PKG activity stimulated with exogenous cGMP.	Nitroglycerin	67-70	protein kinase cGMP-dependent 1	Homo sapiens	153-156
18037907-8	2008	PKG protein and mRNA were down-regulated by a 24 h incubation with NTG at 10(-5) M but not at 10(-7) M. Acute exposure to exogenous superoxide inhibited PKG activity stimulated by NTG at 10(-7) M but not at 10(-5) M. Superoxide had no effect on PKG activity stimulated with exogenous cGMP.	Nitroglycerin	180-183	protein kinase cGMP-dependent 1	Homo sapiens	0-3
18037907-8	2008	PKG protein and mRNA were down-regulated by a 24 h incubation with NTG at 10(-5) M but not at 10(-7) M. Acute exposure to exogenous superoxide inhibited PKG activity stimulated by NTG at 10(-7) M but not at 10(-5) M. Superoxide had no effect on PKG activity stimulated with exogenous cGMP.	Nitroglycerin	180-183	protein kinase cGMP-dependent 1	Homo sapiens	153-156
18037907-8	2008	PKG protein and mRNA were down-regulated by a 24 h incubation with NTG at 10(-5) M but not at 10(-7) M. Acute exposure to exogenous superoxide inhibited PKG activity stimulated by NTG at 10(-7) M but not at 10(-5) M. Superoxide had no effect on PKG activity stimulated with exogenous cGMP.	Nitroglycerin	180-183	protein kinase cGMP-dependent 1	Homo sapiens	153-156
18197882-4	2008	Following NTG administration, CGRP-ir decreased steadily in the NTC, whereas SP-ir increased transiently.	Nitroglycerin	10-13	calcitonin related polypeptide alpha	Homo sapiens	30-34
18197882-5	2008	In the lumbar dorsal horns, NTG induced a decrease in SP-ir 1 h after its administration.	Nitroglycerin	28-31	tachykinin precursor 1	Homo sapiens	54-56
17855351-6	2007	After 4 weeks of aortic banding (transverse aortic constriction (TAC)), increases in left ventricular weight and myocyte size were significantly smaller in Tg than in NTg, indicating that GSK-3alpha inhibits cardiac hypertrophy.	Nitroglycerin	167-170	glycogen synthase kinase 3 alpha	Mus musculus	188-198
18457363-7	2008	550 mg/kg/day SA or NG for 5 days could significantly inhibit ADP-induced platelet aggregation of PRP.	Nitroglycerin	20-22	proline rich protein 2-like 1	Rattus norvegicus	98-101
18457363-8	2008	Moreover, combination of SA and NG at a ratio of 5:1 had a synergistic effect on platelet aggregation of PRP.	Nitroglycerin	32-34	proline rich protein 2-like 1	Rattus norvegicus	105-108
17949246-3	2008	We also evaluated the dose response for forskolin- and nitroglycerin-induced relaxation in phenylephrine-stimulated PLM-/- and PLM+/+ mice.	Nitroglycerin	55-68	FXYD domain-containing ion transport regulator 1	Mus musculus	116-119
17949246-7	2008	In aortae precontracted with phenylephrine, nitroglycerin induced a slightly, but significantly greater relaxation in PLM-/- compared to PLM+/+ aortae.	Nitroglycerin	44-57	FXYD domain-containing ion transport regulator 7	Sus scrofa	118-121
17949246-7	2008	In aortae precontracted with phenylephrine, nitroglycerin induced a slightly, but significantly greater relaxation in PLM-/- compared to PLM+/+ aortae.	Nitroglycerin	44-57	FXYD domain-containing ion transport regulator 7	Sus scrofa	137-140
18061070-1	2007	OBJECTIVES: We tested the hypothesis of whether an inhibition of the nitroglycerin (GTN) bioactivating enzyme mitochondrial aldehyde dehydrogenase (ALDH-2) contributes to GTN tolerance in human blood vessels.	Nitroglycerin	69-82	aldehyde dehydrogenase 2 family member	Homo sapiens	148-154
18061070-1	2007	OBJECTIVES: We tested the hypothesis of whether an inhibition of the nitroglycerin (GTN) bioactivating enzyme mitochondrial aldehyde dehydrogenase (ALDH-2) contributes to GTN tolerance in human blood vessels.	Nitroglycerin	84-87	aldehyde dehydrogenase 2 family member	Homo sapiens	148-154
18061070-1	2007	OBJECTIVES: We tested the hypothesis of whether an inhibition of the nitroglycerin (GTN) bioactivating enzyme mitochondrial aldehyde dehydrogenase (ALDH-2) contributes to GTN tolerance in human blood vessels.	Nitroglycerin	171-174	aldehyde dehydrogenase 2 family member	Homo sapiens	148-154
18061070-7	2007	In vivo GTN tolerance was mimicked in vitro by incubation of nontolerant vessels with the ALDH-2 inhibitor benomyl.	Nitroglycerin	8-11	aldehyde dehydrogenase 2 family member	Homo sapiens	90-96
18061070-8	2007	In vivo GTN treatment decreased vascular aldehyde dehydrogenase activity compared with nontolerant vessels and decreased the expression of ALDH-2 in arterial tissue.	Nitroglycerin	8-11	aldehyde dehydrogenase 2 family member	Homo sapiens	139-145
18061070-10	2007	CONCLUSIONS: Long-term GTN treatment induces tolerance and endothelial dysfunction in human vessels, associated with an inhibition and down-regulation of vascular ALDH-2.	Nitroglycerin	23-26	aldehyde dehydrogenase 2 family member	Homo sapiens	163-169
17891157-3	2007	EXPERIMENTAL APPROACH: Effects of a PKG inhibitor on the basal tension and responses induced by nitroglycerin, DETA NONOate, and 8-Br-cGMP in isolated porcine coronary veins were determined.	Nitroglycerin	96-109	protein kinase cGMP-dependent 1	Homo sapiens	36-39
17585900-0	2007	Decrease in endogenous CGRP release in nitroglycerin tolerance: role of ALDH-2.	Nitroglycerin	39-52	calcitonin related polypeptide alpha	Homo sapiens	23-27
17927648-1	2007	OBJECTIVE: The aim of the present study was to determine which isoform of the cyclooxygenase (COX) enzyme plays a role in the neuronal nitric oxide synthase (nNOS) activation caused by nitroglycerin (NTG), in the most caudal part of the trigeminal caudal nucleus (TNC) of the rat.	Nitroglycerin	185-198	nitric oxide synthase 1	Rattus norvegicus	126-156
17927648-1	2007	OBJECTIVE: The aim of the present study was to determine which isoform of the cyclooxygenase (COX) enzyme plays a role in the neuronal nitric oxide synthase (nNOS) activation caused by nitroglycerin (NTG), in the most caudal part of the trigeminal caudal nucleus (TNC) of the rat.	Nitroglycerin	185-198	nitric oxide synthase 1	Rattus norvegicus	158-162
17927648-1	2007	OBJECTIVE: The aim of the present study was to determine which isoform of the cyclooxygenase (COX) enzyme plays a role in the neuronal nitric oxide synthase (nNOS) activation caused by nitroglycerin (NTG), in the most caudal part of the trigeminal caudal nucleus (TNC) of the rat.	Nitroglycerin	200-203	nitric oxide synthase 1	Rattus norvegicus	126-156
17927648-1	2007	OBJECTIVE: The aim of the present study was to determine which isoform of the cyclooxygenase (COX) enzyme plays a role in the neuronal nitric oxide synthase (nNOS) activation caused by nitroglycerin (NTG), in the most caudal part of the trigeminal caudal nucleus (TNC) of the rat.	Nitroglycerin	200-203	nitric oxide synthase 1	Rattus norvegicus	158-162
17927648-3	2007	In rats, subcutaneous administration of NTG (10 mg/kg) increases significantly the number of nNOS-immunoreactive neurons in the TNC after 4 hours, which could be attenuated by acetyl-salicylate (Aspirin), a nonselective COX-inhibitor.	Nitroglycerin	40-43	nitric oxide synthase 1	Rattus norvegicus	93-97
17927648-7	2007	Results.-The selective COX-2 inhibitor NS398 in contrast to the selective COX-1 inhibitor SC560 attenuates the NTG-induced nNOS expression dose-dependently.	Nitroglycerin	111-114	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	23-28
17927648-7	2007	Results.-The selective COX-2 inhibitor NS398 in contrast to the selective COX-1 inhibitor SC560 attenuates the NTG-induced nNOS expression dose-dependently.	Nitroglycerin	111-114	nitric oxide synthase 1	Rattus norvegicus	123-127
17927648-8	2007	CONCLUSION: These findings suggest that metabolites deriving from COX-2 (but not COX-1) may be the most important factors in the NTG-induced nNOS expression.	Nitroglycerin	129-132	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	66-71
17927648-8	2007	CONCLUSION: These findings suggest that metabolites deriving from COX-2 (but not COX-1) may be the most important factors in the NTG-induced nNOS expression.	Nitroglycerin	129-132	nitric oxide synthase 1	Rattus norvegicus	141-145
17585900-1	2007	In the present study, we tested whether the decreased release of calcitonin gene-related peptide (CGRP) observed in nitroglycerin tolerance is associated with the decrease in aldehyde dehydrogenase (ALDH-2) activity.	Nitroglycerin	116-129	calcitonin related polypeptide alpha	Homo sapiens	65-96
17585900-1	2007	In the present study, we tested whether the decreased release of calcitonin gene-related peptide (CGRP) observed in nitroglycerin tolerance is associated with the decrease in aldehyde dehydrogenase (ALDH-2) activity.	Nitroglycerin	116-129	calcitonin related polypeptide alpha	Homo sapiens	98-102
17585900-4	2007	Pretreatment with ALDH-2 inhibitors and nitroglycerin significantly attenuated vasodilator responses to nitroglycerin concomitantly with a decrease in the release of CGRP from the isolated thoracic aorta.	Nitroglycerin	40-53	calcitonin related polypeptide alpha	Homo sapiens	166-170
17585900-4	2007	Pretreatment with ALDH-2 inhibitors and nitroglycerin significantly attenuated vasodilator responses to nitroglycerin concomitantly with a decrease in the release of CGRP from the isolated thoracic aorta.	Nitroglycerin	104-117	aldehyde dehydrogenase 2 family member	Homo sapiens	18-24
17585900-5	2007	Nitroglycerin produced a depressor effect concomitantly with an increase in plasma concentrations of CGRP, and the effect of nitroglycerin was attenuated after pretreatment with an inhibitor of ALDH-2 or nitroglycerin for 8 days.	Nitroglycerin	0-13	calcitonin related polypeptide alpha	Homo sapiens	101-105
17585900-5	2007	Nitroglycerin produced a depressor effect concomitantly with an increase in plasma concentrations of CGRP, and the effect of nitroglycerin was attenuated after pretreatment with an inhibitor of ALDH-2 or nitroglycerin for 8 days.	Nitroglycerin	0-13	aldehyde dehydrogenase 2 family member	Homo sapiens	194-200
17585900-5	2007	Nitroglycerin produced a depressor effect concomitantly with an increase in plasma concentrations of CGRP, and the effect of nitroglycerin was attenuated after pretreatment with an inhibitor of ALDH-2 or nitroglycerin for 8 days.	Nitroglycerin	125-138	aldehyde dehydrogenase 2 family member	Homo sapiens	194-200
17585900-6	2007	Exposure of HUVEC to nitroglycerin for 16 h increased reactive oxygen species production and decreased ALDH-2 activity as well as cGMP production in a time-and concentration-dependent manner.	Nitroglycerin	21-34	aldehyde dehydrogenase 2 family member	Homo sapiens	103-109
17488770-7	2007	Patients with CSX and CAD had significantly decreased endothelium-dependent flow-mediated vasodilation (FMD) compared with normal controls (normal controls vs CSX vs CAD: 10.6% (3.5%) vs 6.1% (1.8%) vs 4.1% (1.9%), p&lt;0.001), but the difference was not found in endothelium-independent nitroglycerine-mediated vasodilation (p = 0.159).	Nitroglycerin	288-302	NK2 homeobox 5	Homo sapiens	14-17
17488313-7	2007	When ET-1 was used as a constrictor nitroglycerin and milrinone caused nearly complete (80-100%) relaxation, whereas other agents were of limited effectiveness (40-50%).	Nitroglycerin	36-49	endothelin 1	Homo sapiens	5-9
17377806-7	2007	The activity of PKG but not that of PKA was increased by nitroglycerin and DETA NONOate in intact vessels and increased by cGMP in the tissue homogenates.	Nitroglycerin	57-70	protein kinase cGMP-dependent 1	Homo sapiens	16-19
17969895-8	2007	The mechanism of NG in protecting hemor-rhagic brain tissue might be related with its actions in inhibiting the post-cerebral high PAR-1 expression to re-duce cell apoptosis and relieve brain edema.	Nitroglycerin	17-19	coagulation factor II (thrombin) receptor	Rattus norvegicus	131-136
17541025-1	2007	OBJECTIVE: Nitrate tolerance is likely attributable to an increased production of reactive oxygen species (ROS) leading to an inhibition of the mitochondrial aldehyde dehydrogenase (ALDH-2), representing the nitroglycerin (GTN) and pentaerythrityl tetranitrate (PETN) bioactivating enzyme, and to impaired nitric oxide bioactivity and signaling.	Nitroglycerin	208-221	aldehyde dehydrogenase 2 family member	Rattus norvegicus	144-180
17541025-1	2007	OBJECTIVE: Nitrate tolerance is likely attributable to an increased production of reactive oxygen species (ROS) leading to an inhibition of the mitochondrial aldehyde dehydrogenase (ALDH-2), representing the nitroglycerin (GTN) and pentaerythrityl tetranitrate (PETN) bioactivating enzyme, and to impaired nitric oxide bioactivity and signaling.	Nitroglycerin	208-221	aldehyde dehydrogenase 2 family member	Rattus norvegicus	182-188
17541025-1	2007	OBJECTIVE: Nitrate tolerance is likely attributable to an increased production of reactive oxygen species (ROS) leading to an inhibition of the mitochondrial aldehyde dehydrogenase (ALDH-2), representing the nitroglycerin (GTN) and pentaerythrityl tetranitrate (PETN) bioactivating enzyme, and to impaired nitric oxide bioactivity and signaling.	Nitroglycerin	223-226	aldehyde dehydrogenase 2 family member	Rattus norvegicus	144-180
17541025-1	2007	OBJECTIVE: Nitrate tolerance is likely attributable to an increased production of reactive oxygen species (ROS) leading to an inhibition of the mitochondrial aldehyde dehydrogenase (ALDH-2), representing the nitroglycerin (GTN) and pentaerythrityl tetranitrate (PETN) bioactivating enzyme, and to impaired nitric oxide bioactivity and signaling.	Nitroglycerin	223-226	aldehyde dehydrogenase 2 family member	Rattus norvegicus	182-188
17541025-5	2007	Vascular protein and mRNA expression of HO-1 and ferritin were increased in response to PETN but not GTN.	Nitroglycerin	101-104	heme oxygenase 1	Rattus norvegicus	40-44
17541025-7	2007	Inhibition of HO-1 expression by apigenin induced "tolerance" to PETN whereas HO-1 gene induction by hemin prevented tolerance in GTN treated rats.	Nitroglycerin	130-133	heme oxygenase 1	Rattus norvegicus	78-82
17967228-0	2007	[The relationship between aldehyde dehydrogenase-2 gene polymorphisms and efficacy of nitroglycerin].	Nitroglycerin	86-99	aldehyde dehydrogenase 2 family member	Homo sapiens	26-50
17967228-1	2007	OBJECTIVE: To investigate the association among aldehyde dehydrogenase-2 (ALDH2) gene polymorphisms, alcohol flushing and efficacy of nitroglycerin (GTN) in patients with coronary heart disease.	Nitroglycerin	134-147	aldehyde dehydrogenase 2 family member	Homo sapiens	48-72
17967228-1	2007	OBJECTIVE: To investigate the association among aldehyde dehydrogenase-2 (ALDH2) gene polymorphisms, alcohol flushing and efficacy of nitroglycerin (GTN) in patients with coronary heart disease.	Nitroglycerin	134-147	aldehyde dehydrogenase 2 family member	Homo sapiens	74-79
17967228-1	2007	OBJECTIVE: To investigate the association among aldehyde dehydrogenase-2 (ALDH2) gene polymorphisms, alcohol flushing and efficacy of nitroglycerin (GTN) in patients with coronary heart disease.	Nitroglycerin	149-152	aldehyde dehydrogenase 2 family member	Homo sapiens	48-72
17967228-1	2007	OBJECTIVE: To investigate the association among aldehyde dehydrogenase-2 (ALDH2) gene polymorphisms, alcohol flushing and efficacy of nitroglycerin (GTN) in patients with coronary heart disease.	Nitroglycerin	149-152	aldehyde dehydrogenase 2 family member	Homo sapiens	74-79
17967228-9	2007	The rate of efficacious response to GTN was significantly higher in the patients with ALDH2*1 genotype than the patients with ALDH2*2 genotype (81.1% vs 36.1%, P &lt; 0.01) and the efficacious response to GTN in 5 minutes was higher in the patients with ALDH2*1 genotype than those with ALDH2*2 genotype (57.5% vs 11.1%, P &lt; 0.01).	Nitroglycerin	36-39	aldehyde dehydrogenase 2 family member	Homo sapiens	86-91
17967228-9	2007	The rate of efficacious response to GTN was significantly higher in the patients with ALDH2*1 genotype than the patients with ALDH2*2 genotype (81.1% vs 36.1%, P &lt; 0.01) and the efficacious response to GTN in 5 minutes was higher in the patients with ALDH2*1 genotype than those with ALDH2*2 genotype (57.5% vs 11.1%, P &lt; 0.01).	Nitroglycerin	36-39	aldehyde dehydrogenase 2 family member	Homo sapiens	126-131
17967228-9	2007	The rate of efficacious response to GTN was significantly higher in the patients with ALDH2*1 genotype than the patients with ALDH2*2 genotype (81.1% vs 36.1%, P &lt; 0.01) and the efficacious response to GTN in 5 minutes was higher in the patients with ALDH2*1 genotype than those with ALDH2*2 genotype (57.5% vs 11.1%, P &lt; 0.01).	Nitroglycerin	36-39	aldehyde dehydrogenase 2 family member	Homo sapiens	126-131
17967228-9	2007	The rate of efficacious response to GTN was significantly higher in the patients with ALDH2*1 genotype than the patients with ALDH2*2 genotype (81.1% vs 36.1%, P &lt; 0.01) and the efficacious response to GTN in 5 minutes was higher in the patients with ALDH2*1 genotype than those with ALDH2*2 genotype (57.5% vs 11.1%, P &lt; 0.01).	Nitroglycerin	36-39	aldehyde dehydrogenase 2 family member	Homo sapiens	126-131
17967228-10	2007	CONCLUSIONS: There is relationship among ALDH2 gene polymorphisms, alcohol flushing and efficacy of nitroglycerin.	Nitroglycerin	100-113	aldehyde dehydrogenase 2 family member	Homo sapiens	41-46
17488313-9	2007	CONCLUSIONS: Nitroglycerin and milrinone are very effective in reversing ET-1 and U46619-induced pulmonary vasoconstriction in vitro.	Nitroglycerin	13-26	endothelin 1	Homo sapiens	73-77
17493633-12	2007	Similarly, in vascular smooth muscle cells exposed to NTG for 6-24 h, NAD(P)H oxidase activity was increased, in spite of nox1 downregulation.	Nitroglycerin	54-57	NADPH oxidase 1	Rattus norvegicus	122-126
17449545-7	2007	Apocynin caused significant improvement of increased mRNA and protein levels of endothelial nitric oxide synthase (eNOS) in BAECs given nitroglycerin continuously over the treatment period.	Nitroglycerin	136-149	nitric oxide synthase 3	Homo sapiens	80-113
17493633-16	2007	Furthermore, reduced ALDH-2 activity and expression leads to decreased NTG bioconversion.	Nitroglycerin	71-74	aldehyde dehydrogenase 2 family member	Rattus norvegicus	21-27
17040971-4	2007	p38 MAPK activation was earlier, more marked, and longer in the myocardium of the TG group compared with that of the nontransgenic (NTG) group after swimming stress, whereas JNK activation was detected on day 5 and decreased afterward.	Nitroglycerin	132-135	mitogen-activated protein kinase 14	Mus musculus	0-3
17382471-1	2007	The systemic administration of nitroglycerine, regarded as a migraine model, was previously observed to result in an increased number of c-fos immunoreactive secondary sensory neurons in the caudal trigeminal nucleus, which forward nociceptive impulses to the thalamus.	Nitroglycerin	31-45	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	137-142
