PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
15883972-4	2005	Putative structural models have been generated for the interactions of ACE inhibitors (lisinopril, captoril, enalaprilat, keto-ACE, ramiprilat, quinaprilat, peridoprilat, fosinoprilat, and RXP 407) with both the ACE_C and the ACE_N domains.	Enalaprilat	109-120	angiotensin I converting enzyme	Homo sapiens	71-74
15601445-1	2004	The pharmacokinetic (PK) properties and the pharmacokinetic/pharmacodynamic (PK/PD) relationships for the angiotensin-converting enzyme (ACE) inhibitors (ACEIs), such as enalaprilat, benazeprilat, imidaprilat and ramiprilat, differ from those of conventional drugs.	Enalaprilat	170-181	angiotensin I converting enzyme	Homo sapiens	106-135
15467007-9	2005	Incubation of PSTs with ANG 1-9 also led to generation of ANG 1-7, an effect blocked by the ACE inhibitor captopril or enalaprilat, but not by DX600.	Enalaprilat	119-130	angiogenin	Rattus norvegicus	24-31
15467007-9	2005	Incubation of PSTs with ANG 1-9 also led to generation of ANG 1-7, an effect blocked by the ACE inhibitor captopril or enalaprilat, but not by DX600.	Enalaprilat	119-130	angiogenin	Rattus norvegicus	58-65
15475593-2	2005	Three hours after probe implantation, 200 microM of the angiotensin-converting enzyme (ACE) inhibitor enalaprilat were added to the perfusion solution in one of the sides for 30 min.	Enalaprilat	102-113	angiotensin I converting enzyme	Homo sapiens	56-85
15475593-2	2005	Three hours after probe implantation, 200 microM of the angiotensin-converting enzyme (ACE) inhibitor enalaprilat were added to the perfusion solution in one of the sides for 30 min.	Enalaprilat	102-113	angiotensin I converting enzyme	Homo sapiens	87-90
15475593-6	2005	Enalaprilat induced a significant increase in bradykinin levels in the dialysate, without affecting kallidin levels.	Enalaprilat	0-11	kininogen 1	Homo sapiens	46-56
15601445-1	2004	The pharmacokinetic (PK) properties and the pharmacokinetic/pharmacodynamic (PK/PD) relationships for the angiotensin-converting enzyme (ACE) inhibitors (ACEIs), such as enalaprilat, benazeprilat, imidaprilat and ramiprilat, differ from those of conventional drugs.	Enalaprilat	170-181	angiotensin I converting enzyme	Homo sapiens	137-140
15381315-3	2004	Nevertheless, a 1:1 stoichiometry for the binding of lisinopril, captopril or enalaprilat to somatic pig lung ACE is shown by isothermal titration calorimetry (ITC) and enzymatic assays.	Enalaprilat	78-89	angiotensin-converting enzyme	Sus scrofa	110-113
15304551-3	2004	The ACE inhibitor enalaprilat and the peptide ligand desArg(10)-kallidin (in nanomolar concentrations) release NO by activating endothelial NO synthase (eNOS) in bovine and inducible NO synthase (iNOS) in stimulated human endothelial cells.	Enalaprilat	18-29	angiotensin I converting enzyme	Bos taurus	4-7
15304551-3	2004	The ACE inhibitor enalaprilat and the peptide ligand desArg(10)-kallidin (in nanomolar concentrations) release NO by activating endothelial NO synthase (eNOS) in bovine and inducible NO synthase (iNOS) in stimulated human endothelial cells.	Enalaprilat	18-29	nitric oxide synthase 2	Bos taurus	173-194
15304551-3	2004	The ACE inhibitor enalaprilat and the peptide ligand desArg(10)-kallidin (in nanomolar concentrations) release NO by activating endothelial NO synthase (eNOS) in bovine and inducible NO synthase (iNOS) in stimulated human endothelial cells.	Enalaprilat	18-29	nitric oxide synthase 2	Bos taurus	196-200