17395874-5	2007	After 4 weeks, Mst1 was significantly activated in the remodeling area in NTg, but not in Tg-DN-Mst1.	Nitroglycerin	74-77	macrophage stimulating 1	Homo sapiens	15-19
17327228-1	2007	The common mitochondrial aldehyde dehydrogenase (ALDH2) ALDH2(*)2 polymorphism is associated with impaired ethanol metabolism and decreased efficacy of nitroglycerin treatment.	Nitroglycerin	152-165	aldehyde dehydrogenase 2 family member	Homo sapiens	49-54
17327228-1	2007	The common mitochondrial aldehyde dehydrogenase (ALDH2) ALDH2(*)2 polymorphism is associated with impaired ethanol metabolism and decreased efficacy of nitroglycerin treatment.	Nitroglycerin	152-165	aldehyde dehydrogenase 2 family member	Homo sapiens	56-61
16837148-6	2007	In experiment II, EC-SOD levels were examined in NTg-CMEF and Tg-CMEF at 0, 2 and 4 days obtained from EC-SOD transgenic mice generated in our laboratory.	Nitroglycerin	49-52	superoxide dismutase 3, extracellular	Mus musculus	18-24
16806230-4	2007	HDL fractions from both CETP Tg and from nTg mice were removed faster from the plasma of CETP expressing than from nTg mice, suggesting a direct role of CETP in accelerating tissue CE uptake.	Nitroglycerin	41-44	cholesteryl ester transfer protein	Homo sapiens	89-93
16806230-4	2007	HDL fractions from both CETP Tg and from nTg mice were removed faster from the plasma of CETP expressing than from nTg mice, suggesting a direct role of CETP in accelerating tissue CE uptake.	Nitroglycerin	41-44	cholesteryl ester transfer protein	Homo sapiens	89-93
17220910-10	2007	CONCLUSIONS AND IMPLICATIONS: Our results support the crucial role of ALDH-2 in bioactivating highly reactive nitrates like GTN, PETN and PETriN.	Nitroglycerin	124-127	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	70-76
17322376-6	2007	Treatment with GTN during the hy-poxia/reoxygenation cycle blocked the increases in the number of TUNEL-positive nuclei and in the levels of 4-hydroxynonenal, nitrotyrosine, and active caspase-3.	Nitroglycerin	15-18	caspase 3	Homo sapiens	185-194
17329906-2	2007	We have previously reported that cytochrome P450 (P450) plays important role in NO generation from other organic nitrates such as nitroglycerin (NTG) and isosorbide dinitrate (ISDN).	Nitroglycerin	130-143	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	33-48
17329906-2	2007	We have previously reported that cytochrome P450 (P450) plays important role in NO generation from other organic nitrates such as nitroglycerin (NTG) and isosorbide dinitrate (ISDN).	Nitroglycerin	145-148	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	33-48
17160421-6	2007	RESULTS: Both NTG and POAG patients differed from controls in the IC-1 response to the superior quadrants, and POAG patients also differed from controls in the centre.	Nitroglycerin	14-17	ICR1 differentially methylated region	Homo sapiens	66-70
17102135-3	2007	We have recently shown that mitochondria are an important source of nitroglycerin-induced oxidants and that the nitroglycerin-bioactivating mitochondrial aldehyde dehydrogenase is oxidatively inactivated in the setting of tolerance.	Nitroglycerin	112-125	aldehyde dehydrogenase 2 family member	Rattus norvegicus	140-176
17160421-7	2007	The most sensitive parameter was the IC-1 of the superior temporal quadrant with an area under the ROC curve of 0.82 for POAG and 0.79 for NTG.	Nitroglycerin	139-142	ICR1 differentially methylated region	Homo sapiens	37-41
17160421-9	2007	When all five response averages of the IC-1 were taken into consideration 90% of the NTG patients and 85% of the POAG patients were correctly classified as abnormal while 80% of the control subjects were correctly classified as normal.	Nitroglycerin	85-88	ICR1 differentially methylated region	Homo sapiens	39-43
17678972-8	2007	These data support the hypothesis that NTG administration is capable of activating the COX-2 pathway within cerebral areas.	Nitroglycerin	39-42	prostaglandin-endoperoxide synthase 2	Homo sapiens	87-92
17678976-0	2007	Neuroprotective effect of nitroglycerin in a rodent model of ischemic stroke: evaluation of Bcl-2 expression.	Nitroglycerin	26-39	BCL2, apoptosis regulator	Rattus norvegicus	92-97
17162147-8	2006	In patients with CKD, HOMA score and SBP were associated negatively with FMD (model R(2) = 0.28; P &lt; 0.001), and SBP and waist-hip ratio were associated negatively with GTN-mediated dilatation (model R(2) = 0.25; P &lt; 0.001).	Nitroglycerin	172-175	selenium binding protein 1	Homo sapiens	116-119
16897600-1	2007	Nitroglycerin, often used as a migraine model, results in increased number of c-fos immunoreactive secondary sensory neurons in the caudal trigeminal nucleus.	Nitroglycerin	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
16897600-4	2007	Systemic kynurenine + probenecid treatment significantly diminishes nitroglycerin-induced increase of c-fos immunoreactivity in the brainstem.	Nitroglycerin	68-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-107
17880809-10	2007	The detection of proapoptotic molecules showed higher expression of Bak (++/+) and Bax (+) in Graves" thyroid tissues while Bax was in trace amount in NTNG (0/+) and TNG (0/+).	Nitroglycerin	152-155	BCL2 associated X, apoptosis regulator	Homo sapiens	124-127
17053193-9	2006	We propose that, following prolonged treatment with GTN in addition to ALDH-2, complex I is a target for mitochondrially generated reactive oxygen species.	Nitroglycerin	52-55	aldehyde dehydrogenase 2 family member	Homo sapiens	71-77
17603667-3	2006	Nitroglycerine infusion before the reperfusion period decreased the concentration of LPO products, increased activity of the antioxidant system, and improved liver function.	Nitroglycerin	0-14	lactoperoxidase	Oryctolagus cuniculus	85-88
17121895-3	2006	EXPERIMENTAL DESIGN: Seventeen patients with operable lung adenocarcinoma and stable angina pectoris were selected to investigate the effects of nitroglycerin on immunoreactivity for hypoxia-inducible factor 1alpha (HIF-1alpha), vascular endothelial growth factor (VEGF), P-glycoprotein (P-gp), the production of which is regulated by HIF-1, and p53 proteins in their resected tumor by semiquantitative immunohistochemical analyses.	Nitroglycerin	145-158	hypoxia inducible factor 1 subunit alpha	Homo sapiens	183-214
17121895-5	2006	Furthermore, to study the relationship between changes in plasma VEGF levels by nitroglycerin treatment and response to DCb, 29 patients with advanced lung adenocarcinoma were treated with nitroglycerin for 3 days before chemotherapy using DCb.	Nitroglycerin	80-93	vascular endothelial growth factor A	Homo sapiens	65-69
17121895-6	2006	RESULTS: The rates of immunoreactive cells for HIF-1alpha, VEGF, and P-gp in tumor tissues treated with nitroglycerin were lower than those without nitroglycerin, but those for p53 were not different between those treated with and without nitroglycerin.	Nitroglycerin	104-117	hypoxia inducible factor 1 subunit alpha	Homo sapiens	47-57
17121895-6	2006	RESULTS: The rates of immunoreactive cells for HIF-1alpha, VEGF, and P-gp in tumor tissues treated with nitroglycerin were lower than those without nitroglycerin, but those for p53 were not different between those treated with and without nitroglycerin.	Nitroglycerin	104-117	vascular endothelial growth factor A	Homo sapiens	59-63
17121895-6	2006	RESULTS: The rates of immunoreactive cells for HIF-1alpha, VEGF, and P-gp in tumor tissues treated with nitroglycerin were lower than those without nitroglycerin, but those for p53 were not different between those treated with and without nitroglycerin.	Nitroglycerin	104-117	ATP binding cassette subfamily B member 1	Homo sapiens	69-73
17121895-8	2006	The magnitude of decrease in plasma VEGF levels after treatment with nitroglycerin was significantly associated with response to DCb in patients with advanced lung adenocarcinoma.	Nitroglycerin	69-82	vascular endothelial growth factor A	Homo sapiens	36-40
17121895-9	2006	CONCLUSIONS: Nitroglycerin treatment may improve response to DCb in patients with lung adenocarcinoma, partly through decreasing VEGF and P-gp production via reduction of HIF-1alpha.	Nitroglycerin	13-26	vascular endothelial growth factor A	Homo sapiens	129-133
17121895-9	2006	CONCLUSIONS: Nitroglycerin treatment may improve response to DCb in patients with lung adenocarcinoma, partly through decreasing VEGF and P-gp production via reduction of HIF-1alpha.	Nitroglycerin	13-26	ATP binding cassette subfamily B member 1	Homo sapiens	138-142
17121895-9	2006	CONCLUSIONS: Nitroglycerin treatment may improve response to DCb in patients with lung adenocarcinoma, partly through decreasing VEGF and P-gp production via reduction of HIF-1alpha.	Nitroglycerin	13-26	hypoxia inducible factor 1 subunit alpha	Homo sapiens	171-181
17055381-1	2006	The mitochondrial aldehyde dehydrogenase (ALDH2, mtALDH) was recently found to catalyze the reduction of nitroglycerin (glyceryl trinitrate [GTN]) to generate nitrite and 1,2-glyceryl dinitrate.	Nitroglycerin	105-118	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	42-47
17092343-3	2006	METHODS: Tolerance was induced by infusion of wild type (WT) and heterozygous manganese superoxide dismutase mice (Mn-SOD+/-) with ethanolic solution of GTN (12.5 mug/min/kg for 4 d).	Nitroglycerin	153-156	superoxide dismutase 2, mitochondrial	Mus musculus	115-124
17092343-7	2006	RESULTS: Chronic GTN infusion lead to impaired vascular responses to GTN and acetylcholine (ACh), increased the ROS formation in mitochondria and decreased ALDH-2 activity in Mn-SOD+/- mice.	Nitroglycerin	17-20	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	156-162
17092343-7	2006	RESULTS: Chronic GTN infusion lead to impaired vascular responses to GTN and acetylcholine (ACh), increased the ROS formation in mitochondria and decreased ALDH-2 activity in Mn-SOD+/- mice.	Nitroglycerin	17-20	superoxide dismutase 2, mitochondrial	Mus musculus	175-184
17055381-1	2006	The mitochondrial aldehyde dehydrogenase (ALDH2, mtALDH) was recently found to catalyze the reduction of nitroglycerin (glyceryl trinitrate [GTN]) to generate nitrite and 1,2-glyceryl dinitrate.	Nitroglycerin	120-139	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	42-47
17055381-1	2006	The mitochondrial aldehyde dehydrogenase (ALDH2, mtALDH) was recently found to catalyze the reduction of nitroglycerin (glyceryl trinitrate [GTN]) to generate nitrite and 1,2-glyceryl dinitrate.	Nitroglycerin	141-144	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	42-47
16864608-6	2006	Perfusion with PGI2, at variance from NTG and Ado, increased ADSC delivery and entrance into the myocardial interstitium without affecting ventricular or metabolic functions and CF (engrafted ADSCs, as percentage of control, at doses producing 50% of maximum vasodilation: PGI2: 220+/-12, P &lt; 0.001; NTG: 110+/-8, P = N.S.	Nitroglycerin	38-41	prostaglandin I receptor (IP)	Mus musculus	15-19
16978603-6	2006	The Cu/Zn SOD inhibitor, diethyldithiocarbamic acid (DETCA; 8 mM), inhibited the relaxation of intact and denuded mucosa stomach fundus to UV light irradiation, EFS, NO and nitroglycerin but not those to isoproterenol.	Nitroglycerin	173-186	superoxide dismutase 1, soluble	Mus musculus	4-13
17030184-4	2006	RESULTS: GTN induces beta-catenin degradation and down-regulates its transcriptional activity in colon cancer cells.	Nitroglycerin	9-12	catenin beta 1	Homo sapiens	21-33
17030184-5	2006	This effect is preceded by GTN-induced tyrosine nitration of beta-catenin, together with its dephosphorylation on serine 33, 37, and 45 and threonine 41.	Nitroglycerin	27-30	catenin beta 1	Homo sapiens	61-73
17030184-6	2006	GTN-induced beta-catenin degradation involves proteases that are sensitive to a broad-spectrum caspase inhibitor, z-VAD-fmk, and to serine protease inhibitors N-tosyl-L-phenylalaline chloromethyl ketone (TPCK) and [4-(2-aminoethyl)-benzenesulfonylfluoride] (AEBSF), whereas the ubiquitin/proteasome pathway is not involved.	Nitroglycerin	0-3	catenin beta 1	Homo sapiens	12-24
17030184-7	2006	Interestingly, only TPCK and AEBSF restore beta-catenin transcriptional activity and preserve beta-catenin nuclear localization in GTN-treated colon cancer cells.	Nitroglycerin	131-134	catenin beta 1	Homo sapiens	94-106
16864608-6	2006	Perfusion with PGI2, at variance from NTG and Ado, increased ADSC delivery and entrance into the myocardial interstitium without affecting ventricular or metabolic functions and CF (engrafted ADSCs, as percentage of control, at doses producing 50% of maximum vasodilation: PGI2: 220+/-12, P &lt; 0.001; NTG: 110+/-8, P = N.S.	Nitroglycerin	303-306	prostaglandin I receptor (IP)	Mus musculus	15-19
16972651-13	2006	CONCLUSION: His26Asp mutation in the optineurin gene showed low penetrance in a Japanese family with NTG.	Nitroglycerin	101-104	optineurin	Homo sapiens	37-47
16886948-0	2006	Sumatriptan causes parallel decrease in plasma CGRP concentration and migraine headache during nitroglycerin-induced migraine attack.	Nitroglycerin	95-108	calcitonin related polypeptide alpha	Homo sapiens	47-51
16720755-0	2006	Biotransformation of glyceryl trinitrate by rat hepatic microsomal glutathione S-transferase 1.	Nitroglycerin	21-40	microsomal glutathione S-transferase 1	Rattus norvegicus	56-94
16720755-2	2006	We therefore compared the denitration of glyceryl trinitrate (GTN) by purified rat liver MGST1 and cytosolic GSTs.	Nitroglycerin	41-60	microsomal glutathione S-transferase 1	Rattus norvegicus	89-94
16720755-2	2006	We therefore compared the denitration of glyceryl trinitrate (GTN) by purified rat liver MGST1 and cytosolic GSTs.	Nitroglycerin	62-65	microsomal glutathione S-transferase 1	Rattus norvegicus	89-94
16720755-3	2006	Both MGST1 and cytosolic GSTs catalyzed the denitration of GTN, but the activity of MGST1 toward GTN was 2- to 3-fold higher.	Nitroglycerin	59-62	microsomal glutathione S-transferase 1	Rattus norvegicus	5-10
16720755-3	2006	Both MGST1 and cytosolic GSTs catalyzed the denitration of GTN, but the activity of MGST1 toward GTN was 2- to 3-fold higher.	Nitroglycerin	97-100	microsomal glutathione S-transferase 1	Rattus norvegicus	84-89
16720755-5	2006	Both oxidants and nitrating reagents increased the activity of MGST1 toward the GST substrate, 1-chloro-2,4-dinitrobenzene (CDNB) whereas these treatments inhibited GTN denitration by MGST1.	Nitroglycerin	165-168	microsomal glutathione S-transferase 1	Rattus norvegicus	63-68
16720755-5	2006	Both oxidants and nitrating reagents increased the activity of MGST1 toward the GST substrate, 1-chloro-2,4-dinitrobenzene (CDNB) whereas these treatments inhibited GTN denitration by MGST1.	Nitroglycerin	165-168	microsomal glutathione S-transferase 1	Rattus norvegicus	184-189
16720755-6	2006	Alkylation of the sole cysteine residue of MGST1 by N-ethylmaleimide markedly increased enzyme activity with CDNB as substrate but decreased the rate of GTN denitration.	Nitroglycerin	153-156	microsomal glutathione S-transferase 1	Rattus norvegicus	43-48
16720755-7	2006	In aortic microsomes from GTN-tolerant animals, there was a decreased abundance of MGST1 dimers and trimers.	Nitroglycerin	26-29	microsomal glutathione S-transferase 1	Rattus norvegicus	83-88
16720755-9	2006	Collectively, these data indicate that MGST1 contributes significantly to the biotransformation of GTN and that chemical modification of the microsomal enzyme has differential effects on the catalytic activity toward different substrates.	Nitroglycerin	99-102	microsomal glutathione S-transferase 1	Rattus norvegicus	39-44
16864937-4	2006	The frequencies of SstI major allele (S1) and minor allele (S2) of ApoCIII were 66.1% and 33.9% in HTG and 73.6% and 26.4% in NTG (p&lt;0.1).	Nitroglycerin	126-129	apolipoprotein C3	Homo sapiens	67-74
16765342-6	2006	Gastric ulceration was occurred in a rat in Group L. Malondialdehyde, TNF-alpha, and IL-6 levels decreased in NTG and L-NTG groups, whereas catalase and glutathion levels increased in NTG, L and L-NTG groups compared to control group (p &lt; 0.05).	Nitroglycerin	110-113	tumor necrosis factor	Rattus norvegicus	70-79
16765342-6	2006	Gastric ulceration was occurred in a rat in Group L. Malondialdehyde, TNF-alpha, and IL-6 levels decreased in NTG and L-NTG groups, whereas catalase and glutathion levels increased in NTG, L and L-NTG groups compared to control group (p &lt; 0.05).	Nitroglycerin	110-113	interleukin 6	Rattus norvegicus	85-89
16765342-6	2006	Gastric ulceration was occurred in a rat in Group L. Malondialdehyde, TNF-alpha, and IL-6 levels decreased in NTG and L-NTG groups, whereas catalase and glutathion levels increased in NTG, L and L-NTG groups compared to control group (p &lt; 0.05).	Nitroglycerin	120-123	tumor necrosis factor	Rattus norvegicus	70-79
16765342-6	2006	Gastric ulceration was occurred in a rat in Group L. Malondialdehyde, TNF-alpha, and IL-6 levels decreased in NTG and L-NTG groups, whereas catalase and glutathion levels increased in NTG, L and L-NTG groups compared to control group (p &lt; 0.05).	Nitroglycerin	120-123	interleukin 6	Rattus norvegicus	85-89
16622039-9	2006	In vivo, GTN exposure significantly increased the percentage of circulating cells expressing the EPC marker CD34 and increased the susceptibility of expanded EPCs to apoptosis but had no impact on the phenotypic differentiation or migration of EPCs.	Nitroglycerin	9-12	CD34 molecule	Homo sapiens	108-112
16182446-3	2006	Phosphorylated Ng reduces the affinity of Ng to bind CaM, which may affect the activities of calmodulin-dependent downstream enzymes, such as nitric oxide synthase (NOS), CaM-dependent protein kinase II (CaMKII) and adenylate cyclase (AC).	Nitroglycerin	15-17	calmodulin 2	Mus musculus	53-56
16554355-2	2006	In this study, we examined the effects of NG-acylated imidazolylpropylguanidines substituted with a single phenyl or cyclohexyl substituent on H1R and H2R species isoforms expressed in Sf9 insect cells.	Nitroglycerin	42-44	histamine receptor H1	Homo sapiens	143-146
16554355-2	2006	In this study, we examined the effects of NG-acylated imidazolylpropylguanidines substituted with a single phenyl or cyclohexyl substituent on H1R and H2R species isoforms expressed in Sf9 insect cells.	Nitroglycerin	42-44	histamine receptor H2	Homo sapiens	151-154
16775503-13	2006	We conclude that delayed PC through transdermal nitroglycerin application increases the production of the endocannabinoid 2-AG which elicits protective effects against myocardial infarction via CB1 cannabinoid receptors which represents one new mechanism of NO-mediated PC.	Nitroglycerin	48-61	cannabinoid receptor 1	Rattus norvegicus	194-197
16424150-6	2006	Differently from NOBA, GTN is also metabolized in blood plasma and more quickly metabolized by different GST isoforms in liver cytosol.	Nitroglycerin	23-26	glutathione S-transferase kappa 1	Homo sapiens	105-108