15492767-2	2004	Its active form, temocaprilat, is slightly more potent than enalaprilat in inhibiting ACE isolated from rabbit lung.	Enalaprilat	60-71	angiotensin-converting enzyme	Oryctolagus cuniculus	86-89
15100096-5	2004	Luminally perfusing with either enalaprilat (10(-4) M) to inhibit production of angiotensin II or losartan (10(-8) M) to block the angiotensin receptor decreased the proximal tubule volume reabsorptive rate in DHT-treated rats to a significantly greater degree than in control vehicle-injected rats.	Enalaprilat	32-43	angiotensinogen	Rattus norvegicus	80-94
12831415-3	2003	Enalaprilat, the only intravenous angiotensin-converting enzyme inhibitor, is used to treat hypertension in pediatric patients in other settings.	Enalaprilat	0-11	angiotensin I converting enzyme	Homo sapiens	34-63
14743484-1	2004	Dynamic capillary electrophoresis (DCE) and computer simulation of the elution profiles with the stochastic model has been applied to determine the isomerization barriers of the angiotensin converting enzyme inhibitor enalaprilat.	Enalaprilat	218-229	angiotensin I converting enzyme	Homo sapiens	178-207
14694157-4	2004	Bradykinin, enalaprilat, and amlodipine significantly suppressed cortical oxygen consumption in 4-mo-old rats (bradykinin: -2.5 +/- 0.9% to -21 +/- 1.5%; enalaprilat: -0.7 +/- 0.5% to -26 +/- 1.2%; amlodipine: -1.3 +/- 0.9% to -18 +/- 1.2%; P < 0.05).	Enalaprilat	12-23	kininogen 1	Homo sapiens	111-121
14694157-4	2004	Bradykinin, enalaprilat, and amlodipine significantly suppressed cortical oxygen consumption in 4-mo-old rats (bradykinin: -2.5 +/- 0.9% to -21 +/- 1.5%; enalaprilat: -0.7 +/- 0.5% to -26 +/- 1.2%; amlodipine: -1.3 +/- 0.9% to -18 +/- 1.2%; P < 0.05).	Enalaprilat	154-165	kininogen 1	Homo sapiens	0-10
14694157-6	2004	However, in 23-mo-old animals, the responses to bradykinin and enalaprilat were attenuated (bradykinin: 0 +/- 0% to -13 +/- 0.9%; enalaprilat: -0.3 +/- 0.3% to -17 +/- 2.1%; P < 0.05), whereas the response to an NO donor was unaffected, suggesting decreased bioavailability of NO.	Enalaprilat	63-74	kininogen 1	Homo sapiens	92-102
14694157-6	2004	However, in 23-mo-old animals, the responses to bradykinin and enalaprilat were attenuated (bradykinin: 0 +/- 0% to -13 +/- 0.9%; enalaprilat: -0.3 +/- 0.3% to -17 +/- 2.1%; P < 0.05), whereas the response to an NO donor was unaffected, suggesting decreased bioavailability of NO.	Enalaprilat	130-141	kininogen 1	Homo sapiens	48-58
15236580-0	2004	Structural details on the binding of antihypertensive drugs captopril and enalaprilat to human testicular angiotensin I-converting enzyme.	Enalaprilat	74-85	angiotensin I converting enzyme	Homo sapiens	106-137
15236580-2	2004	Here we report the high-resolution crystal structures of testis ACE (tACE) in complex with the first successfully designed ACE inhibitor captopril and enalaprilat, the Phe-Ala-Pro analogue.	Enalaprilat	151-162	angiotensin I converting enzyme	Homo sapiens	64-67
15236580-2	2004	Here we report the high-resolution crystal structures of testis ACE (tACE) in complex with the first successfully designed ACE inhibitor captopril and enalaprilat, the Phe-Ala-Pro analogue.	Enalaprilat	151-162	angiotensin I converting enzyme	Homo sapiens	70-73
14733716-8	2003	In both groups, the ACE inhibitors captopril and enalaprilat, caused a significant inhibition of the ACE activity in the choroid and ciliary body, with enalaprilat being more potent.	Enalaprilat	49-60	angiotensin-converting enzyme	Sus scrofa	20-23