16111685-7	2006	The results demonstrated that (i) E2 esterification occurring mainly in HDL3 was significantly more efficient in HTG-HDL3 compared to NTG-HDL3, (ii) triglyceride content in HDL3 correlated positively with E2 esterification rate, and (iii) addition of both exogenous LCAT and E2 into the incubation prolonged lag time of HDL3 oxidation.	Nitroglycerin	134-137	HDL3	Homo sapiens	72-76
16446342-8	2006	CONCLUSION: Use of nitroglycerin combined with vinorelbine and cisplatin may improve overall response and TTP in patients with stage IIIB/IV NSCLC.	Nitroglycerin	19-32	ZFP36 ring finger protein	Homo sapiens	106-109
16520233-9	2006	Cardiac P450 expression (CYP1A2) assessed by immunoblotting, markedly decreased 48 h after NTG administration in control rats.	Nitroglycerin	91-94	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	25-31
16520233-15	2006	NTG markedly reduced the vasodilator-stimulated phosphoprotein (VASP) serine 239 phosphorylation (specific substrate of cGMP-activated protein kinase I; cGK-I) in tolerant hearts.	Nitroglycerin	0-3	vasodilator-stimulated phosphoprotein	Rattus norvegicus	25-62
16520233-15	2006	NTG markedly reduced the vasodilator-stimulated phosphoprotein (VASP) serine 239 phosphorylation (specific substrate of cGMP-activated protein kinase I; cGK-I) in tolerant hearts.	Nitroglycerin	0-3	vasodilator-stimulated phosphoprotein	Rattus norvegicus	64-68
16633087-9	2006	Diminished relaxation to GTN is partially restored after removing endothelium or L(G)-nitro-L-arginine (L-NOARG, 10 M) or superoxide dismutase (20 and 200 U/mL) or catalase (200 U/mL) pretreatments.	Nitroglycerin	25-28	catalase	Homo sapiens	122-172
16440063-0	2006	Mitochondrial aldehyde dehydrogenase-2 (ALDH2) Glu504Lys polymorphism contributes to the variation in efficacy of sublingual nitroglycerin.	Nitroglycerin	125-138	aldehyde dehydrogenase 2 family member	Homo sapiens	40-45
16440063-2	2006	Recently, it was shown that mitochondrial aldehyde dehydrogenase-2 (ALDH2) is responsible for formation of NO, the metabolite needed for GTN efficacy.	Nitroglycerin	137-140	aldehyde dehydrogenase 2 family member	Homo sapiens	68-73
16440063-3	2006	In the present study, we show that the common G-to-A polymorphism in exon 12 of ALDH2--resulting in a Glu504Lys replacement that virtually eliminates ALDH2 activity in both heterozygotes and homozygotes--is associated with a lack of efficacy of sublingual GTN in Chinese subjects.	Nitroglycerin	256-259	aldehyde dehydrogenase 2 family member	Homo sapiens	80-85
16440063-3	2006	In the present study, we show that the common G-to-A polymorphism in exon 12 of ALDH2--resulting in a Glu504Lys replacement that virtually eliminates ALDH2 activity in both heterozygotes and homozygotes--is associated with a lack of efficacy of sublingual GTN in Chinese subjects.	Nitroglycerin	256-259	aldehyde dehydrogenase 2 family member	Homo sapiens	150-155
16182446-3	2006	Phosphorylated Ng reduces the affinity of Ng to bind CaM, which may affect the activities of calmodulin-dependent downstream enzymes, such as nitric oxide synthase (NOS), CaM-dependent protein kinase II (CaMKII) and adenylate cyclase (AC).	Nitroglycerin	15-17	calmodulin 2	Mus musculus	93-103
16182446-3	2006	Phosphorylated Ng reduces the affinity of Ng to bind CaM, which may affect the activities of calmodulin-dependent downstream enzymes, such as nitric oxide synthase (NOS), CaM-dependent protein kinase II (CaMKII) and adenylate cyclase (AC).	Nitroglycerin	15-17	nitric oxide synthase 1, neuronal	Mus musculus	142-163
16182446-3	2006	Phosphorylated Ng reduces the affinity of Ng to bind CaM, which may affect the activities of calmodulin-dependent downstream enzymes, such as nitric oxide synthase (NOS), CaM-dependent protein kinase II (CaMKII) and adenylate cyclase (AC).	Nitroglycerin	15-17	calmodulin 2	Mus musculus	171-174
16182446-3	2006	Phosphorylated Ng reduces the affinity of Ng to bind CaM, which may affect the activities of calmodulin-dependent downstream enzymes, such as nitric oxide synthase (NOS), CaM-dependent protein kinase II (CaMKII) and adenylate cyclase (AC).	Nitroglycerin	42-44	calmodulin 2	Mus musculus	53-56
16182446-3	2006	Phosphorylated Ng reduces the affinity of Ng to bind CaM, which may affect the activities of calmodulin-dependent downstream enzymes, such as nitric oxide synthase (NOS), CaM-dependent protein kinase II (CaMKII) and adenylate cyclase (AC).	Nitroglycerin	42-44	calmodulin 2	Mus musculus	93-103
16182446-3	2006	Phosphorylated Ng reduces the affinity of Ng to bind CaM, which may affect the activities of calmodulin-dependent downstream enzymes, such as nitric oxide synthase (NOS), CaM-dependent protein kinase II (CaMKII) and adenylate cyclase (AC).	Nitroglycerin	42-44	nitric oxide synthase 1, neuronal	Mus musculus	142-163
16182446-3	2006	Phosphorylated Ng reduces the affinity of Ng to bind CaM, which may affect the activities of calmodulin-dependent downstream enzymes, such as nitric oxide synthase (NOS), CaM-dependent protein kinase II (CaMKII) and adenylate cyclase (AC).	Nitroglycerin	42-44	calmodulin 2	Mus musculus	171-174
16155108-4	2006	MHC-PPARalpha hearts had significantly higher FAO rates during aerobic and postischemic reperfusion (aerobic 1,479 +/- 171 vs. 699 +/- 117, reperfusion 1,062 +/- 214 vs. 601 +/- 70 nmol x g dry wt(-1) x min(-1); P &lt; 0.05) and significantly lower glucose oxidation rates compared with NTG hearts (aerobic 225 +/- 36 vs. 1,563 +/- 165, reperfusion 402 +/- 54 vs. 1,758 +/- 165 nmol x g dry wt(-1) x min(-1); P &lt; 0.05).	Nitroglycerin	287-290	peroxisome proliferator activated receptor alpha	Mus musculus	4-13
16155108-6	2006	Increased FAO rates in MHC-PPARalpha hearts were associated with a markedly lower recovery of cardiac power (45 +/- 9% vs. 71 +/- 6% of preischemic levels in NTG hearts; P &lt; 0.05).	Nitroglycerin	158-161	peroxisome proliferator activated receptor alpha	Mus musculus	27-36
17083157-8	2006	In NTG group triglyceride concentrations, as well as BMI in early pregnancy and at the time of sampling were significant predictors, explaining together 62% of the variance in TNF-alpha concentration.	Nitroglycerin	3-6	tumor necrosis factor	Homo sapiens	176-185
17303920-10	2006	By manipulating GSTs, physiological tolerance to NTG may be diminished or eliminated.	Nitroglycerin	49-52	glutathione S-transferase alpha 4	Homo sapiens	16-20
16157314-6	2006	Mice lacking iNOS exhibited a decrease in resting indices of cardiac function as well as an impairment in the positive inotropic actions of isoproterenol following treatment with ADR compared to nTg mice.	Nitroglycerin	195-198	nitric oxide synthase 2, inducible	Mus musculus	13-17
17303920-3	2006	Our previous work showed that an alpha-class glutathione-S-transferase (GSTA4-4) defends against oxidative damage in the vascular wall; therefore, we asked whether overexpression of GSTA4-4 in endothelial cells and smooth muscle cells might alter the development of tolerance to NTG.	Nitroglycerin	279-282	glutathione S-transferase alpha 4	Homo sapiens	72-79
17303920-6	2006	Endothelial cells overexpressing mGSTA4-4, and smooth muscle cells overexpressing hGSTA4-4 were more resistant to cytotoxic injury by NTG, assessed at 24 h (p &lt; 0.05).	Nitroglycerin	134-137	glutathione S-transferase, alpha 4	Mus musculus	33-41
17303920-6	2006	Endothelial cells overexpressing mGSTA4-4, and smooth muscle cells overexpressing hGSTA4-4 were more resistant to cytotoxic injury by NTG, assessed at 24 h (p &lt; 0.05).	Nitroglycerin	134-137	glutathione S-transferase alpha 4	Homo sapiens	82-90
17303920-8	2006	Following dosing in a relevant tolerance-inducing NTG protocol, we found that GSTA4-4-overexpressing cells demonstrated significant downregulation of NOS enzymes; NO release, unchanged by the tolerance protocol in both wild-type and vector-transfected cells, was augmented in GST-overexpressing cells (p &lt; 0.01); cGMP levels in control cells fell, whereas it rose in GSTA4-4-overexpressing cells (p &lt; 0.05).	Nitroglycerin	50-53	glutathione S-transferase alpha 4	Homo sapiens	78-85
16024565-10	2005	Only NTG hearts demonstrated a significant increase in cTnI phosphorylation.	Nitroglycerin	5-8	troponin I, cardiac 3	Mus musculus	55-59
16462911-0	2005	Glyceryl trinitrate-induced angiotensin-converting enzyme (ACE) inhibition in healthy volunteers is dependent on ACE genotype.	Nitroglycerin	0-19	angiotensin I converting enzyme	Homo sapiens	28-57
16462911-0	2005	Glyceryl trinitrate-induced angiotensin-converting enzyme (ACE) inhibition in healthy volunteers is dependent on ACE genotype.	Nitroglycerin	0-19	angiotensin I converting enzyme	Homo sapiens	59-62
16462911-0	2005	Glyceryl trinitrate-induced angiotensin-converting enzyme (ACE) inhibition in healthy volunteers is dependent on ACE genotype.	Nitroglycerin	0-19	angiotensin I converting enzyme	Homo sapiens	113-116
16462911-2	2005	The aim of this study was to investigate if nitric oxide (NO), generated from glyceryl trinitrate (GTN), affects human serum ACE activity in vivo, and if so, whether this effect was dependent on ACE genotype and (or) reflected in blood pressure reduction.	Nitroglycerin	99-102	angiotensin I converting enzyme	Homo sapiens	125-128
16462911-6	2005	Sixty minutes after GTN administration, serum ACE activity was reduced in individuals with the insertion/insertion (II) and insertion/deletion (ID) genotypes, but not the DD genotype.	Nitroglycerin	20-23	angiotensin I converting enzyme	Homo sapiens	46-49
16462911-9	2005	In conclusion, GTN inhibits serum ACE in vivo in individuals with the II and ID, but not the DD genotype.	Nitroglycerin	15-18	angiotensin I converting enzyme	Homo sapiens	34-37
16006548-6	2005	In iNOS-/- mice, however, the late PC effect elicited by DETA/NO, NTG, SNAP, TAN-670, and CCPA was completely abrogated.	Nitroglycerin	66-69	nitric oxide synthase 2, inducible	Mus musculus	3-7
16119201-4	2005	Studies reported here show that the red cell activity of antioxidant enzymes, catalase and glutathione peroxidase, are significantly decreased after intravenous nitroglycerin treatment.	Nitroglycerin	161-174	catalase	Homo sapiens	78-86
16140321-7	2005	3-[4, 5-Dimethylthiazol-2-yl]-2, 5-diphenyltetrazolium bromide (MTT) assay showed that basal level of mitochondrial function was lower in MnSOD(+/-) cardiomyocytes than in NTg or TgH, and that MnSOD(+/-) was more sensitive to ADR.	Nitroglycerin	172-175	superoxide dismutase 2, mitochondrial	Mus musculus	138-143
16140321-7	2005	3-[4, 5-Dimethylthiazol-2-yl]-2, 5-diphenyltetrazolium bromide (MTT) assay showed that basal level of mitochondrial function was lower in MnSOD(+/-) cardiomyocytes than in NTg or TgH, and that MnSOD(+/-) was more sensitive to ADR.	Nitroglycerin	172-175	superoxide dismutase 2, mitochondrial	Mus musculus	138-148
16259771-5	2005	The slower CL(NR) of DA-8159 could have been due to the inhibition of the metabolism of DA-8159 by nitroglycerin, since DA-8159 is metabolized via CYP3A1/2 in rats and nitroglycerin inhibits CYP3A1/2 in rats.	Nitroglycerin	99-112	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	147-153
16259771-5	2005	The slower CL(NR) of DA-8159 could have been due to the inhibition of the metabolism of DA-8159 by nitroglycerin, since DA-8159 is metabolized via CYP3A1/2 in rats and nitroglycerin inhibits CYP3A1/2 in rats.	Nitroglycerin	99-112	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	191-197
16226933-11	2005	Recent experimental work has defined new tolerance mechanisms, including inhibition of the enzyme that bioactivates NTG (ie, mitochondrial aldehyde dehydrogenase isoform 2 [ALDH2]) and mitochondria as potential sources of ROS.	Nitroglycerin	116-119	aldehyde dehydrogenase 2 family member	Homo sapiens	173-178
16226933-12	2005	NTG-induced ROS inhibit the bioactivation of NTG by ALDH2.	Nitroglycerin	0-3	aldehyde dehydrogenase 2 family member	Homo sapiens	52-57
16226933-12	2005	NTG-induced ROS inhibit the bioactivation of NTG by ALDH2.	Nitroglycerin	45-48	aldehyde dehydrogenase 2 family member	Homo sapiens	52-57
16226933-13	2005	Both mechanisms increase oxidative stress and impair NTG bioactivation, and now converge at the level of ALDH2 to support a new theory for NTG tolerance and NTG-induced endothelial dysfunction.	Nitroglycerin	139-142	aldehyde dehydrogenase 2 family member	Homo sapiens	105-110
16226933-13	2005	Both mechanisms increase oxidative stress and impair NTG bioactivation, and now converge at the level of ALDH2 to support a new theory for NTG tolerance and NTG-induced endothelial dysfunction.	Nitroglycerin	139-142	aldehyde dehydrogenase 2 family member	Homo sapiens	105-110
16195486-10	2005	The consequences of these processes for the nitroglycerin downstream targets soluble guanylyl cyclase, cGMP-dependent protein kinase, cGMP-degrading phosphodiesterases, and toxic side effects contributing to endothelial dysfunction, such as inhibition of prostacyclin synthase, are discussed in this review.	Nitroglycerin	44-57	prostaglandin I2 synthase	Homo sapiens	255-276
16051882-0	2005	Aldehyde dehydrogenase 2 plays a role in the bioactivation of nitroglycerin in humans.	Nitroglycerin	62-75	aldehyde dehydrogenase 2 family member	Homo sapiens	0-24
16051882-4	2005	We investigated the role of ALDH2 in the vascular effects of nitroglycerin (NTG) in humans in vivo.	Nitroglycerin	61-74	aldehyde dehydrogenase 2 family member	Homo sapiens	28-33
16051882-8	2005	Separately, 11 subjects of East Asian origin, with the loss-of-function glu504lys mutation in the ALDH2 gene, received intra-arterial NTG, SNP, and verapamil.	Nitroglycerin	134-137	aldehyde dehydrogenase 2 family member	Homo sapiens	98-103
16051882-10	2005	CONCLUSIONS: The findings suggest that ALDH2 is involved in the bioactivation of NTG in humans in vivo but accounts for less than half of the total bioactivation.	Nitroglycerin	81-84	aldehyde dehydrogenase 2 family member	Homo sapiens	39-44
17162860-5	2005	RESULTS: The levels of renin of NTG patients and normal controls are (769.085+/-183.217) pg/ml/n and (822.035+/-124.140) pg/ml/n, while the levels of angiotensin A II of NTG patients and normal controls are (37.347+/-10.669) pg/ml and (24.836+/-10.665) pg/ml respectively.	Nitroglycerin	32-35	renin	Homo sapiens	23-28
17162860-5	2005	RESULTS: The levels of renin of NTG patients and normal controls are (769.085+/-183.217) pg/ml/n and (822.035+/-124.140) pg/ml/n, while the levels of angiotensin A II of NTG patients and normal controls are (37.347+/-10.669) pg/ml and (24.836+/-10.665) pg/ml respectively.	Nitroglycerin	170-173	renin	Homo sapiens	23-28
15855227-7	2005	Only LPS-treated NTG hearts showed a significant increase in cTnI phosphorylation.	Nitroglycerin	17-20	troponin I, cardiac 3	Mus musculus	61-65
15976786-10	2005	CONCLUSIONS: Use of morphine either alone or in combination with nitroglycerin for patients presenting with NSTE ACS was associated with higher mortality even after risk adjustment and matching on propensity score for treatment.	Nitroglycerin	65-78	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	113-116
15904666-6	2005	We further demonstrate that, in addition to the TX-100 resistance at 4 degrees C, Can1p and Pma1pa exhibit different accessibility to nonyl glucoside (NG), which points to distinct intimate lipid surroundings of these two proteins.	Nitroglycerin	151-153	arginine permease CAN1	Saccharomyces cerevisiae S288C	82-87
16247215-0	2005	Low-renin (volume dependent) mild-hypertensive patients have impaired flow-mediated and glyceryl-trinitrate stimulated vascular reactivity.	Nitroglycerin	88-107	renin	Homo sapiens	4-9
16247215-13	2005	CONCLUSION: This study showed impaired FMD and reduced GTN response in mildly hypertensive patients with low-renin plasma levels.	Nitroglycerin	55-58	renin	Homo sapiens	109-114
16237174-6	2005	Surprisingly, levels of active Fyn were lower in high expresser hAPP mice than in NTG controls and lower in FYN/hAPP mice than in FYN mice.	Nitroglycerin	82-85	Fyn proto-oncogene	Mus musculus	31-34
15936821-6	2005	A significant increase of nuclear immunostaining of p65, an indicator of NF-kappaB activation, was detected in lamina I and II of nucleus trigeminalis caudalis in rats injected with NTG when compared with the control group.	Nitroglycerin	182-185	synaptotagmin 1	Rattus norvegicus	52-55
15933216-6	2005	Aortic rings from Mn-SOD+/- mice showed normal endothelial function and vasodilator responses to GTN.	Nitroglycerin	97-100	superoxide dismutase 2, mitochondrial	Mus musculus	18-24
15933216-7	2005	In contrast, preincubation of aorta with GTN or long-term GTN infusion caused a marked higher degree of tolerance as well as endothelial dysfunction in Mn-SOD+/- compared with wild type.	Nitroglycerin	41-44	superoxide dismutase 2, mitochondrial	Mus musculus	152-158
15933216-7	2005	In contrast, preincubation of aorta with GTN or long-term GTN infusion caused a marked higher degree of tolerance as well as endothelial dysfunction in Mn-SOD+/- compared with wild type.	Nitroglycerin	58-61	superoxide dismutase 2, mitochondrial	Mus musculus	152-158
15933216-8	2005	Basal as well as GTN-stimulated ROS formation was significantly increased in isolated heart mitochondria from Mn-SOD+/- mice, correlating well with a marked decrease in ALDH-2 activity in response to in vitro and in vivo GTN treatment.	Nitroglycerin	17-20	superoxide dismutase 2, mitochondrial	Mus musculus	110-116
15933216-8	2005	Basal as well as GTN-stimulated ROS formation was significantly increased in isolated heart mitochondria from Mn-SOD+/- mice, correlating well with a marked decrease in ALDH-2 activity in response to in vitro and in vivo GTN treatment.	Nitroglycerin	17-20	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	169-175
15933216-8	2005	Basal as well as GTN-stimulated ROS formation was significantly increased in isolated heart mitochondria from Mn-SOD+/- mice, correlating well with a marked decrease in ALDH-2 activity in response to in vitro and in vivo GTN treatment.	Nitroglycerin	221-224	superoxide dismutase 2, mitochondrial	Mus musculus	110-116
15933216-8	2005	Basal as well as GTN-stimulated ROS formation was significantly increased in isolated heart mitochondria from Mn-SOD+/- mice, correlating well with a marked decrease in ALDH-2 activity in response to in vitro and in vivo GTN treatment.	Nitroglycerin	221-224	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	169-175
15933216-9	2005	The data presented indicate that deficiency in Mn-SOD leads to a higher degree of tolerance and endothelial dysfunction associated with increased mitochondrial ROS production in response to in vitro and in vivo GTN challenges.	Nitroglycerin	211-214	superoxide dismutase 2, mitochondrial	Mus musculus	47-53
15933216-10	2005	These data further point to a crucial role of ALDH-2 in mediating GTN bioactivation as well as development of GTN tolerance and underline the important contribution of ROS to these processes.	Nitroglycerin	66-69	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	46-52
15933216-10	2005	These data further point to a crucial role of ALDH-2 in mediating GTN bioactivation as well as development of GTN tolerance and underline the important contribution of ROS to these processes.	Nitroglycerin	110-113	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	46-52
16103363-1	2005	The identity of the cellular mechanisms through which nitroglycerin (glyceryl trinitrate, GTN) elicits nitric oxide (NO)-based signaling to dilate blood vessels remains one of the longest standing foci of investigation and sources of controversy in cardiovascular biology.	Nitroglycerin	54-67	guanine nucleotide binding protein, alpha transducing 3	Mus musculus	90-93
15910863-3	2005	Reductions in LDL apoB-100 production rate (PR) were also observed in these two patients compared with NTG and HTG controls.	Nitroglycerin	103-106	apolipoprotein B	Homo sapiens	18-26
16119201-5	2005	Catalase activity (739.6 +/- 92.3 k/gHb) decreased to 440.1 +/- 111.9 and 459.8 +/- 130.7 k/gHb after 1 and 24 hr GTN infusion, respectively.	Nitroglycerin	114-117	catalase	Homo sapiens	0-8
15847642-11	2005	Ser16-HSP20 phosphorylation was increased with hypoxia and nitroglycerin treatment and ser16-HSP20 phosphorylation correlated with changes in diameters (n = 29, r2 = 0.64, P &lt; 0.001).	Nitroglycerin	59-72	HSPB6	Sus scrofa	6-11
16025966-4	2005	RESULTS: The VEGF mRNA expression was significantly lower in nitric oxide synthesis inhibited model rats than that in rats non-modeled, or in model rats treated by ASC abstracts or nitroglycerin (P &lt; 0.05, P &lt; 0.01).	Nitroglycerin	181-194	vascular endothelial growth factor A	Rattus norvegicus	13-17
15870202-7	2005	Similarly, GLUT-4 translocation was significantly reduced in NTG (74 +/- 7%) and 8-Br-cGMP (120 +/- 11%), compared with control (165 +/- 17%).	Nitroglycerin	61-64	solute carrier family 2 member 4	Canis lupus familiaris	11-17
15699266-7	2005	Circulating tumor necrosis factor-alpha was significantly reduced (4.0+/-0.3 to 3.6+/-0.2 pg/mL, P=0.02); resistance vessel responses to acetylcholine, bradykinin, and verapamil were significantly enhanced; and responses to nitroglycerin and conduit-vessel vasoreactivity were unchanged after ACAT inhibition.	Nitroglycerin	224-237	tumor necrosis factor	Homo sapiens	12-39
15837093-7	2005	At the follow-up, G-CSF treated had improved in CCS classification, NTG consumption and angina attacks, but the controls only in CCS classification.	Nitroglycerin	68-71	colony stimulating factor 3	Homo sapiens	18-23
15689199-0	2005	CGRP release and c-fos expression within trigeminal nucleus caudalis of the rat following glyceryltrinitrate infusion.	Nitroglycerin	90-108	calcitonin-related polypeptide alpha	Rattus norvegicus	0-4
15689199-6	2005	Surprisingly, GTN attenuated capsaicin-induced c-fos expression by 64%.	Nitroglycerin	14-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
15689199-10	2005	Both GTN and L-NAME reduced capsaicin-induced c-fos LI.	Nitroglycerin	5-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
15851979-8	2005	CONCLUSIONS: The findings in the current study provide further evidence that MYOC and OPTN gene variants are rare causes of NTG.	Nitroglycerin	124-127	myocilin	Homo sapiens	77-81
15851979-8	2005	CONCLUSIONS: The findings in the current study provide further evidence that MYOC and OPTN gene variants are rare causes of NTG.	Nitroglycerin	124-127	optineurin	Homo sapiens	86-90
15471984-3	2005	Ventricular myocytes isolated from transgenic (TG) mice that overexpress the specific GDP dissociation inhibitor Rho GDI-alpha exhibited significantly decreased basal L-type Ca2+ current density (approximately 40%) compared with myocytes from nontransgenic (NTG) mice.	Nitroglycerin	258-261	Rho GDP dissociation inhibitor (GDI) alpha	Mus musculus	113-126
15632822-2	2005	This study compared the vasopressin-induced contraction and the effects of milrinone, nitroglycerin, and nitroprusside in vasopressin-induced contraction between the human radial artery and the internal thoracic artery to find effective antispastic methods for arterial grafts.	Nitroglycerin	86-99	arginine vasopressin	Homo sapiens	122-133
15377279-0	2005	Contribution of aldehyde dehydrogenase to mitochondrial bioactivation of nitroglycerin: evidence for the activation of purified soluble guanylate cyclase through direct formation of nitric oxide.	Nitroglycerin	73-86	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	128-153
15377279-1	2005	Vascular relaxation to GTN (nitroglycerin) and other antianginal nitrovasodilators requires bioactivation of the drugs to NO or a related activator of sGC (soluble guanylate cyclase).	Nitroglycerin	23-26	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	151-154
15377279-1	2005	Vascular relaxation to GTN (nitroglycerin) and other antianginal nitrovasodilators requires bioactivation of the drugs to NO or a related activator of sGC (soluble guanylate cyclase).	Nitroglycerin	23-26	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	156-181
15377279-1	2005	Vascular relaxation to GTN (nitroglycerin) and other antianginal nitrovasodilators requires bioactivation of the drugs to NO or a related activator of sGC (soluble guanylate cyclase).	Nitroglycerin	28-41	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	151-154
15377279-1	2005	Vascular relaxation to GTN (nitroglycerin) and other antianginal nitrovasodilators requires bioactivation of the drugs to NO or a related activator of sGC (soluble guanylate cyclase).	Nitroglycerin	28-41	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	156-181
15377279-2	2005	Conversion of GTN into 1,2-GDN (1,2-glycerol dinitrate) and nitrite by mitochondrial ALDH2 (aldehyde dehydrogenase 2) may be an essential pathway of GTN bioactivation in blood vessels.	Nitroglycerin	14-17	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	85-90
15377279-2	2005	Conversion of GTN into 1,2-GDN (1,2-glycerol dinitrate) and nitrite by mitochondrial ALDH2 (aldehyde dehydrogenase 2) may be an essential pathway of GTN bioactivation in blood vessels.	Nitroglycerin	14-17	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	92-116
15377279-2	2005	Conversion of GTN into 1,2-GDN (1,2-glycerol dinitrate) and nitrite by mitochondrial ALDH2 (aldehyde dehydrogenase 2) may be an essential pathway of GTN bioactivation in blood vessels.	Nitroglycerin	149-152	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	85-90
15377279-2	2005	Conversion of GTN into 1,2-GDN (1,2-glycerol dinitrate) and nitrite by mitochondrial ALDH2 (aldehyde dehydrogenase 2) may be an essential pathway of GTN bioactivation in blood vessels.	Nitroglycerin	149-152	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	92-116
15377279-3	2005	In the present study, we characterized the profile of GTN biotransformation by purified human liver ALDH2 and rat liver mitochondria, and we used purified sGC as a sensitive detector of GTN bioactivity to examine whether ALDH2-catalysed nitrite formation is linked to sGC activation.	Nitroglycerin	54-57	aldehyde dehydrogenase 2 family member	Homo sapiens	100-105
15377279-4	2005	In the presence of mitochondria, GTN activated sGC with an EC50 (half-maximally effective concentration) of 3.77+/-0.83 microM.	Nitroglycerin	33-36	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	47-50
15377279-5	2005	The selective ALDH2 inhibitor, daidzin (0.1 mM), increased the EC50 of GTN to 7.47+/-0.93 microM.	Nitroglycerin	71-74	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	14-19
15377279-7	2005	However, since co-incubation of sGC with purified ALDH2 led to significant stimulation of cGMP formation by GTN that was completely inhibited by 0.1 mM daidzin and NO scavengers, ALDH2 may convert GTN directly into NO or a related species.	Nitroglycerin	108-111	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	32-35
15377279-7	2005	However, since co-incubation of sGC with purified ALDH2 led to significant stimulation of cGMP formation by GTN that was completely inhibited by 0.1 mM daidzin and NO scavengers, ALDH2 may convert GTN directly into NO or a related species.	Nitroglycerin	108-111	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	50-55
15377279-7	2005	However, since co-incubation of sGC with purified ALDH2 led to significant stimulation of cGMP formation by GTN that was completely inhibited by 0.1 mM daidzin and NO scavengers, ALDH2 may convert GTN directly into NO or a related species.	Nitroglycerin	108-111	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	179-184
15377279-7	2005	However, since co-incubation of sGC with purified ALDH2 led to significant stimulation of cGMP formation by GTN that was completely inhibited by 0.1 mM daidzin and NO scavengers, ALDH2 may convert GTN directly into NO or a related species.	Nitroglycerin	197-200	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	32-35
15377279-7	2005	However, since co-incubation of sGC with purified ALDH2 led to significant stimulation of cGMP formation by GTN that was completely inhibited by 0.1 mM daidzin and NO scavengers, ALDH2 may convert GTN directly into NO or a related species.	Nitroglycerin	197-200	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	50-55
15377279-7	2005	However, since co-incubation of sGC with purified ALDH2 led to significant stimulation of cGMP formation by GTN that was completely inhibited by 0.1 mM daidzin and NO scavengers, ALDH2 may convert GTN directly into NO or a related species.	Nitroglycerin	197-200	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	179-184
15377279-8	2005	Studies with rat aortic rings suggested that ALDH2 contributes to GTN bioactivation and showed that maximal relaxation to GTN occurred at cGMP levels that were only 3.4% of the maximal levels obtained with NO.	Nitroglycerin	66-69	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	45-50
15377279-8	2005	Studies with rat aortic rings suggested that ALDH2 contributes to GTN bioactivation and showed that maximal relaxation to GTN occurred at cGMP levels that were only 3.4% of the maximal levels obtained with NO.	Nitroglycerin	122-125	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	45-50
15377279-9	2005	Comparison of sGC activation in the presence of mitochondria with cGMP accumulation in rat aorta revealed a slightly higher potency of GTN to activate sGC in vitro compared with blood vessels.	Nitroglycerin	135-138	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	14-17
15377279-9	2005	Comparison of sGC activation in the presence of mitochondria with cGMP accumulation in rat aorta revealed a slightly higher potency of GTN to activate sGC in vitro compared with blood vessels.	Nitroglycerin	135-138	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	151-154
15377279-10	2005	Our results suggest that ALDH2 catalyses the mitochondrial bioactivation of GTN by the formation of a reactive NO-related intermediate that activates sGC.	Nitroglycerin	76-79	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	25-30
15377279-10	2005	Our results suggest that ALDH2 catalyses the mitochondrial bioactivation of GTN by the formation of a reactive NO-related intermediate that activates sGC.	Nitroglycerin	76-79	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	150-153
16244377-2	2005	A commonly used NBV, glyceryl trinitrate (GTN) is bioactivated by mitochondrial, class 2 aldehyde dehydrogenase (ALDH2).	Nitroglycerin	21-40	aldehyde dehydrogenase 2 family member	Rattus norvegicus	113-118
16244377-2	2005	A commonly used NBV, glyceryl trinitrate (GTN) is bioactivated by mitochondrial, class 2 aldehyde dehydrogenase (ALDH2).	Nitroglycerin	42-45	aldehyde dehydrogenase 2 family member	Rattus norvegicus	113-118
16244377-4	2005	The GTN bioactivation step, however, inac-tivates ALDH2 and may alter the metabolism of these aldehydes.	Nitroglycerin	4-7	aldehyde dehydrogenase 2 family member	Rattus norvegicus	50-55
16244377-7	2005	GTN (1 microM) inhibited ALDH2 activity (55 +/- 6% of control) and ablated ALDH3 activity.	Nitroglycerin	0-3	aldehyde dehydrogenase 2 family member	Rattus norvegicus	25-30
16244377-7	2005	GTN (1 microM) inhibited ALDH2 activity (55 +/- 6% of control) and ablated ALDH3 activity.	Nitroglycerin	0-3	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	75-80
15494775-5	2004	RESULTS: Subjects with the eNOS Asp298 allele (n=15) showed significantly reduced FMD:GTN compared with those without this allele (n=38) (0.23+/-0.13 [mean +/- SD] versus 0.35+/-0.14, P=0.0072), whereas there was no significant difference in GTN between these two groups.	Nitroglycerin	242-245	nitric oxide synthase 3	Homo sapiens	27-31
15331769-1	2004	Mitochondrial aldehyde dehydrogenase (ALDH-2) was recently identified to be essential for the bioactivation of glyceryl trinitrate (GTN).	Nitroglycerin	111-130	aldehyde dehydrogenase 2 family member	Rattus norvegicus	0-36
15331769-1	2004	Mitochondrial aldehyde dehydrogenase (ALDH-2) was recently identified to be essential for the bioactivation of glyceryl trinitrate (GTN).	Nitroglycerin	111-130	aldehyde dehydrogenase 2 family member	Rattus norvegicus	38-44
15331769-1	2004	Mitochondrial aldehyde dehydrogenase (ALDH-2) was recently identified to be essential for the bioactivation of glyceryl trinitrate (GTN).	Nitroglycerin	132-135	aldehyde dehydrogenase 2 family member	Rattus norvegicus	0-36
15331769-1	2004	Mitochondrial aldehyde dehydrogenase (ALDH-2) was recently identified to be essential for the bioactivation of glyceryl trinitrate (GTN).	Nitroglycerin	132-135	aldehyde dehydrogenase 2 family member	Rattus norvegicus	38-44
15331769-4	2004	Likewise, benomyl decreased GTN- and PETN-elicited phosphorylation of the cGMP-activated protein kinase substrate vasodilator-stimulated phosphoprotein (VASP) but not that elicited by other nitrates.	Nitroglycerin	28-31	vasodilator-stimulated phosphoprotein	Rattus norvegicus	114-151
15331769-4	2004	Likewise, benomyl decreased GTN- and PETN-elicited phosphorylation of the cGMP-activated protein kinase substrate vasodilator-stimulated phosphoprotein (VASP) but not that elicited by other nitrates.	Nitroglycerin	28-31	vasodilator-stimulated phosphoprotein	Rattus norvegicus	153-157
15331769-6	2004	In contrast, mitochondrial ALDH-2 esterase activity was not affected by PETN and its metabolites, whereas it was inhibited by benomyl, GTN applied in vitro and in vivo, and some sulfhydryl oxidants.	Nitroglycerin	135-138	aldehyde dehydrogenase 2 family member	Rattus norvegicus	27-33
15331769-7	2004	The bioactivation-related metabolism of GTN to glyceryl-1,2-dinitrate by isolated RAW macrophages was reduced by the ALDH-2 inhibitors benomyl and daidzin, as well as by GTN at concentrations &gt;1 microM.	Nitroglycerin	40-43	aldehyde dehydrogenase 2 family member	Rattus norvegicus	117-123
15331769-8	2004	We conclude that mitochondrial ALDH-2, specifically its esterase activity, is required for the bioactivation of the organic nitrates with high vasodilator potency, such as GTN and PETN, but not for the less potent nitrates.	Nitroglycerin	172-175	aldehyde dehydrogenase 2 family member	Rattus norvegicus	31-37
15331769-9	2004	It is interesting that ALDH-2 esterase activity was inhibited by GTN only, not by the other nitrates tested.	Nitroglycerin	65-68	aldehyde dehydrogenase 2 family member	Rattus norvegicus	23-29
16106903-12	2004	Previous results of the authors supported that lower platelet serotonin concentration and higher plasma CGRP concentration, during the headache free period, are risk factors that express greater susceptibility to develop both spontaneous and nitroglycerin-induced migraine attack.	Nitroglycerin	242-255	calcitonin related polypeptide alpha	Homo sapiens	104-108
15465035-4	2004	We investigated the effect of the clinically used nitrates nitroglycerin (NTG), isosorbide dinitrate (ISDN), and sodium nitroprusside (SNP) on HIF-1-mediated transcriptional responses to hypoxia.	Nitroglycerin	59-72	hypoxia inducible factor 1 subunit alpha	Homo sapiens	143-148
15465035-4	2004	We investigated the effect of the clinically used nitrates nitroglycerin (NTG), isosorbide dinitrate (ISDN), and sodium nitroprusside (SNP) on HIF-1-mediated transcriptional responses to hypoxia.	Nitroglycerin	74-77	hypoxia inducible factor 1 subunit alpha	Homo sapiens	143-148
15205173-9	2004	CBF responses to ACh and nitroglycerin were maintained during ET-1 delivery.	Nitroglycerin	25-38	endothelin 1	Canis lupus familiaris	62-66
15494775-5	2004	RESULTS: Subjects with the eNOS Asp298 allele (n=15) showed significantly reduced FMD:GTN compared with those without this allele (n=38) (0.23+/-0.13 [mean +/- SD] versus 0.35+/-0.14, P=0.0072), whereas there was no significant difference in GTN between these two groups.	Nitroglycerin	86-89	nitric oxide synthase 3	Homo sapiens	27-31
15494775-6	2004	Although subjects with the MTHFR T677 allele did not show significantly reduced levels of FMD:GTN, subjects with the eNOS Asp298 allele and who were carriers of the MTHFR T677 allele demonstrated markedly reduced levels of FMD:GTN compared with noncarriers (0.14+/-0.05 versus 0.28+/-0.13, P=0.04).	Nitroglycerin	227-230	nitric oxide synthase 3	Homo sapiens	117-121
15494775-6	2004	Although subjects with the MTHFR T677 allele did not show significantly reduced levels of FMD:GTN, subjects with the eNOS Asp298 allele and who were carriers of the MTHFR T677 allele demonstrated markedly reduced levels of FMD:GTN compared with noncarriers (0.14+/-0.05 versus 0.28+/-0.13, P=0.04).	Nitroglycerin	227-230	methylenetetrahydrofolate reductase	Homo sapiens	165-170
15355613-0	2004	[Changes in tissue plasminogen activator and plasminogen activator inhibitor during administration of nitroglycerine into internal thoracic artery in dogs with acute myocardial ischemia].	Nitroglycerin	102-116	tissue-type plasminogen activator	Canis lupus familiaris	12-40
15336617-5	2004	Serum OPG levels were found to be significantly higher in hyperthyroid patients than in the healthy subjects (4.3 pmol/l, range: 1.6-12.0, vs. 2.2 pmol/l, range: 1.4-6.0; P &lt; 0.001), the values being higher in GD patients than TNG.	Nitroglycerin	230-233	TNF receptor superfamily member 11b	Homo sapiens	6-9
15471166-7	2004	Glyceryl trinitrate-induced dilatation was similar in the ACE group, the non-ACE group, and in the control subjects.	Nitroglycerin	0-19	angiotensin I converting enzyme	Homo sapiens	58-61
15336617-10	2004	After 6 months of MMI treatment, serum OPG concentrations decreased significantly in TNG patients (from 3.5 pmol/l, range: 1.6-8.0, to 2.3 pmol/l, range: 1.0-4.3; P &lt; 0.001), whereas a not significant change in OPG levels occurred in GD patients (from 4.8 pmol/l, range: 1.8-12.0, to 4.2 pmol/l, range: 1.0-14.0; P = 0.7).	Nitroglycerin	85-88	TNF receptor superfamily member 11b	Homo sapiens	39-42