14733716-8	2003	In both groups, the ACE inhibitors captopril and enalaprilat, caused a significant inhibition of the ACE activity in the choroid and ciliary body, with enalaprilat being more potent.	Enalaprilat	49-60	angiotensin-converting enzyme	Sus scrofa	101-104
14733716-8	2003	In both groups, the ACE inhibitors captopril and enalaprilat, caused a significant inhibition of the ACE activity in the choroid and ciliary body, with enalaprilat being more potent.	Enalaprilat	152-163	angiotensin-converting enzyme	Sus scrofa	20-23
14733716-8	2003	In both groups, the ACE inhibitors captopril and enalaprilat, caused a significant inhibition of the ACE activity in the choroid and ciliary body, with enalaprilat being more potent.	Enalaprilat	152-163	angiotensin-converting enzyme	Sus scrofa	101-104
14511680-8	2003	Similar analyses can be made using the alternative ACE inhibitors captopril and enalaprilat.	Enalaprilat	80-91	angiotensin I converting enzyme	Homo sapiens	51-54
12427424-0	2002	Influence of propranolol, enalaprilat, verapamil, and caffeine on adenosine A(2A)-receptor-mediated coronary vasodilation.	Enalaprilat	26-37	adenosine A2a receptor	Canis lupus familiaris	66-90
12623947-2	2003	We compared intravenously administered ACE inhibitors, perindoprilat and enalaprilat, for myocardial drug uptake and effects on angiotensin and bradykinin peptides versus hemodynamic effects in 25 patients with stable angina and well-preserved left ventricular systolic function.	Enalaprilat	73-84	kininogen 1	Homo sapiens	144-154
12566370-6	2003	In contrast, enalaprilat significantly increased resting net t-PA release (from 0.6+/-0.4 to 1.7+/-0.6 ng.	Enalaprilat	13-24	plasminogen activator, tissue type	Homo sapiens	61-65
12566370-8	2003	Enalaprilat increased the effect of exogenous bradykinin on FBF 60% (from 17.5+/-2.5 to 28.1+/-4.0 mL.	Enalaprilat	0-11	kininogen 1	Homo sapiens	46-56
14520012-9	2003	Enalaprilat decreased the fibronectin mRNA synthesis dramatically (>50%, p < 0.0001) under high-glucose conditions.	Enalaprilat	0-11	fibronectin 1	Mus musculus	26-37
14520012-10	2003	CONCLUSIONS: Enalaprilat normalizes the abnormal, high-glucose-induced concentration of laminin, while it decreases the fibronectin synthesis.	Enalaprilat	13-24	fibronectin 1	Mus musculus	120-131
12489793-3	2002	Enalaprilat and other ACE inhibitors at nanomolar concentrations activate the BK B1 receptor directly in the absence of ACE and the peptide ligands, des-Arg-kinins.	Enalaprilat	0-11	bradykinin receptor B1	Homo sapiens	81-92
12651915-4	2003	Similar effects were obtained using CV-11974 (another AT1R blocker) and enalaprilat (another ACE inhibitor).	Enalaprilat	72-83	angiotensin-converting enzyme	Oryctolagus cuniculus	93-96
12566370-10	2003	Enalaprilat increased the t-PA response to bradykinin to a greater extent than the FBF response, shifting the relationship between net t-PA release and FBF (P=0.005).	Enalaprilat	0-11	plasminogen activator, tissue type	Homo sapiens	26-30
12566370-10	2003	Enalaprilat increased the t-PA response to bradykinin to a greater extent than the FBF response, shifting the relationship between net t-PA release and FBF (P=0.005).	Enalaprilat	0-11	kininogen 1	Homo sapiens	43-53
12566370-10	2003	Enalaprilat increased the t-PA response to bradykinin to a greater extent than the FBF response, shifting the relationship between net t-PA release and FBF (P=0.005).	Enalaprilat	0-11	plasminogen activator, tissue type	Homo sapiens	135-139