15355613-12	2004	CONCLUSION: Introduction of nitroglycerine through internal thoracic artery under pressure is effective to accelerate release of t-PA from the endothelium while inhibit secretion of PAI, therefore it is useful to modulate the balance of fibrinolysis.	Nitroglycerin	28-42	tissue-type plasminogen activator	Canis lupus familiaris	129-133
15066953-6	2004	Sublingual administration of the NO donor glyceryl trinitrate normalized platelet VASP phosphorylation and restored markers of platelet activation to baseline levels.	Nitroglycerin	42-61	vasodilator stimulated phosphoprotein	Homo sapiens	82-86
15154853-2	2004	We found previously in rats that nitroglycerin (10 mg/kg s.c.) is able to increase significantly after 4 h the number of neuronal nitric oxide synthase (nNOS)-immunoreactive neurones in the cervical part of trigeminal nucleus caudalis.	Nitroglycerin	33-46	nitric oxide synthase 1	Rattus norvegicus	121-151
15154853-2	2004	We found previously in rats that nitroglycerin (10 mg/kg s.c.) is able to increase significantly after 4 h the number of neuronal nitric oxide synthase (nNOS)-immunoreactive neurones in the cervical part of trigeminal nucleus caudalis.	Nitroglycerin	33-46	nitric oxide synthase 1	Rattus norvegicus	153-157
15154853-5	2004	attenuates the NTG-induced nNOS expression in the superficial laminae of trigeminal nucleus caudalis.	Nitroglycerin	15-18	nitric oxide synthase 1	Rattus norvegicus	27-31
15154853-6	2004	These findings suggest that effect of NTG on nNOS at a high dosage may involve the cycloxygenase pathway and that activation of the peripheral 5-HT1B/D receptors is not able to modify this effect.	Nitroglycerin	38-41	nitric oxide synthase 1	Rattus norvegicus	45-49
15288585-1	2004	The role of aldehyde dehydrogenase (ALDH) in ex vivo tolerance to transdermal glyceryl trinitrate was explored in rat aorta.	Nitroglycerin	78-97	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	12-34
15288585-1	2004	The role of aldehyde dehydrogenase (ALDH) in ex vivo tolerance to transdermal glyceryl trinitrate was explored in rat aorta.	Nitroglycerin	78-97	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	36-40
15288585-3	2004	ALDH inhibitors, chloral hydrate (0.3 mM) and cyanamide (0.1-1 mM) inhibited relaxation to glyceryl trinitrate in non-tolerant and tolerant arteries.	Nitroglycerin	91-110	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	0-4
15288585-9	2004	The discrepancies are consistent with evidence that (a) organic nitrates, unlike chloral and cyanamide, irreversibly inactivate ALDH (hence reduced enzyme saturability can explain the biphasic curve) and (b) eNOS contributes to tolerance by a mechanism independent of glyceryl trinitrate metabolism.	Nitroglycerin	268-287	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	128-132
15154853-0	2004	Nitroglycerin-induced nNOS increase in rat trigeminal nucleus caudalis is inhibited by systemic administration of lysine acetylsalicylate but not of sumatriptan.	Nitroglycerin	0-13	nitric oxide synthase 1	Rattus norvegicus	22-26
15118032-7	2004	RESULTS: Compared with the control group, the glyceryl trinitrate group showed reduced pain with activity at twelve weeks (p = 0.02) and twenty-four weeks (p = 0.03), reduced night pain at twelve weeks (p = 0.04), reduced tenderness at twelve weeks (p = 0.02), decreased pain scores after the hop test at twenty-four weeks (p = 0.005), and increased ankle plantar flexor mean total work compared with the baseline level at twenty-four weeks (p = 0.04).	Nitroglycerin	46-65	HOP homeobox	Homo sapiens	293-296
14988295-8	2004	In the latter, adiponectin levels were positively associated with arterial vasodilation in response to nitroglycerin (endothelium-independent vasodilation [EIVD], r=0.41, P=0.002) but not with flux-induced, endothelium-dependent vasodilation (EDVD) (r=0.007, P=NS).	Nitroglycerin	103-116	adiponectin, C1Q and collagen domain containing	Homo sapiens	15-26
15139508-3	2004	Concentration-response curves for nitroglycerin, vasoactive intestinal polypeptide (VIP), and sodium nitroprusside (SNP) were shifted to the right in the presence of (p-chloro-D-Phe6, Leu17)-VIP (VIPa), a VIP receptor antagonist.	Nitroglycerin	34-47	VIP peptides	Oryctolagus cuniculus	191-194
15139508-3	2004	Concentration-response curves for nitroglycerin, vasoactive intestinal polypeptide (VIP), and sodium nitroprusside (SNP) were shifted to the right in the presence of (p-chloro-D-Phe6, Leu17)-VIP (VIPa), a VIP receptor antagonist.	Nitroglycerin	34-47	VIP peptides	Oryctolagus cuniculus	191-194
15095278-5	2004	In accordance with these temporal effects, reduced bone mineral density, bone microhardness, and osteocalcin expression could be restored to normal, wild-type values after 21 days in vivo administration of the nitric oxide donor glyceryl trinitrate to 4-week-old endothelial nitric oxide synthase knockout mice, but there was no significant effect in older animals.	Nitroglycerin	229-248	bone gamma-carboxyglutamate protein	Homo sapiens	97-108
15095278-5	2004	In accordance with these temporal effects, reduced bone mineral density, bone microhardness, and osteocalcin expression could be restored to normal, wild-type values after 21 days in vivo administration of the nitric oxide donor glyceryl trinitrate to 4-week-old endothelial nitric oxide synthase knockout mice, but there was no significant effect in older animals.	Nitroglycerin	229-248	nitric oxide synthase 3	Homo sapiens	263-296
14988262-5	2004	Inulin clearance (C(IN)) and urinary excretion of guanosine 3",5"-cyclic monophosphate (U(cGMP)) were increased in SOD-Tg-db/db mice compared with corresponding values in nondiabetic mice or NTg-db/db mice.	Nitroglycerin	191-194	superoxide dismutase 1	Homo sapiens	115-118
12969888-10	2004	Left ventricular end-diastolic pressure was significantly (P &lt; 0.05 vs. NTG) reduced in the eNOS TG-Kobe strain at 7 days of reperfusion.	Nitroglycerin	75-78	nitric oxide synthase 3, endothelial cell	Mus musculus	95-99
15076233-1	2004	Clinical evidence has been raised to suggest that transdermal nitroglycerin increases the sensitivity of peripheral tissues to the hypoglycemic effect of insulin.	Nitroglycerin	62-75	insulin	Oryctolagus cuniculus	154-161
15076233-2	2004	In this study we determined whether development of tolerance to the hypotensive effect of nitroglycerin also resulted in tolerance to the insulin-sensitizing effect in rabbits.	Nitroglycerin	90-103	insulin	Oryctolagus cuniculus	138-145
15076233-6	2004	A six-hour exposure to transdermal nitroglycerin significantly increased insulin sensitivity determined by hyperinsulinemic (100 microU/ml) euglycemic (5.5 mmol/l) glucose clamping as compared with that seen in rabbits treated with placebo patches.	Nitroglycerin	35-48	insulin	Oryctolagus cuniculus	73-80
15076233-7	2004	A significant decrease in insulin sensitivity was observed in the nitroglycerin patch-treated animals both in the presence and after the removal of the last patch when the patches were applied over 7 days.	Nitroglycerin	66-79	insulin	Oryctolagus cuniculus	26-33
14755345-2	2004	The extent to which ALDH-2 contributes to GTN tolerance (impaired relaxation to GTN) and cross-tolerance (impaired endothelium-dependent relaxation) in vivo remain to be elucidated.	Nitroglycerin	80-83	aldehyde dehydrogenase 2 family member	Rattus norvegicus	20-26
14755345-5	2004	Further, whereas in control vessels, multiple inhibitors and substrates of ALDH-2 reduced both GTN-stimulation of cGKI and GTN-induced vasodilation, these agents had little effect on tolerant vessels.	Nitroglycerin	95-98	aldehyde dehydrogenase 2 family member	Rattus norvegicus	75-81
14755345-5	2004	Further, whereas in control vessels, multiple inhibitors and substrates of ALDH-2 reduced both GTN-stimulation of cGKI and GTN-induced vasodilation, these agents had little effect on tolerant vessels.	Nitroglycerin	123-126	aldehyde dehydrogenase 2 family member	Rattus norvegicus	75-81
14732477-10	2004	Nitroglycerin significantly enhanced aortic Mn-SOD, CAT, GR and glutathione-S-transferase (GST) activities and protein expressions with decreased MDA levels, protein carbonyls and BP.	Nitroglycerin	0-13	superoxide dismutase 2	Rattus norvegicus	44-50
14732477-10	2004	Nitroglycerin significantly enhanced aortic Mn-SOD, CAT, GR and glutathione-S-transferase (GST) activities and protein expressions with decreased MDA levels, protein carbonyls and BP.	Nitroglycerin	0-13	catalase	Rattus norvegicus	52-55
14732477-10	2004	Nitroglycerin significantly enhanced aortic Mn-SOD, CAT, GR and glutathione-S-transferase (GST) activities and protein expressions with decreased MDA levels, protein carbonyls and BP.	Nitroglycerin	0-13	hematopoietic prostaglandin D synthase	Rattus norvegicus	64-89
14732477-10	2004	Nitroglycerin significantly enhanced aortic Mn-SOD, CAT, GR and glutathione-S-transferase (GST) activities and protein expressions with decreased MDA levels, protein carbonyls and BP.	Nitroglycerin	0-13	hematopoietic prostaglandin D synthase	Rattus norvegicus	91-94
14755345-0	2004	Central role of mitochondrial aldehyde dehydrogenase and reactive oxygen species in nitroglycerin tolerance and cross-tolerance.	Nitroglycerin	84-97	aldehyde dehydrogenase 2 family member	Rattus norvegicus	16-52
14755345-1	2004	Recent studies suggest that mitochondrial aldehyde dehydrogenase (ALDH-2) plays a central role in the process of nitroglycerin (glyceryl trinitrate, GTN) biotransformation in vivo and that its inhibition accounts for mechanism-based tolerance in vitro.	Nitroglycerin	113-126	aldehyde dehydrogenase 2 family member	Rattus norvegicus	28-64
14755345-1	2004	Recent studies suggest that mitochondrial aldehyde dehydrogenase (ALDH-2) plays a central role in the process of nitroglycerin (glyceryl trinitrate, GTN) biotransformation in vivo and that its inhibition accounts for mechanism-based tolerance in vitro.	Nitroglycerin	113-126	aldehyde dehydrogenase 2 family member	Rattus norvegicus	66-72
14755345-1	2004	Recent studies suggest that mitochondrial aldehyde dehydrogenase (ALDH-2) plays a central role in the process of nitroglycerin (glyceryl trinitrate, GTN) biotransformation in vivo and that its inhibition accounts for mechanism-based tolerance in vitro.	Nitroglycerin	128-147	aldehyde dehydrogenase 2 family member	Rattus norvegicus	28-64
14755345-1	2004	Recent studies suggest that mitochondrial aldehyde dehydrogenase (ALDH-2) plays a central role in the process of nitroglycerin (glyceryl trinitrate, GTN) biotransformation in vivo and that its inhibition accounts for mechanism-based tolerance in vitro.	Nitroglycerin	128-147	aldehyde dehydrogenase 2 family member	Rattus norvegicus	66-72
14755345-1	2004	Recent studies suggest that mitochondrial aldehyde dehydrogenase (ALDH-2) plays a central role in the process of nitroglycerin (glyceryl trinitrate, GTN) biotransformation in vivo and that its inhibition accounts for mechanism-based tolerance in vitro.	Nitroglycerin	149-152	aldehyde dehydrogenase 2 family member	Rattus norvegicus	28-64
14755345-1	2004	Recent studies suggest that mitochondrial aldehyde dehydrogenase (ALDH-2) plays a central role in the process of nitroglycerin (glyceryl trinitrate, GTN) biotransformation in vivo and that its inhibition accounts for mechanism-based tolerance in vitro.	Nitroglycerin	149-152	aldehyde dehydrogenase 2 family member	Rattus norvegicus	66-72
14755345-2	2004	The extent to which ALDH-2 contributes to GTN tolerance (impaired relaxation to GTN) and cross-tolerance (impaired endothelium-dependent relaxation) in vivo remain to be elucidated.	Nitroglycerin	42-45	aldehyde dehydrogenase 2 family member	Rattus norvegicus	20-26
14729435-0	2004	Delayed cardioprotection afforded by nitroglycerin is mediated by alpha-CGRP via activation of inducible nitric oxide synthase.	Nitroglycerin	37-50	calcitonin-related polypeptide alpha	Rattus norvegicus	72-76
15510511-4	2004	Impact of CCT on results of Goldman aplanation tonometry was detected in 55.7% of NTG eyes--overestimated in 20% and underestimated in 35% of them.	Nitroglycerin	82-85	CCT	Homo sapiens	10-13
14729435-0	2004	Delayed cardioprotection afforded by nitroglycerin is mediated by alpha-CGRP via activation of inducible nitric oxide synthase.	Nitroglycerin	37-50	nitric oxide synthase 2	Rattus norvegicus	95-126
14729435-1	2004	Previous investigations have demonstrated that delayed preconditioning induced by nitroglycerin is mediated by endogenous calcitonin gene-related peptide (CGRP).	Nitroglycerin	82-95	calcitonin-related polypeptide alpha	Rattus norvegicus	122-153
14729435-1	2004	Previous investigations have demonstrated that delayed preconditioning induced by nitroglycerin is mediated by endogenous calcitonin gene-related peptide (CGRP).	Nitroglycerin	82-95	calcitonin-related polypeptide alpha	Rattus norvegicus	155-159
14729435-2	2004	In the present study, we examined whether CGRP-mediated delayed preconditioning induced by nitroglycerin is involved in activation of inducible nitric oxide synthase (iNOS).	Nitroglycerin	91-104	calcitonin-related polypeptide alpha	Rattus norvegicus	42-46
14729435-2	2004	In the present study, we examined whether CGRP-mediated delayed preconditioning induced by nitroglycerin is involved in activation of inducible nitric oxide synthase (iNOS).	Nitroglycerin	91-104	nitric oxide synthase 2	Rattus norvegicus	134-165
14729435-2	2004	In the present study, we examined whether CGRP-mediated delayed preconditioning induced by nitroglycerin is involved in activation of inducible nitric oxide synthase (iNOS).	Nitroglycerin	91-104	nitric oxide synthase 2	Rattus norvegicus	167-171
14729435-7	2004	Nitroglycerin caused a significant increase in the expression of alpha-CGRP mRNA, but not beta-CGRP mRNA, concomitant with an increase in plasma concentrations of cGMP and CGRP.	Nitroglycerin	0-13	calcitonin-related polypeptide alpha	Rattus norvegicus	71-75
14729435-11	2004	The present results suggest that delayed cardioprotection afforded by nitroglycerin is mediated by the alpha-CGRP isoform via generation of NO derived from iNOS.	Nitroglycerin	70-83	calcitonin-related polypeptide alpha	Rattus norvegicus	109-113
14729435-11	2004	The present results suggest that delayed cardioprotection afforded by nitroglycerin is mediated by the alpha-CGRP isoform via generation of NO derived from iNOS.	Nitroglycerin	70-83	nitric oxide synthase 2	Rattus norvegicus	156-160
14563789-0	2004	Roles of superoxide, peroxynitrite, and protein kinase C in the development of tolerance to nitroglycerin.	Nitroglycerin	92-105	protein kinase C, gamma	Rattus norvegicus	40-56
14563789-2	2004	Studies showing that inhibitors of protein kinase C (PKC) prevent tolerance to GTN suggest the involvement of PKC activation, which can also increase O2*-.	Nitroglycerin	79-82	protein kinase C, gamma	Rattus norvegicus	35-51
14563789-2	2004	Studies showing that inhibitors of protein kinase C (PKC) prevent tolerance to GTN suggest the involvement of PKC activation, which can also increase O2*-.	Nitroglycerin	79-82	protein kinase C, gamma	Rattus norvegicus	53-56
14563789-2	2004	Studies showing that inhibitors of protein kinase C (PKC) prevent tolerance to GTN suggest the involvement of PKC activation, which can also increase O2*-.	Nitroglycerin	79-82	protein kinase C, gamma	Rattus norvegicus	110-113
15510511-2	2004	MATERIAL AND METHODS: CCT (measured by specular microscope Topcon SP2000P) was evaluated in 70 eyes of 39 patients with diagnosed NTG, 35 women and 4 men in age 31-78 years (mean 68 years).	Nitroglycerin	130-133	CCT	Homo sapiens	22-25
14644393-5	2003	Rosuvastatin reduced cholesteryl ester transfer protein (CETP) by 33% in NTG and 37% in HTG (both P &lt; 0.001); a reduction in cholesteryl ester transfer activity (-59%, P &lt; 0.001) was observed in HTG only.	Nitroglycerin	73-76	cholesteryl ester transfer protein	Homo sapiens	21-55
15588129-2	2004	In the presence of NADH or NADPH, diaphorase can convert selected NO donors, glycerol trinitrate (GTN) and formaldoxime (FAL) to nitrites and nitrates with NO as an intermediate.	Nitroglycerin	77-96	dihydrolipoamide dehydrogenase	Homo sapiens	34-44
15588129-2	2004	In the presence of NADH or NADPH, diaphorase can convert selected NO donors, glycerol trinitrate (GTN) and formaldoxime (FAL) to nitrites and nitrates with NO as an intermediate.	Nitroglycerin	98-101	dihydrolipoamide dehydrogenase	Homo sapiens	34-44
15588129-3	2004	This activity of diaphorase was inhibited by diphenyleneiodonium (DPI) (inhibitor of some NADPH-dependent flavoprotein oxidoreductases), while it remained uninhibited by NG-nitro-L-arginine methyl ester (inhibitor of NO synthase) 7-Ethoxyresorufin (inhibitor of cytochrome P-450 1A1 and cytochrome P-450 NADPH-dependent reductase) inhibited the conversion of GTN only.	Nitroglycerin	359-362	dihydrolipoamide dehydrogenase	Homo sapiens	17-27
15720833-6	2004	hemeoxygenase-1 (HO-1) was induced within 24 h of continuous NTG infusion, but it returned to normal levels 48 h after cessation of the NTG.	Nitroglycerin	61-64	heme oxygenase 1	Rattus norvegicus	0-21
15720833-6	2004	hemeoxygenase-1 (HO-1) was induced within 24 h of continuous NTG infusion, but it returned to normal levels 48 h after cessation of the NTG.	Nitroglycerin	136-139	heme oxygenase 1	Rattus norvegicus	0-21
15033804-6	2003	Cerebellar extracts from both nTg and Tg mice displayed the highest level of nNOS activity, which was fourfold higher than cortical extracts.	Nitroglycerin	30-33	nitric oxide synthase 1, neuronal	Mus musculus	77-81
14644393-5	2003	Rosuvastatin reduced cholesteryl ester transfer protein (CETP) by 33% in NTG and 37% in HTG (both P &lt; 0.001); a reduction in cholesteryl ester transfer activity (-59%, P &lt; 0.001) was observed in HTG only.	Nitroglycerin	73-76	cholesteryl ester transfer protein	Homo sapiens	57-61
14688690-6	2003	RESULTS: Verapamil/nitroglycerin solution reduced vasoconstriction in response to epinephrine, angiotensin II, prostaglandin F(2alpha), and phenylephrine but its effect had almost completely waned after 5 hours.	Nitroglycerin	19-32	angiotensinogen	Homo sapiens	95-109
14642695-1	2003	OBJECTIVES: We tested whether in vivo nitroglycerin (NTG) treatment causes tyrosine nitration of prostacyclin synthase (PGI(2)-S), one of the nitration targets of peroxynitrite, and whether this may contribute to nitrate tolerance.	Nitroglycerin	38-51	prostaglandin I2 synthase	Rattus norvegicus	97-118
14642695-1	2003	OBJECTIVES: We tested whether in vivo nitroglycerin (NTG) treatment causes tyrosine nitration of prostacyclin synthase (PGI(2)-S), one of the nitration targets of peroxynitrite, and whether this may contribute to nitrate tolerance.	Nitroglycerin	53-56	prostaglandin I2 synthase	Rattus norvegicus	97-118
14586390-0	2003	Venous response to nitroglycerin is enhanced in young, healthy carriers of the 825T allele of the G protein beta3 subunit gene (GNB3).	Nitroglycerin	19-32	G protein subunit beta 3	Homo sapiens	98-113
14586390-0	2003	Venous response to nitroglycerin is enhanced in young, healthy carriers of the 825T allele of the G protein beta3 subunit gene (GNB3).	Nitroglycerin	19-32	G protein subunit beta 3	Homo sapiens	128-132
14586390-11	2003	CONCLUSION: Our results suggest that the GNB3 C825T polymorphism determines venous response to nitroglycerin and that G proteins may be involved in the signal transduction pathway.	Nitroglycerin	95-108	G protein subunit beta 3	Homo sapiens	41-45
12960101-9	2003	Also, ANG II decreased effective renal plasma flow and glomerular filtration rate in both groups of animals, but the reductions were less in TG than in NTG mice.	Nitroglycerin	152-155	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	6-12
14573760-4	2003	However, the mitochondrial aldehyde dehydrogenase (ALDH2) is inhibited in GTN-tolerant tissues and produces NO2- from GTN, which is proposed to be converted to NO within mitochondria.	Nitroglycerin	118-121	aldehyde dehydrogenase 2 family member	Rattus norvegicus	13-49
14573760-4	2003	However, the mitochondrial aldehyde dehydrogenase (ALDH2) is inhibited in GTN-tolerant tissues and produces NO2- from GTN, which is proposed to be converted to NO within mitochondria.	Nitroglycerin	118-121	aldehyde dehydrogenase 2 family member	Rattus norvegicus	51-56
14573760-4	2003	However, the mitochondrial aldehyde dehydrogenase (ALDH2) is inhibited in GTN-tolerant tissues and produces NO2- from GTN, which is proposed to be converted to NO within mitochondria.	Nitroglycerin	74-77	aldehyde dehydrogenase 2 family member	Rattus norvegicus	13-49
14573760-4	2003	However, the mitochondrial aldehyde dehydrogenase (ALDH2) is inhibited in GTN-tolerant tissues and produces NO2- from GTN, which is proposed to be converted to NO within mitochondria.	Nitroglycerin	74-77	aldehyde dehydrogenase 2 family member	Rattus norvegicus	51-56
14573760-7	2003	The in vivo protocol resulted in almost complete inhibition of ALDH2 activity and GTN biotransformation in hepatic mitochondria, indicating that long-term GTN exposure results in inactivation of the enzyme.	Nitroglycerin	155-158	aldehyde dehydrogenase 2 family member	Rattus norvegicus	63-68
14573760-10	2003	Immunoblot analysis indicated that the majority of vascular ALDH2 is present in the cytoplasm, suggesting that mitochondrial biotransformation of GTN by ALDH2 plays a minor role in the overall vascular biotransformation of GTN by this enzyme.	Nitroglycerin	146-149	aldehyde dehydrogenase 2 family member	Rattus norvegicus	153-158
14573760-10	2003	Immunoblot analysis indicated that the majority of vascular ALDH2 is present in the cytoplasm, suggesting that mitochondrial biotransformation of GTN by ALDH2 plays a minor role in the overall vascular biotransformation of GTN by this enzyme.	Nitroglycerin	223-226	aldehyde dehydrogenase 2 family member	Rattus norvegicus	60-65
14508317-4	2003	Then, 2.5 microg x kg-1 x min-1 nitroglycerin liquid nebulized by a 2-l gas flow of 40% oxygen and air mixture was administered to the patients who were diagnosed as having pulmonary hypertension (mean pulmonary arterial pressures &gt; 25 mmHg).	Nitroglycerin	32-45	CD59 molecule (CD59 blood group)	Homo sapiens	26-31
14572907-7	2003	Similarly, in hyperproliferation protection studies, GTN pretreatment showed a strong inhibition of Fe-NTA-induced renal ornithine decarboxylase (ODC) activity (51-57% inhibition, P&lt;0.001) and [3H]thymidine incorporation (43-58% inhibition, P&lt;0.001) into renal DNA.	Nitroglycerin	53-56	ornithine decarboxylase, structural 1	Mus musculus	121-144
14572907-7	2003	Similarly, in hyperproliferation protection studies, GTN pretreatment showed a strong inhibition of Fe-NTA-induced renal ornithine decarboxylase (ODC) activity (51-57% inhibition, P&lt;0.001) and [3H]thymidine incorporation (43-58% inhibition, P&lt;0.001) into renal DNA.	Nitroglycerin	53-56	ornithine decarboxylase, structural 1	Mus musculus	146-149
14572907-10	2003	In addition, exogenously produced NO can also inhibit Fe-NTA-induced hyperproliferative response by down-regulating the activity of ODC and the rate of [3H]thymidine incorporation into renal DNA and could be suggested as another possible clinical application for this NO-donor (GTN, traditionally used as a vasodilator) in oncological medicine.	Nitroglycerin	278-281	ornithine decarboxylase 1	Homo sapiens	132-135
14564337-10	2003	On the contrary, nitroglycerin significantly reduced plasma levels of C-reactive protein and sE-selectin and increased the levels of intraplatelet cGMP.	Nitroglycerin	17-30	C-reactive protein	Homo sapiens	70-88
13679085-6	2003	GTN administration also inhibited malondialdehyde (MDA) formation, induction of ODC activity, enhanced rate of DNA synthesis, and pathological deterioration in a dose-dependent fashion.	Nitroglycerin	0-3	ornithine decarboxylase 1	Homo sapiens	80-83
14519438-3	2003	We modified the C-lobe of cTnC directly by addition of the Ca(2+)-sensitizer, EMD 57033, and indirectly by replacing native cTnI with cTnI-containing Glu residues at Ser-43 and Ser-45 (cTnI-S43E/S45E) in myofilaments from hearts of non-transgenic (NTG) and transgenic (TG) mice expressing a point mutation on alpha-Tm (E180G) linked to familial hypertrophic cardiomyopathy.	Nitroglycerin	248-251	troponin C, cardiac/slow skeletal	Mus musculus	26-30
14510930-0	2003	5-HT(1B/1D) serotonin receptor agonist attenuates nitroglycerin-evoked nitric oxide synthase expression in trigeminal pathway.	Nitroglycerin	50-63	5-hydroxytryptamine receptor 1B	Rattus norvegicus	0-7
14510930-1	2003	This study was conducted to investigate the effect of 5-HT(1B/1D) receptor activation on nitroglycerin (NTG)-induced cerebral hyperaemia and neuronal nitric oxide synthase (nNOS) expression in trigeminovascular neurones.	Nitroglycerin	89-102	5-hydroxytryptamine receptor 1B	Rattus norvegicus	54-61
14510930-1	2003	This study was conducted to investigate the effect of 5-HT(1B/1D) receptor activation on nitroglycerin (NTG)-induced cerebral hyperaemia and neuronal nitric oxide synthase (nNOS) expression in trigeminovascular neurones.	Nitroglycerin	104-107	5-hydroxytryptamine receptor 1B	Rattus norvegicus	54-61
14510930-5	2003	Sumatriptan pretreatment also attenuated the NTG-evoked expression of nNOS in all studied areas.	Nitroglycerin	45-48	nitric oxide synthase 1	Rattus norvegicus	70-74
14519438-4	2003	Introduction of cTnI-S43E/S45E induced a significantly greater reduction in tension in TG myofilaments compared to NTG controls.	Nitroglycerin	115-118	troponin I, cardiac 3	Mus musculus	16-20
14519438-5	2003	Furthermore, the effect of EMD 57033 to restore Ca(2+)-sensitivity was higher in TG compared to NTG fiber bundles containing cTnI-S43E/S45E and compared to TG or NTG fiber bundles containing native TnI.	Nitroglycerin	96-99	troponin I, cardiac 3	Mus musculus	125-129
14619385-9	2003	Meaningful complications related to the use of vasopressin were observed in 5 patients (chest pain or abdominal pain requiring nitroglycerin), but no complications were associated with the use of somatostatin (p &lt; 0.05).	Nitroglycerin	127-140	arginine vasopressin	Homo sapiens	47-58
12860835-6	2003	Plasma adiponectin level was highly correlated with the vasodilator response to reactive hyperemia in the total (r=0.257, P&lt;0.001) and no-medication (r=0.296, P=0.026) groups but not with nitroglycerin-induced hyperemia, indicating that adiponectin affected endothelium-dependent vasodilation.	Nitroglycerin	191-204	adiponectin, C1Q and collagen domain containing	Mus musculus	7-18
12913759-9	2003	Co-incubation of PC-3 and TRAMP-C2 cells with GTN (0.1 nM) inhibited the hypoxia induced resistance to doxorubicin.	Nitroglycerin	46-49	chromobox 8	Mus musculus	17-21
12913759-9	2003	Co-incubation of PC-3 and TRAMP-C2 cells with GTN (0.1 nM) inhibited the hypoxia induced resistance to doxorubicin.	Nitroglycerin	46-49	tumor necrosis factor receptor superfamily, member 25	Mus musculus	26-31
12952843-9	2003	The plasma level of thioredoxin (a marker of oxidative stress) was increased in the GTN group after treatment (P&lt;0.01) but not in the control or GTN+ARB groups.	Nitroglycerin	84-87	thioredoxin	Homo sapiens	20-31
12890708-5	2003	(4) In contrast, the potency of ANP and CNP in aortae from eNOS KO animals was reduced following pretreatment of tissues with supramaximal concentrations of the NO-donor, glyceryl trinitrate (3 x 10(-5) M, 30 min) or ANP (10(-7) M, 30 min).	Nitroglycerin	171-190	2',3'-cyclic nucleotide 3' phosphodiesterase	Mus musculus	40-43
12900349-8	2003	The reduced response to bradykinin remained significant (P=0.045) after adjusting for the response to glyceryl trinitrate and was independent of conventional risk factors.	Nitroglycerin	102-121	kininogen 1	Homo sapiens	24-34
12860443-10	2003	Nitroglycerin administration significantly enhanced cardiac Mn-SOD, CAT, and GST activities, and protein expression with decreased MDA levels and BP.	Nitroglycerin	0-13	superoxide dismutase 2	Rattus norvegicus	60-66
12860443-10	2003	Nitroglycerin administration significantly enhanced cardiac Mn-SOD, CAT, and GST activities, and protein expression with decreased MDA levels and BP.	Nitroglycerin	0-13	catalase	Rattus norvegicus	68-71
12860443-11	2003	Interaction of training and chronic nitroglycerin treatment increased cardiac NO levels with enhanced eNOS and iNOS protein expressions, GSH/GSSG ratio, and the up-regulation of antioxidant enzymes.	Nitroglycerin	36-49	nitric oxide synthase 2	Rattus norvegicus	111-115
14653081-0	2003	[Effects of nitroglycerin on plasma calcitonin gene-related peptide and endothelin in congestive heart failure].	Nitroglycerin	12-25	calcitonin related polypeptide alpha	Homo sapiens	36-67
12847683-7	2003	The expression of Cas-L protein and its tyrosine phosphorylation were increased in ATg mice compared with NTg and control mice, and this was accompanied by enhanced autophosphorylation of Fyn and Lck.	Nitroglycerin	106-109	neural precursor cell expressed, developmentally down-regulated gene 9	Mus musculus	18-23
12906031-11	2003	Beta-endorphin and epinephrine might participate in the pathophysiology in conventional tilt-induced as well as nitroglycerin provocation tilt-induced syncope in patients with neurally mediated syncope.	Nitroglycerin	112-125	proopiomelanocortin	Homo sapiens	0-14
14653081-7	2003	During the nitroglycerin treatment, the plasma concentration of CGRP significantly increased (P &lt; 0.001), whereas the concentration of ET significantly decreased (P &lt; 0.01).	Nitroglycerin	11-24	calcitonin related polypeptide alpha	Homo sapiens	64-68
14653081-9	2003	CONCLUSION: Nitroglycerin can increase the peripheral plasma CGRP level and decrease the concentration of ET when treating CHF.	Nitroglycerin	12-25	calcitonin related polypeptide alpha	Homo sapiens	61-65
12789484-11	2003	Since NO donors such as nitroglycerin are known to provoke headache and CGRP is released during migraine pain, the NO-stimulated CGRP release may be relevant for the development of vascular headaches that are accompanied by meningeal hyperaemia.	Nitroglycerin	24-37	calcitonin-related polypeptide alpha	Rattus norvegicus	129-133
12704544-3	2003	Coronary blood flow increase after intracoronary infusion of 10 mg VEGF (2.63 +/- 0.49x) was comparable to that seen after 40 mg of intracoronary adenosine (2.5 +/- 0.53x, p = 0.67) and was significantly higher then after 200 mg of intracoronary nitroglycerine (1.9 +/- 0.12x, p = 0.0005).	Nitroglycerin	246-260	vascular endothelial growth factor A	Sus scrofa	67-71
12562915-9	2003	We conclude: (1) PKA-dependent phosphorylation enhances length-dependent activation in NTG hearts; (2) replacement of native TnI with ssTnI increases Ca2+ sensitivity of tension but reduces length-dependent activation; (3) MyBP-C phosphorylation by PKA does not alter calcium responsiveness and induces a decrease in myofilament lattice spacing at all sarcomere lengths and (4) length-dependent activation in the heart cannot be entirely explained by alterations in myofilament lattice spacing.	Nitroglycerin	87-90	troponin I, skeletal, slow 1	Mus musculus	134-139
12710904-0	2003	CGRP-mediated cardiovascular effect of nitroglycerin.	Nitroglycerin	39-52	calcitonin related polypeptide alpha	Homo sapiens	0-4
12710904-4	2003	Nitroglycerin activates sensory nerves fibres to release CGRP by generating NO and increasing cGMP level, and that the cardiovascular effects of nitroglycerin are partly mediated by endogenous CGRP.	Nitroglycerin	0-13	calcitonin related polypeptide alpha	Homo sapiens	57-61
12710904-4	2003	Nitroglycerin activates sensory nerves fibres to release CGRP by generating NO and increasing cGMP level, and that the cardiovascular effects of nitroglycerin are partly mediated by endogenous CGRP.	Nitroglycerin	145-158	calcitonin related polypeptide alpha	Homo sapiens	193-197
12841629-10	2003	Interaction of exercise training and chronic nitroglycerin treatment resulted in normalization of plasma NO, MDA, lactate levels, and CAT activity.	Nitroglycerin	45-58	catalase	Rattus norvegicus	134-137
13129819-13	2003	VEGF increased after infusion of nitroglycerine (+35%; p &lt;.05) and dropped after 1 h of 30-min exercising (-31%, p &lt;.05).	Nitroglycerin	33-47	vascular endothelial growth factor A	Homo sapiens	0-4
12538209-4	2003	Nitroglycerin, hydralazine, and nicardipine produced concentration-dependent relaxation of U46619-preconstricted HUA segments from normotensive and PIH patients.	Nitroglycerin	0-13	pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included)	Homo sapiens	148-151
12527144-3	2003	In the female eNOS (+/+) mice, but not in males, in vitro NTG (0.73 mM) induced significant increases in the release of CGRP-like immunoreactivity (CGRP-LI) from the aorta and the heart but not from the small intestine.	Nitroglycerin	58-61	nitric oxide synthase 3, endothelial cell	Mus musculus	14-18
12527144-3	2003	In the female eNOS (+/+) mice, but not in males, in vitro NTG (0.73 mM) induced significant increases in the release of CGRP-like immunoreactivity (CGRP-LI) from the aorta and the heart but not from the small intestine.	Nitroglycerin	58-61	calcitonin/calcitonin-related polypeptide, alpha	Mus musculus	120-124
12527144-3	2003	In the female eNOS (+/+) mice, but not in males, in vitro NTG (0.73 mM) induced significant increases in the release of CGRP-like immunoreactivity (CGRP-LI) from the aorta and the heart but not from the small intestine.	Nitroglycerin	58-61	calcitonin/calcitonin-related polypeptide, alpha	Mus musculus	148-152
12527144-5	2003	These results suggest that NTG-induced CGRP release is eNOS-dependent and tissue- and gender-selective.	Nitroglycerin	27-30	calcitonin/calcitonin-related polypeptide, alpha	Mus musculus	39-43
12527144-5	2003	These results suggest that NTG-induced CGRP release is eNOS-dependent and tissue- and gender-selective.	Nitroglycerin	27-30	nitric oxide synthase 3, endothelial cell	Mus musculus	55-59
12487622-3	2003	In the Vasodilation in the Management of Acute Congestive Heart Failure (VMAC) study, patients hospitalised with acute decompensated CHF who received nesiritide had significantly greater mean reductions from baseline in pulmonary capillary wedge pressure 3 hours after starting treatment than nitroglycerin or placebo recipients (-5.8 vs -3.8 and -2 mm Hg, respectively); all patients also received standard therapy (e.g. intravenous diuretics).	Nitroglycerin	293-306	vimentin type intermediate filament associated coiled-coil protein	Homo sapiens	73-77
12487622-11	2003	In VMAC, significantly more adverse events occurred with nitroglycerin than with nesiritide.	Nitroglycerin	57-70	vimentin type intermediate filament associated coiled-coil protein	Homo sapiens	3-7
12094019-5	2002	Peripheral CD4(+) and CD8(+) T cell populations were significantly lower in tg than in Ntg, df, or Ndf mice.	Nitroglycerin	87-90	CD4 antigen	Mus musculus	11-14
12512688-1	2002	In retrospect, basic research in the fields of NO and cyclic GMP during the past two decades appears to have followed a logical course beginning with the findings that NO and cyclic GMP are vascular smooth muscle relaxants, that nitroglycerin relaxes smooth muscle by metabolism to NO, progressing to the discovery that mammalian cells synthesize NO, and finally the revelation that NO is a neurotransmitter mediating vasodilation in specialized vascular beds.	Nitroglycerin	229-242	5'-nucleotidase, cytosolic II	Homo sapiens	61-64
12383586-11	2002	Treatment of NZWR with NTG also decreased plasma extracellular superoxide dismutase (EC-SOD)-activity.	Nitroglycerin	23-26	extracellular superoxide dismutase [Cu-Zn]	Oryctolagus cuniculus	49-83
12383586-11	2002	Treatment of NZWR with NTG also decreased plasma extracellular superoxide dismutase (EC-SOD)-activity.	Nitroglycerin	23-26	extracellular superoxide dismutase [Cu-Zn]	Oryctolagus cuniculus	85-91
19649229-6	2002	Treatment of diabetic rats with CP (50 mg/kg intraperitoneally, bid) abolished not only the differences in superoxide, MDA and 8-ISO levels, but also the differences in the relaxation and cGMP responses of vascular tissue between control and diabetic rats to both ACh and nitroglycerine.	Nitroglycerin	272-286	BH3 interacting domain death agonist	Rattus norvegicus	64-67
12133854-5	2002	Heat and nitroglycerin induced a similar relation between Ser16-HSP20 phosphorylation and force.	Nitroglycerin	9-22	HSPB6	Sus scrofa	64-69
12161299-11	2002	Addition of nitroglycerin to the combination of low dose epinephrine with vasopressin during cardiac arrest may be beneficial.	Nitroglycerin	12-25	vasopressin	Sus scrofa	74-85
12094193-6	2002	During period 2, there was an increased use of percutaneous transluminal coronary angioplasty, coronary artery bypass grafting, angiotensin-converting enzyme inhibitors, heparin, and intravenous nitroglycerin.	Nitroglycerin	195-208	period circadian regulator 2	Homo sapiens	7-15
12105852-12	2002	CONCLUSIONS: Our results indicate that GTN (1) activates an unusual caspase cascade to induce apoptosis in colon cancer cells and (2) sensitizes these cells to Fas-mediated cell death by increasing the expression of Fas and decreasing the expression of several IAPs.	Nitroglycerin	39-42	caspase 1	Homo sapiens	68-75
12390297-0	2002	Effects of glutathione S-transferase inhibitors on nitroglycerin action in pig isolated coronary arteries.	Nitroglycerin	51-64	microsomal glutathione S-transferase 1	Sus scrofa	11-36
12390297-2	2002	The present study was designed to clarify the role of glutathione S-transferase (GST) in the vasorelaxation response and development of tolerance to nitroglycerin (GTN) using GST inhibitors.	Nitroglycerin	149-162	microsomal glutathione S-transferase 1	Sus scrofa	54-79