14727943-13	2003	Enalaprilat is the only ACE inhibitor available for parenteral use and may be particularly useful in treating hypertensive emergencies in patients with heart failure.	Enalaprilat	0-11	angiotensin I converting enzyme	Homo sapiens	24-27
12845221-11	2003	Administration of the ACE inhibitor, enalaprilat at the beginning of the experimental period, completely abrogated this decline and protected pO(2) levels throughout this period with no effect on blood pressure or renal blood flow.	Enalaprilat	37-48	angiotensin I converting enzyme	Rattus norvegicus	22-25
12489810-6	2002	Moreover, two renin inhibitors, pepstatin-A and BILA 2157 BS, the ACE inhibitor enalaprilat and the AT1-receptor antagonist EXP3174 prevented ischemic NE release.	Enalaprilat	80-91	angiotensin I converting enzyme	Homo sapiens	66-69
12427424-1	2002	OBJECTIVES: The study was done to determine the effects of propranolol, enalaprilat, verapamil, and caffeine on the vasodilatory properties of the adenosine A(2A)-receptor agonist ATL-146e (ATL).	Enalaprilat	72-83	adenosine A2a receptor	Canis lupus familiaris	147-171
12393362-2	2002	This study aimed to compare the haemodynamic profile of anaesthetized pigs, which were subjected to haemorrhage in the presence of the ACE inhibitor enalaprilat or the AT(1) antagonist valsartan.	Enalaprilat	149-160	angiotensin-converting enzyme	Sus scrofa	135-138
12393362-9	2002	CONCLUSION: Blockade of the renin-angiotensin system by either enalaprilat or valsartan leads to a similar decrease in arterial pressure during anaesthesia and haemorrhage but the haemodynamic profiles are quite different.	Enalaprilat	63-74	renin	Sus scrofa	28-33
12191964-11	2002	These results indicate that addition of AngI in the interstitial compartment leads to low but significant conversion to AngII via ACE activity (blocked by enalaprilat).	Enalaprilat	155-166	angiotensinogen	Rattus norvegicus	120-125
12191964-11	2002	These results indicate that addition of AngI in the interstitial compartment leads to low but significant conversion to AngII via ACE activity (blocked by enalaprilat).	Enalaprilat	155-166	angiotensin I converting enzyme	Rattus norvegicus	130-133
12191964-1	2002	It was recently demonstrated that angiotensin II (AngII) concentrations in the renal interstitial fluid (RIF) of anesthetized rats were in the nanomolar range and were not reduced by intra-arterial infusion of an angiotensin-converting enzyme (ACE) inhibitor (enalaprilat).	Enalaprilat	260-271	angiotensinogen	Rattus norvegicus	34-48
12191964-1	2002	It was recently demonstrated that angiotensin II (AngII) concentrations in the renal interstitial fluid (RIF) of anesthetized rats were in the nanomolar range and were not reduced by intra-arterial infusion of an angiotensin-converting enzyme (ACE) inhibitor (enalaprilat).	Enalaprilat	260-271	angiotensinogen	Rattus norvegicus	50-55
11983548-14	2002	Enalaprilat inhibited caspase 3, which was reversed by L-NAME.	Enalaprilat	0-11	caspase 3	Homo sapiens	22-31
12191964-2	2002	This study was performed to determine changes in RIF AngI and AngII concentrations during interstitial administration of ACE inhibitors (enalaprilat and perindoprilat).	Enalaprilat	137-148	angiotensin I converting enzyme	Rattus norvegicus	121-124
12191964-3	2002	Studies were also performed to determine the effects of enalaprilat on the de novo formation of RIF AngII elicited by interstitial infusion of AngI.	Enalaprilat	56-67	angiotensinogen	Rattus norvegicus	100-105