12390297-2	2002	The present study was designed to clarify the role of glutathione S-transferase (GST) in the vasorelaxation response and development of tolerance to nitroglycerin (GTN) using GST inhibitors.	Nitroglycerin	149-162	microsomal glutathione S-transferase 1	Sus scrofa	81-84
12390297-2	2002	The present study was designed to clarify the role of glutathione S-transferase (GST) in the vasorelaxation response and development of tolerance to nitroglycerin (GTN) using GST inhibitors.	Nitroglycerin	164-167	microsomal glutathione S-transferase 1	Sus scrofa	54-79
12390297-2	2002	The present study was designed to clarify the role of glutathione S-transferase (GST) in the vasorelaxation response and development of tolerance to nitroglycerin (GTN) using GST inhibitors.	Nitroglycerin	164-167	microsomal glutathione S-transferase 1	Sus scrofa	81-84
12451322-6	2002	This vascular tolerance seen after GTN treatment was paralleled by an upregulation of ex vivo platelet activity, which was evident from a rise in aggregation from 29.2 +/- 2.8% at control day to 85.4 +/- 8.5% at day 3, and additionally from thrombin-induced increases of intracellular Ca concentration from 494 +/- 60 nM at control day to 741 +/- 37 nM at day 3.	Nitroglycerin	35-38	coagulation factor II, thrombin	Homo sapiens	241-249
12387407-1	2002	Gas chromatography/mass spectrometry was used to analyze the pyrolytic byproducts from an Army-unique propellant compound (AA2) that is composed of predominantly nitrocellulose and nitroglycerin.	Nitroglycerin	181-194	AA2	Homo sapiens	123-126
12351453-7	2002	Treatment with L-NAME increased, whereas treatment with L-arginine or nitroglycerine patches decreased AR activity and sorbitol content in tissues of diabetic rats.	Nitroglycerin	70-84	aldo-keto reductase family 1 member B1	Rattus norvegicus	103-105
12546077-2	2002	The biological importance of NO was first shown by the findings that nitroglycerin causes vasodilation by liberating NO in the smooth muscle, and activating guanylate cyclase to raise smooth muscle levels of cyclic GMP.	Nitroglycerin	69-82	5'-nucleotidase, cytosolic II	Homo sapiens	215-218
12081660-0	2002	Effect of systemic nitroglycerin on CGRP and 5-HT afferents to rat caudal spinal trigeminal nucleus and its modulation by estrogen.	Nitroglycerin	19-32	calcitonin-related polypeptide alpha	Rattus norvegicus	36-40
12084592-9	2002	Nitroglycerin treatment stimulated a dose-dependent increase in MMP-9 mRNA levels (NTG 200 pmol: 193 +/- 6% and NTG 2,000 pmol: 372 +/- 9% compared to controls, p &lt; 0.005) and MMP-9 activity (NTG 200: 142 +/- 5.5% and NTG 2,000: 167 +/- 11% compared to controls, p &lt; 0.005).	Nitroglycerin	0-13	matrix metallopeptidase 9	Homo sapiens	64-69
12084592-9	2002	Nitroglycerin treatment stimulated a dose-dependent increase in MMP-9 mRNA levels (NTG 200 pmol: 193 +/- 6% and NTG 2,000 pmol: 372 +/- 9% compared to controls, p &lt; 0.005) and MMP-9 activity (NTG 200: 142 +/- 5.5% and NTG 2,000: 167 +/- 11% compared to controls, p &lt; 0.005).	Nitroglycerin	0-13	matrix metallopeptidase 9	Homo sapiens	179-184
12084592-9	2002	Nitroglycerin treatment stimulated a dose-dependent increase in MMP-9 mRNA levels (NTG 200 pmol: 193 +/- 6% and NTG 2,000 pmol: 372 +/- 9% compared to controls, p &lt; 0.005) and MMP-9 activity (NTG 200: 142 +/- 5.5% and NTG 2,000: 167 +/- 11% compared to controls, p &lt; 0.005).	Nitroglycerin	83-86	matrix metallopeptidase 9	Homo sapiens	64-69
12084592-10	2002	Nitroglycerin 2,000 pmol also increased MMP-2 and MMP-7 mRNA levels to 187 +/- 8% and 183 +/- 21% of control values, respectively (p &lt; 0.05).	Nitroglycerin	0-13	matrix metallopeptidase 2	Homo sapiens	40-45
12084592-10	2002	Nitroglycerin 2,000 pmol also increased MMP-2 and MMP-7 mRNA levels to 187 +/- 8% and 183 +/- 21% of control values, respectively (p &lt; 0.05).	Nitroglycerin	0-13	matrix metallopeptidase 7	Homo sapiens	50-55
12084592-11	2002	Furthermore, tissue inhibitor of metalloproteinase (TIMP)-1 (the major tissue inhibitor of MMPs) mRNA and protein levels were decreased in NTG 2,000 pmol-treated MDMs compared with control cells (mRNA: 67 +/- 7%, p &lt; 0.005; protein: 45 +/- 5%, p &lt; 0.005).	Nitroglycerin	139-142	TIMP metallopeptidase inhibitor 1	Homo sapiens	13-59
12084592-11	2002	Furthermore, tissue inhibitor of metalloproteinase (TIMP)-1 (the major tissue inhibitor of MMPs) mRNA and protein levels were decreased in NTG 2,000 pmol-treated MDMs compared with control cells (mRNA: 67 +/- 7%, p &lt; 0.005; protein: 45 +/- 5%, p &lt; 0.005).	Nitroglycerin	139-142	matrix metallopeptidase 2	Homo sapiens	91-95
12084592-12	2002	CONCLUSIONS: Nitroglycerin in pharmacologically relevant concentrations activates MMP but represses TIMP expression in human macrophages.	Nitroglycerin	13-26	TIMP metallopeptidase inhibitor 1	Homo sapiens	100-104
12084592-13	2002	The subsequent imbalance in MMP/TIMP expression associated with NTG treatment could promote matrix degradation, with potentially adverse effects on plaque stability.	Nitroglycerin	64-67	TIMP metallopeptidase inhibitor 1	Homo sapiens	32-36
12187120-7	2002	Specifically, mRNA levels of beta-globin, tropoelastin, gelsolin and a small G protein were confirmed to be upregulated consistently by NTG treatment.	Nitroglycerin	136-139	elastin	Rattus norvegicus	42-54
12187120-7	2002	Specifically, mRNA levels of beta-globin, tropoelastin, gelsolin and a small G protein were confirmed to be upregulated consistently by NTG treatment.	Nitroglycerin	136-139	gelsolin	Rattus norvegicus	56-64
12087347-0	2002	Angiotensin II attenuates the vasodilating effect of a nitric oxide donor, glyceryl trinitrate: roles of superoxide and angiotensin II type 1 receptors.	Nitroglycerin	75-94	angiotensinogen	Homo sapiens	0-14
12087347-0	2002	Angiotensin II attenuates the vasodilating effect of a nitric oxide donor, glyceryl trinitrate: roles of superoxide and angiotensin II type 1 receptors.	Nitroglycerin	75-94	angiotensinogen	Homo sapiens	120-134
12087347-3	2002	We investigated the effect of subpressor doses of angiotensin II on the vasodilating effect of glyceryl trinitrate in human forearm resistance vessels of healthy male subjects by using venous occlusion strain-gauge plethysmography.	Nitroglycerin	95-114	angiotensinogen	Homo sapiens	50-64
12087347-4	2002	METHODS: Glyceryl trinitrate was infused intra-arterially with angiotensin II or vehicle.	Nitroglycerin	9-28	angiotensinogen	Homo sapiens	63-77
12087347-6	2002	RESULTS: Angiotensin II infused at 5 pmol/min significantly attenuated the vasodilating effect of glyceryl trinitrate (mean +/- standard deviation [SD] of percentage change in forearm blood flow [FBF]: 28% +/- 20%, 79% +/- 59%, and 208% +/- 72% at 100, 250, and 1000 ng/min of glyceryl trinitrate with placebo; 8% +/- 18%, 47% +/- 41%, and 173% +/- 98% with angiotensin II at 1 pmol/min; and 2% +/- 27%, 39% +/- 40%, and 132% +/- 74% with angiotension II at 5 pmo;/min; P =.0259).	Nitroglycerin	98-117	angiotensinogen	Homo sapiens	9-23
12087347-6	2002	RESULTS: Angiotensin II infused at 5 pmol/min significantly attenuated the vasodilating effect of glyceryl trinitrate (mean +/- standard deviation [SD] of percentage change in forearm blood flow [FBF]: 28% +/- 20%, 79% +/- 59%, and 208% +/- 72% at 100, 250, and 1000 ng/min of glyceryl trinitrate with placebo; 8% +/- 18%, 47% +/- 41%, and 173% +/- 98% with angiotensin II at 1 pmol/min; and 2% +/- 27%, 39% +/- 40%, and 132% +/- 74% with angiotension II at 5 pmo;/min; P =.0259).	Nitroglycerin	98-117	angiotensinogen	Homo sapiens	358-372
12087347-6	2002	RESULTS: Angiotensin II infused at 5 pmol/min significantly attenuated the vasodilating effect of glyceryl trinitrate (mean +/- standard deviation [SD] of percentage change in forearm blood flow [FBF]: 28% +/- 20%, 79% +/- 59%, and 208% +/- 72% at 100, 250, and 1000 ng/min of glyceryl trinitrate with placebo; 8% +/- 18%, 47% +/- 41%, and 173% +/- 98% with angiotensin II at 1 pmol/min; and 2% +/- 27%, 39% +/- 40%, and 132% +/- 74% with angiotension II at 5 pmo;/min; P =.0259).	Nitroglycerin	277-296	angiotensinogen	Homo sapiens	9-23
12087347-7	2002	Either a single dose of candesartan or coinfusion with vitamin C abolished the angiotensin II-induced attenuation of vasodilation of glyceryl trinitrate.	Nitroglycerin	133-152	angiotensinogen	Homo sapiens	79-93
12087347-8	2002	CONCLUSION: Our results suggest that angiotensin II may attenuate the arterial vasodilating effect of glyceryl trinitrate through angiotensin type 1 receptors and presumably through receptor-mediated superoxide production, which may be relevant to the development of nitrate tolerance.	Nitroglycerin	102-121	angiotensinogen	Homo sapiens	37-51
12081660-4	2002	We studied the effect of nitroglycerin on the innervated area of calcitonin gene-related peptide (CGRP) and serotonin-immunoreactive afferents to the superficial laminae of the spinal portion of trigeminal nucleus caudalis, and its modulation by estrogen.	Nitroglycerin	25-38	calcitonin-related polypeptide alpha	Rattus norvegicus	65-96
12081660-5	2002	In male rats, nitroglycerin produced after 4 h a significant decrease of the area innervated by CGRP-immunoreactive afferents and an increase of that covered by serotonin-immunoreactive fibres.	Nitroglycerin	14-27	calcitonin-related polypeptide alpha	Rattus norvegicus	96-100
12162941-11	2002	The administration of the NO donor nitroglycerin (NG) in the vasopressin treated animals restored NO values, and was capable of preventing the appearance of the plasma cardiac necrosis markers and altered coagulation values.	Nitroglycerin	35-48	arginine vasopressin	Homo sapiens	61-72
12054156-6	2002	These defective responses after reloading were rescued in iNOS-/- mice by treatment with an NO donor nitroglycerine (NG).	Nitroglycerin	101-115	nitric oxide synthase 2, inducible	Mus musculus	58-62
12054156-6	2002	These defective responses after reloading were rescued in iNOS-/- mice by treatment with an NO donor nitroglycerine (NG).	Nitroglycerin	117-119	nitric oxide synthase 2, inducible	Mus musculus	58-62
12162941-11	2002	The administration of the NO donor nitroglycerin (NG) in the vasopressin treated animals restored NO values, and was capable of preventing the appearance of the plasma cardiac necrosis markers and altered coagulation values.	Nitroglycerin	50-52	arginine vasopressin	Homo sapiens	61-72
12162941-12	2002	The protective activity of NG was attributed to NO release, which lowers BP values and counteracts coagulation activity in vasopressin-treated animals.	Nitroglycerin	27-29	arginine vasopressin	Homo sapiens	123-134
12044813-2	2002	Intraportal nitroglycerin restored insulin sensitivity in either case.	Nitroglycerin	12-25	insulin	Oryctolagus cuniculus	35-42
11923046-3	2002	The trigger for this is unknown, but there is evidence that GTN alters nitric oxide synthase (NOS) function and also leads to reduced L-arginine availability at its site of action with NOS.	Nitroglycerin	60-63	nitric oxide synthase 2	Homo sapiens	71-92
11994256-10	2002	To examine if another NO donor would have a similar effect, cardiomyocytes were treated with nitroglycerin before H-R. With nitroglycerin treatment, similar to SIN-1 treatment, myocyte injury was diminished, TGF-beta1 release increased, and total TGF-beta1 expression decreased.	Nitroglycerin	124-137	transforming growth factor beta 1	Homo sapiens	208-217
11919648-0	2002	Delayed cardioprotection induced by nitroglycerin is mediated by alpha-calcitonin gene-related peptide.	Nitroglycerin	36-49	calcitonin-related polypeptide alpha	Rattus norvegicus	71-102
11921057-2	2002	The NO donor glyceryl trinitrate (GTN) provokes delayed migraine attacks when infused into migraineurs and also causes iNOS expression and delayed inflammation within rodent dura mater.	Nitroglycerin	13-32	nitric oxide synthase 2	Homo sapiens	119-123
11921057-2	2002	The NO donor glyceryl trinitrate (GTN) provokes delayed migraine attacks when infused into migraineurs and also causes iNOS expression and delayed inflammation within rodent dura mater.	Nitroglycerin	34-37	nitric oxide synthase 2	Homo sapiens	119-123
11921057-4	2002	Because inflammation and iNOS are potential therapeutic targets, we examined transcriptional regulation of iNOS following GTN infusion and the consequences of its inhibition within dura mater.	Nitroglycerin	122-125	nitric oxide synthase 2	Homo sapiens	107-111
11921057-7	2002	iNOS expression is preceded by significant nuclear factor kappa B (NF-kappaB) activity, as reflected by a reduction in the inhibitory protein-kappa-Balpha (IkappaBalpha) and activation of NF-kappaB after GTN infusion.	Nitroglycerin	204-207	nitric oxide synthase 2	Homo sapiens	0-4
11921057-7	2002	iNOS expression is preceded by significant nuclear factor kappa B (NF-kappaB) activity, as reflected by a reduction in the inhibitory protein-kappa-Balpha (IkappaBalpha) and activation of NF-kappaB after GTN infusion.	Nitroglycerin	204-207	nuclear factor kappa B subunit 1	Homo sapiens	67-76
11921057-9	2002	These findings suggest that GTN promotes NF-kappaB activity and inflammation with a time course consistent with migraine attacks in susceptible individuals.	Nitroglycerin	28-31	nuclear factor kappa B subunit 1	Homo sapiens	41-50
11919648-1	2002	Previous investigations have demonstrated that early preconditioning induced by nitroglycerin is mediated by calcitonin gene-related peptide (CGRP).	Nitroglycerin	80-93	calcitonin-related polypeptide alpha	Rattus norvegicus	109-140
11919648-1	2002	Previous investigations have demonstrated that early preconditioning induced by nitroglycerin is mediated by calcitonin gene-related peptide (CGRP).	Nitroglycerin	80-93	calcitonin-related polypeptide alpha	Rattus norvegicus	142-146
11919648-2	2002	In the present study, we addressed the question of whether delayed preconditioning induced by nitroglycerin in the rat is related to stimulation of the release and synthesis of CGRP.	Nitroglycerin	94-107	calcitonin-related polypeptide alpha	Rattus norvegicus	177-181
11919648-11	2002	The present results suggest that the delayed cardioprotection induced by nitroglycerin is mediated mainly by the alpha-CGRP isoform via the NO-cGMP pathway.	Nitroglycerin	73-86	calcitonin-related polypeptide alpha	Rattus norvegicus	119-123
11937102-1	2002	Previous studies have shown that the development of tolerance to nitroglycerin is related to a decrease in the release of endogenous calcitonin gene-related peptide (CGRP).	Nitroglycerin	65-78	calcitonin-related polypeptide alpha	Rattus norvegicus	166-170
11979979-9	2002	CONCLUSION: Since the Asp 208 Glu mutation was found in NTG, the pathogenesis of glaucoma with myocilin mutation might be more complex and it may be related to weakness of the optic nerve head.	Nitroglycerin	56-59	myocilin	Homo sapiens	95-103
11937102-2	2002	In the present study, we explored whether endogenous CGRP is involved in reversal of tolerance to nitroglycerin with N-acetylcysteine or captopril in rats in vivo and vitro.	Nitroglycerin	98-111	calcitonin-related polypeptide alpha	Rattus norvegicus	53-57
11937102-1	2002	Previous studies have shown that the development of tolerance to nitroglycerin is related to a decrease in the release of endogenous calcitonin gene-related peptide (CGRP).	Nitroglycerin	65-78	calcitonin-related polypeptide alpha	Rattus norvegicus	133-164
11937102-4	2002	Nitroglycerin (3 x 10(-9)-10(-6) M) caused a concentration-dependent relaxation in the isolated rat thoracic aorta, an effect that was reduced by CGRP-(8-37) (3 x 10(-7) M) or capsaicin (3 x 10(-7) M).	Nitroglycerin	0-13	calcitonin-related polypeptide alpha	Rattus norvegicus	146-150
11937102-9	2002	The present results suggest that reversal of tolerance to nitroglycerin with N-acetylcysteine or captopril is related to the increased release of CGRP in the rat.	Nitroglycerin	58-71	calcitonin-related polypeptide alpha	Rattus norvegicus	146-150
11845867-10	2002	However, nitroglycerin only slightly depressed the AVP-induced contraction.	Nitroglycerin	9-22	arginine vasopressin	Homo sapiens	51-54
12039421-0	2002	Fos and nitric oxide synthase in rat brain with chronic mesostriatal dopamine deficiency: effects of nitroglycerin and hypoxia.	Nitroglycerin	101-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
12039421-2	2002	Systemic administration of nitroglycerin (NTG) or mild hypoxia resulted in a decreased of c-fos expression in the dorsolateral part of the denervated neostriatum.	Nitroglycerin	27-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
12039421-2	2002	Systemic administration of nitroglycerin (NTG) or mild hypoxia resulted in a decreased of c-fos expression in the dorsolateral part of the denervated neostriatum.	Nitroglycerin	42-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
12039421-3	2002	However, in other brain structures NTG or mild hypoxia evoked sustained c-fos expression in NOS-containing neurons and in the sources catecholaminergic projections involved in the control of cardiovascular function.	Nitroglycerin	35-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
12039421-4	2002	We propose that the administration of NTG, an NO donor, or hypoxia partially attenuate the consequences of an excessively increased glutamate level in the denervated neostriatum which are manifest in high level of c-fos expression.	Nitroglycerin	38-41	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	214-219
11953077-6	2002	The mean level of CRH concentration in nitroglycerin patch group before treatment was (257 +/- 61) ng/L, and it was decreased sharply to (38 +/- 17) ng/L after treatment.	Nitroglycerin	39-52	corticotropin releasing hormone	Homo sapiens	18-21
11953077-8	2002	CONCLUSION: Reduction of CRH secretion may be the mechanism of nitroglycerin patch on preterm labour therapy.	Nitroglycerin	63-76	corticotropin releasing hormone	Homo sapiens	25-28
11889009-7	2002	CONCLUSIONS: We conclude that long-term NTG treatment induces endothelial dysfunction and impaired vascular NO/cGMP signaling in humans, which can be monitored by measuring P-VASP levels.	Nitroglycerin	40-43	vasodilator stimulated phosphoprotein	Homo sapiens	175-179
11751199-7	2002	Transplanted lung graft ET-1 mRNA, measured by Northern blotting and in situ hybridization, and protein, measured by Western blotting and immunohistochemistry, were suppressed only with Early NTG (P &lt; 0.05 versus all other groups).	Nitroglycerin	192-195	endothelin 1	Homo sapiens	24-28
11751199-3	2002	Because endothelin-1 (ET-1), a potent vasoconstrictor, and nitric oxide (NO) are reciprocally regulated in vitro, we hypothesized that early administration of the NO donor NTG may suppress ET-1 and thereby improve lung preservation.	Nitroglycerin	172-175	endothelin 1	Homo sapiens	8-20
11739123-10	2002	Membrane PKC-zeta activity measured by immunoprecipitation and (32)P phosphorylation of PKC-epsilon pseudosubstrate peptide was 190 +/- 18% of NG (P &lt; 0.01, n = 4), which was completely inhibited by pretreatment with a myristoylated peptide inhibitor (ZI).	Nitroglycerin	143-145	protein kinase C zeta	Homo sapiens	9-17
11751199-8	2002	Post-transplantation benefits of NTG are restricted to lung grafts which received NTG during the early harvest and immersion periods, and are coincident with suppression of graft ET-1 expression.	Nitroglycerin	33-36	endothelin 1	Homo sapiens	179-183
11751199-3	2002	Because endothelin-1 (ET-1), a potent vasoconstrictor, and nitric oxide (NO) are reciprocally regulated in vitro, we hypothesized that early administration of the NO donor NTG may suppress ET-1 and thereby improve lung preservation.	Nitroglycerin	172-175	endothelin 1	Homo sapiens	22-26
11751199-3	2002	Because endothelin-1 (ET-1), a potent vasoconstrictor, and nitric oxide (NO) are reciprocally regulated in vitro, we hypothesized that early administration of the NO donor NTG may suppress ET-1 and thereby improve lung preservation.	Nitroglycerin	172-175	endothelin 1	Homo sapiens	189-193
11751199-9	2002	When viewed in the context of improved graft survival and function with ET-1 receptor blockade, these data suggest that early administration of NTG to donor lungs improves primary graft function, in part, by suppressing graft ET-1 expression.	Nitroglycerin	144-147	endothelin 1	Homo sapiens	72-76
11751199-9	2002	When viewed in the context of improved graft survival and function with ET-1 receptor blockade, these data suggest that early administration of NTG to donor lungs improves primary graft function, in part, by suppressing graft ET-1 expression.	Nitroglycerin	144-147	endothelin 1	Homo sapiens	226-230
12688525-3	2002	CYP1A2 effectively formed NO from isosorbide dinitrate and nitroglycerine (NTG).	Nitroglycerin	75-78	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	0-6
14600946-14	2002	In GD patients a statistically significant increase of ICAM-1 was observed in the 6th week (301.1 +/- 33.2 ng/ml, p &lt; 0.05) of RAI whereas in TNG group there was no statistical difference compared to initial values (249.7 +/- 42.6 ng/ml, N.S.).	Nitroglycerin	145-148	intercellular adhesion molecule 1	Homo sapiens	55-61
11815364-4	2002	In both the eNOS (-/-) and (+/+) mice, the EC(50) from NTG concentration-response curve was increased by approximately 3 fold, and vascular cyclic GMP accumulation was similarly decreased after NTG pretreatment.	Nitroglycerin	194-197	5'-nucleotidase, cytosolic II	Mus musculus	147-150
12688525-3	2002	CYP1A2 effectively formed NO from isosorbide dinitrate and nitroglycerine (NTG).	Nitroglycerin	59-73	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	0-6
12688525-6	2002	At 48 h after infusion, NTG-induced NO generation of the vessels increased in acetone (a P450 inducer)-pretreated rats, and nitrite and nitrate levels were markedly greater than in normal rats.	Nitroglycerin	24-27	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	89-93
11742226-3	2001	Subcutaneous treatment of rats with the NO-donor glyceryl trinitrate (GTN) induced an increase of sGC expression and activity in dural blood vessels after 20-30 min.	Nitroglycerin	49-68	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	98-101
11742226-3	2001	Subcutaneous treatment of rats with the NO-donor glyceryl trinitrate (GTN) induced an increase of sGC expression and activity in dural blood vessels after 20-30 min.	Nitroglycerin	70-73	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	98-101
11742226-0	2001	Glyceryl trinitrate treatment up-regulates soluble guanylyl cyclase in rat dura mater.	Nitroglycerin	0-19	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	43-67
11701602-9	2001	In addition to cytokine induction, macrophage iNOS upregulation and oedema formation after GTN infusion, dural mast cells exhibited granular changes consistent with secretion at 4 and 6 h. Because iNOS was expressed in dural macrophages following topical GTN, and in the spleen after intravenous injection, the data suggest that the inflammatory response is mediated by direct actions on the dura and does not develop secondary to events within the brain.	Nitroglycerin	91-94	nitric oxide synthase 2	Rattus norvegicus	197-201
11701602-9	2001	In addition to cytokine induction, macrophage iNOS upregulation and oedema formation after GTN infusion, dural mast cells exhibited granular changes consistent with secretion at 4 and 6 h. Because iNOS was expressed in dural macrophages following topical GTN, and in the spleen after intravenous injection, the data suggest that the inflammatory response is mediated by direct actions on the dura and does not develop secondary to events within the brain.	Nitroglycerin	255-258	nitric oxide synthase 2	Rattus norvegicus	197-201
11679441-10	2001	Cardiac surgery increased plasma insulin in patients with and without diabetes; this increase was delayed by the infusion of GTN, but it was not related to the changes in NO production.	Nitroglycerin	125-128	insulin	Homo sapiens	33-40
11744139-6	2001	Nitroglycerin (60 microg/kg or 120 microg/kg) caused an improvement of cardiac function, a decrease in the release of creatine kinase in coronary effluent and a decrease in the content of TNF-alpha in myocardial tissues.	Nitroglycerin	0-13	tumor necrosis factor	Rattus norvegicus	188-197
11744139-7	2001	Nitroglycerin significantly increased plasma concentrations of CGRP and NO.	Nitroglycerin	0-13	calcitonin-related polypeptide alpha	Rattus norvegicus	63-67
11744139-8	2001	After pretreatment with capsaicin, which depletes neurotransmitters in sensory nerves, or methylene blue, a selective guanylate cyclase inhibitor, the protection and the elevated release of CGRP induced by nitroglycerin were abolished.	Nitroglycerin	206-219	calcitonin-related polypeptide alpha	Rattus norvegicus	190-194
11744139-9	2001	The present study suggests that improvement of preservation with cardioplegic solution by nitroglycerin-induced delayed preconditioning is due to stimulation of CGRP release in the rat heart, and that the protection of CGRP-mediated nitroglycerin is related to inhibition of TNF-alpha production.	Nitroglycerin	90-103	calcitonin-related polypeptide alpha	Rattus norvegicus	161-165
11744139-9	2001	The present study suggests that improvement of preservation with cardioplegic solution by nitroglycerin-induced delayed preconditioning is due to stimulation of CGRP release in the rat heart, and that the protection of CGRP-mediated nitroglycerin is related to inhibition of TNF-alpha production.	Nitroglycerin	90-103	calcitonin-related polypeptide alpha	Rattus norvegicus	219-223
11744139-9	2001	The present study suggests that improvement of preservation with cardioplegic solution by nitroglycerin-induced delayed preconditioning is due to stimulation of CGRP release in the rat heart, and that the protection of CGRP-mediated nitroglycerin is related to inhibition of TNF-alpha production.	Nitroglycerin	90-103	tumor necrosis factor	Rattus norvegicus	275-284
11744139-9	2001	The present study suggests that improvement of preservation with cardioplegic solution by nitroglycerin-induced delayed preconditioning is due to stimulation of CGRP release in the rat heart, and that the protection of CGRP-mediated nitroglycerin is related to inhibition of TNF-alpha production.	Nitroglycerin	233-246	calcitonin-related polypeptide alpha	Rattus norvegicus	219-223
11711050-0	2001	Protective effects of nitroglycerin-induced preconditioning mediated by calcitonin gene-related peptide in rat small intestine.	Nitroglycerin	22-35	calcitonin-related polypeptide alpha	Rattus norvegicus	72-103
11711050-1	2001	Previous studies of myocardium have shown that ischemic preconditioning could be mimicked by nitroglycerin through stimulating the release of calcitonin gene-related peptide (CGRP).	Nitroglycerin	93-106	calcitonin-related polypeptide alpha	Rattus norvegicus	142-173
11711050-1	2001	Previous studies of myocardium have shown that ischemic preconditioning could be mimicked by nitroglycerin through stimulating the release of calcitonin gene-related peptide (CGRP).	Nitroglycerin	93-106	calcitonin-related polypeptide alpha	Rattus norvegicus	175-179
11711050-6	2001	However, the protection afforded by nitroglycerin was abolished by CGRP-(8-37), a selective CGRP acceptor antagonist.	Nitroglycerin	36-49	calcitonin-related polypeptide alpha	Rattus norvegicus	67-71
11711050-6	2001	However, the protection afforded by nitroglycerin was abolished by CGRP-(8-37), a selective CGRP acceptor antagonist.	Nitroglycerin	36-49	calcitonin-related polypeptide alpha	Rattus norvegicus	92-96
11711050-8	2001	In addition, the content of CGRP-like immunoreactivity in the effluent was increased during nitroglycerin perfusion.	Nitroglycerin	92-105	calcitonin-related polypeptide alpha	Rattus norvegicus	28-32
11711050-11	2001	All these findings suggest that nitroglycerin-induced preconditioning is related to stimulation of CGRP release in the rat small intestine.	Nitroglycerin	32-45	calcitonin-related polypeptide alpha	Rattus norvegicus	99-103
11583888-0	2001	Evidence supporting abnormalities in nitric oxide synthase function induced by nitroglycerin in humans.	Nitroglycerin	79-92	nitric oxide synthase 2	Homo sapiens	37-58
11691878-11	2001	Compared to NTG controls, the force generated by fibre bundles from TG mice expressing ssTnI was more sensitive to Ca(2+).	Nitroglycerin	12-15	troponin I, skeletal, slow 1	Mus musculus	87-92
11576096-6	2001	The mean value of dRoR during baseline and during induced hypotension was 14.2 (2.9) and 14.2 (1.6) % x s(-1), respectively, in the nitroglycerin group, and 14.6 (2.6) and 14.4 (2.4) % x s(-1), in the prostaglandin E1 group.	Nitroglycerin	132-145	Ror	Drosophila melanogaster	18-22
11574422-5	2001	Likewise, downstream of ERK1/2, ET-1 stimulated Elk-1-driven GAL4 luciferase activity to 11 +/- 1-fold (P &lt; 0.002 vs. NG + ET-1) in HG, and DN-PKC-delta, -epsilon, or -zeta attenuated this response to NG levels.	Nitroglycerin	121-123	mitogen-activated protein kinase 3	Homo sapiens	24-30
11574422-5	2001	Likewise, downstream of ERK1/2, ET-1 stimulated Elk-1-driven GAL4 luciferase activity to 11 +/- 1-fold (P &lt; 0.002 vs. NG + ET-1) in HG, and DN-PKC-delta, -epsilon, or -zeta attenuated this response to NG levels.	Nitroglycerin	121-123	endothelin 1	Homo sapiens	32-36
11574422-5	2001	Likewise, downstream of ERK1/2, ET-1 stimulated Elk-1-driven GAL4 luciferase activity to 11 +/- 1-fold (P &lt; 0.002 vs. NG + ET-1) in HG, and DN-PKC-delta, -epsilon, or -zeta attenuated this response to NG levels.	Nitroglycerin	121-123	ETS transcription factor ELK1	Homo sapiens	48-53
11574422-5	2001	Likewise, downstream of ERK1/2, ET-1 stimulated Elk-1-driven GAL4 luciferase activity to 11 +/- 1-fold (P &lt; 0.002 vs. NG + ET-1) in HG, and DN-PKC-delta, -epsilon, or -zeta attenuated this response to NG levels.	Nitroglycerin	121-123	galectin 4	Homo sapiens	61-65
11583888-12	2001	The responses to L-NMMA suggest that GTN therapy causes abnormalities in nitric oxide synthase (NOS) function; the vasodilation observed at the lowest infused concentration of L-NMMA in the GTN group also suggests that continuous GTN therapy is associated with a NOS-mediated production of a vasoconstrictor.	Nitroglycerin	37-40	nitric oxide synthase 2	Homo sapiens	73-94
11557266-0	2001	Involvement of calcitonin gene-related peptide in the development of tolerance to nitroglycerin in the rat.	Nitroglycerin	82-95	calcitonin-related polypeptide alpha	Rattus norvegicus	15-46
11571238-5	2001	MLD of patients with elevated CRP levels exhibited a greater reduction during CPT and a greater increase after NTG than of patients with normal CRP levels (-15+/-12% versus -7+/-14%, P=0.037, and 31+/-23% versus 13+/-25%, P=0.011, respectively).	Nitroglycerin	111-114	C-reactive protein	Homo sapiens	30-33
11557266-1	2001	Previous studies have shown that the depressor effect of nitroglycerin is related to stimulation of endogenous calcitonin gene-related peptide (CGRP) release.	Nitroglycerin	57-70	calcitonin-related polypeptide alpha	Rattus norvegicus	111-142
11557266-1	2001	Previous studies have shown that the depressor effect of nitroglycerin is related to stimulation of endogenous calcitonin gene-related peptide (CGRP) release.	Nitroglycerin	57-70	calcitonin-related polypeptide alpha	Rattus norvegicus	144-148
11557266-2	2001	In the present study, we explored whether endogenous CGRP is involved in the development of tolerance to nitroglycerin in the rat.	Nitroglycerin	105-118	calcitonin-related polypeptide alpha	Rattus norvegicus	53-57
11557266-6	2001	significantly decreased blood pressure concomitantly with an increase in plasma concentration of nitric oxide (NO) and CGRP, and these effects of nitroglycerin disappeared after pretreatment with nitroglycerin for 8 days.	Nitroglycerin	196-209	calcitonin-related polypeptide alpha	Rattus norvegicus	119-123
11557266-7	2001	However, the nitroglycerin-induced depressor effect and elevation of NO and CGRP content were restored, partially or completely, 4 or 8 days after nitroglycerin removal in the tolerant rat.	Nitroglycerin	13-26	calcitonin-related polypeptide alpha	Rattus norvegicus	76-80
11557266-8	2001	The present study suggests that the development of tolerance to nitroglycerin is related to the decreased release of CGRP in the rat.	Nitroglycerin	64-77	calcitonin-related polypeptide alpha	Rattus norvegicus	117-121
11509549-5	2001	With addition of nitroglycerin to histamine-stimulated swine carotid media, the initial relaxation transient was associated with a decrease in MRLC phosphorylation without an increase in Ser(16)-HSP20 phosphorylation.	Nitroglycerin	17-30	HSPB6	Sus scrofa	195-200
11509549-6	2001	During the sustained phase of nitroglycerin-induced relaxation and during force redevelopment induced by washout of nitroglycerin in the continued presence of histamine, the level of Ser(16)-HSP20 phosphorylation, but not MRLC phosphorylation, correlated with inhibition of force.	Nitroglycerin	30-43	HSPB6	Sus scrofa	191-196
11509549-0	2001	Selected contribution: HSP20 phosphorylation in nitroglycerin- and forskolin-induced sustained reductions in swine carotid media tone.	Nitroglycerin	48-61	HSPB6	Sus scrofa	23-28
21171413-2	2001	RESULTS: CNP had the dose-dependent vasodilation effects on abdominal artery and celiac vein at the range of 10(-10)-10(-6) mol/L, its action on vein was just like nitroglycerin, its action on artery was weaker than that of ANP.	Nitroglycerin	164-177	2',3'-cyclic-nucleotide 3'-phosphodiesterase	Oryctolagus cuniculus	9-12
11718022-1	2001	OBJECTIVE: To evaluate the effects and possibility of nitroglycerin on Pregnancy induced hypertension (PIH) treatment.	Nitroglycerin	54-67	pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included)	Homo sapiens	103-106
11397846-5	2001	Vasodilator response to bradykinin, expressed as the within-subject mean difference in the area under the dose-response curve between phases, was significantly increased at midcycle compared with that in the early menstrual phase (486.5 +/- 165.0; P = 0.01), whereas there was no significant difference in response to glyceryl trinitrate (185.8 +/- 239.0; P = 0.45).	Nitroglycerin	318-337	kininogen 1	Homo sapiens	24-34
11521755-0	2001	The depressor effect of nitroglycerin is mediated by calcitonin gene-related peptide.	Nitroglycerin	24-37	calcitonin-related polypeptide alpha	Rattus norvegicus	53-84
11521755-1	2001	Previous investigations have suggested that vasodilator responses to nitroglycerin involve in stimulation of calcitonin gene-related peptide (CGRP) release.	Nitroglycerin	69-82	calcitonin-related polypeptide alpha	Rattus norvegicus	109-140
11521755-1	2001	Previous investigations have suggested that vasodilator responses to nitroglycerin involve in stimulation of calcitonin gene-related peptide (CGRP) release.	Nitroglycerin	69-82	calcitonin-related polypeptide alpha	Rattus norvegicus	142-146
11521755-5	2001	Nitroglycerin (30 or 150 microg/kg) caused a depressor effect with an increase in plasma concentrations of CGRP.	Nitroglycerin	0-13	calcitonin-related polypeptide alpha	Rattus norvegicus	107-111
11521755-7	2001	The present study suggests that the depressor effect of nitroglycerin is related to stimulation of CGRP release in the rat.	Nitroglycerin	56-69	calcitonin-related polypeptide alpha	Rattus norvegicus	99-103
11470751-3	2001	We also observed that GTN application led to a significant reduction in the ornithine decarboxylase (ODC) activity and decreased the rate of [3H]thymidine incorporation into epidermal DNA when compared with the acetone-treated control (P &lt; 0.001).	Nitroglycerin	22-25	ornithine decarboxylase, structural 1	Mus musculus	76-99
11470751-3	2001	We also observed that GTN application led to a significant reduction in the ornithine decarboxylase (ODC) activity and decreased the rate of [3H]thymidine incorporation into epidermal DNA when compared with the acetone-treated control (P &lt; 0.001).	Nitroglycerin	22-25	ornithine decarboxylase, structural 1	Mus musculus	101-104
11531896-4	2001	Intradermal injection of capsaicin in the periorbital area increased c-fos expression in nucleus trigeminalis caudalis; this was significantly potentiated by glyceryl trinitrate.	Nitroglycerin	158-177	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-74
11408036-1	2001	The delayed preconditioning of the heart by monophosphoryl lipid A is mediated by endogenous nitric oxide (NO), and the cardioprotection afforded by nitroglycerin is related to stimulation of calcitonin gene-related peptide (CGRP) release.	Nitroglycerin	149-162	calcitonin-related polypeptide alpha	Rattus norvegicus	192-223
11408036-1	2001	The delayed preconditioning of the heart by monophosphoryl lipid A is mediated by endogenous nitric oxide (NO), and the cardioprotection afforded by nitroglycerin is related to stimulation of calcitonin gene-related peptide (CGRP) release.	Nitroglycerin	149-162	calcitonin-related polypeptide alpha	Rattus norvegicus	225-229
11331261-0	2001	Effects of in vivo nitroglycerin treatment on activity and expression of the guanylyl cyclase and cGMP-dependent protein kinase and their downstream target vasodilator-stimulated phosphoprotein in aorta.	Nitroglycerin	19-32	vasodilator-stimulated phosphoprotein	Rattus norvegicus	156-193
11331261-4	2001	METHODS AND RESULTS: We therefore studied the effects of 3-day NTG treatment of rats and rabbits on activity and expression of the immediate NO target soluble guanylyl cyclase (sGC) and on the cGMP-activated protein kinase I (cGK-I).	Nitroglycerin	63-66	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	177-180