12057995-3	2002	The purpose of the present study was to determine the effects and the mechanism of action of the ACE inhibitor enalaprilat and the AT1 antagonist losartan on regional myocardial perfusion and coronary flow and vasodilator reserve in conscious dogs with pacing-induced dilated cardiomyopathy (DCM).	Enalaprilat	111-122	angiotensin I converting enzyme	Canis lupus familiaris	97-100
12057995-9	2002	CONCLUSIONS: The ACE inhibitor enalaprilat improves transmural myocardial perfusion at rest and after chronotropic stress and restores impaired subendocardial coronary flow and vasodilator reserve in DCM.	Enalaprilat	31-42	angiotensin I converting enzyme	Canis lupus familiaris	17-20
12057995-10	2002	The effects of enalaprilat were bradykinin mediated and NO dependent and were not recapitulated by losartan.	Enalaprilat	15-26	kininogen 1	Canis lupus familiaris	32-42
11997320-4	2002	The effect of angiotensin II was assessed by measuring the decrease in volume reabsorption with the addition of 10(-4) M luminal enalaprilat.	Enalaprilat	129-140	angiotensinogen	Homo sapiens	14-28
11880373-3	2002	We found that enalaprilat and other ACE inhibitors in nanomolar concentrations activate human bradykinin B(1) receptors directly in the absence of ACE and the B(1) agonist des-Arg(10)-Lys(1)-bradykinin.	Enalaprilat	14-25	kininogen 1	Homo sapiens	94-104
11880373-3	2002	We found that enalaprilat and other ACE inhibitors in nanomolar concentrations activate human bradykinin B(1) receptors directly in the absence of ACE and the B(1) agonist des-Arg(10)-Lys(1)-bradykinin.	Enalaprilat	14-25	kininogen 1	Homo sapiens	191-201
11741551-7	2001	Enalaprilat induced a 70% reduction of ACE activity and a significant increase of bradykinin in pulmonary arterial blood.	Enalaprilat	0-11	angiotensin I converting enzyme	Homo sapiens	39-42
11836639-8	2002	To investigate the PCE in this manner we tested the hypothesis that PCEB-ACE is depressed in patients diagnosed with acute lung injury and estimated interaction of an ACE inhibitor (enalaprilat) with PCE in human subjects.	Enalaprilat	182-193	angiotensin I converting enzyme	Homo sapiens	167-170
11836639-13	2002	When normalized to pre-drug (T(1)) activity levels, enalaprilat inhibited PCEB and SE ACE activity at T(2) by 74 +/- 6 and 68 +/- 6%, respectively.	Enalaprilat	52-63	angiotensin I converting enzyme	Homo sapiens	86-89
11879921-5	2002	The ACE inhibition assay was further validated by enalapril, its active derivative enalaprilat and the ACE-inhibitory peptide Ala-Leu-Pro-Met-His-Ile-Arg, corresponding to a tryptic fragment of bovine beta-lactoglobulin.	Enalaprilat	83-94	angiotensin I converting enzyme	Bos taurus	4-7
11799091-2	2002	In the present study, we performed experiments to explore renal interstitial fluid concentrations of Ang I and Ang II further and to determine whether these levels are altered by acute arterial infusion of an ACE inhibitor (enalaprilat) or by volume expansion.	Enalaprilat	224-235	angiotensin I converting enzyme	Rattus norvegicus	209-212
11799091-6	2002	Intra-arterial infusion of enalaprilat (7.5 micromol/kg/min, n=5) for 120 minutes resulted in a significant decrease in mean arterial pressure (from 114+/-4 to 68+/-4 mm Hg) along with reductions in plasma and renal ACE activity (by -99% and -52%, respectively).	Enalaprilat	27-38	angiotensin I converting enzyme	Rattus norvegicus	216-219
11741551-7	2001	Enalaprilat induced a 70% reduction of ACE activity and a significant increase of bradykinin in pulmonary arterial blood.	Enalaprilat	0-11	kininogen 1	Homo sapiens	82-92
11741551-11	2001	Effective cardiac ACE inhibition can be achieved by low-dose intracoronary enalaprilat, which primarily causes a potentiation of bradykinin.	Enalaprilat	75-86	angiotensin I converting enzyme	Homo sapiens	18-21
11741551-11	2001	Effective cardiac ACE inhibition can be achieved by low-dose intracoronary enalaprilat, which primarily causes a potentiation of bradykinin.	Enalaprilat	75-86	kininogen 1	Homo sapiens	129-139
11583902-8	2001	Pretreatment with the bradykinin antagonist HOE-140 attenuated the enalaprilat-induced increase in coronary blood flow.	Enalaprilat	67-78	kininogen 1	Canis lupus familiaris	22-32
11515896-5	2001	RESULTS: Wall motion scores (4, normal, to -1, dyskinesia) were higher in animals treated with ACE inhibitors (3.20+/-0.15 SE enalaprilat versus 3.08+/-0.23 quinaprilat versus 1.52+/-0.07 no ACE; both p < 0.0001 from no ACE).	Enalaprilat	126-137	angiotensin-converting enzyme	Sus scrofa	95-98
11578111-0	2001	Inhibition of serum angiotensin-converting enzyme in rabbits after intravenous administration of enalaprilat-loaded intact erythrocytes.	Enalaprilat	97-108	angiotensin-converting enzyme	Oryctolagus cuniculus	20-49
11578111-2	2001	In this study, the inhibition time courses of serum angiotensin-converting enzyme (ACE) activity after intravenous administration of enalaprilat encapsulated in intact erythrocytes was evaluated and compared with free drug, in a rabbit model.	Enalaprilat	133-144	angiotensin-converting enzyme	Oryctolagus cuniculus	52-81
11578111-2	2001	In this study, the inhibition time courses of serum angiotensin-converting enzyme (ACE) activity after intravenous administration of enalaprilat encapsulated in intact erythrocytes was evaluated and compared with free drug, in a rabbit model.	Enalaprilat	133-144	angiotensin-converting enzyme	Oryctolagus cuniculus	83-86
28095236-7	2001	The inhibitory effects of candesartan were selective and were similar in animals pretreated with enalaprilat to reduce endogenous Ang II production.	Enalaprilat	97-108	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	130-136
11453472-12	2001	Enalaprilat inhibited ACE activity to < 25% of baseline activity without changing cardiorespiratory or blood gas values, compared with horses administered saline solution.	Enalaprilat	0-11	angiotensin I converting enzyme	Equus caballus	22-25
11453472-13	2001	CONCLUSIONS AND CLINICAL RELEVANCE: Enalaprilat administration almost completely inhibited ACE activity in horses without changing the hemodynamic responses to intense exercise and is unlikely to be of value in preventing exercise-induced pulmonary hemorrhage.	Enalaprilat	36-47	angiotensin I converting enzyme	Equus caballus	91-94
11393708-1	2001	The chromatographic behaviour of the ACE inhibitors lisinopril, enalapril and its two degradation products, enalaprilat (hydrolytic degradation product) and diketopiperazine (DKP) (cyclization degradation product) was studied as a function of column temperature and pH of the mobile phase.	Enalaprilat	108-119	angiotensin I converting enzyme	Homo sapiens	37-40
11342966-0	2001	The bladder angiotensin system in female rats: response to infusions of angiotensin I and the angiotensin converting enzyme inhibitor enalaprilat.	Enalaprilat	134-145	angiotensin I converting enzyme	Rattus norvegicus	94-123
11181415-3	2001	The decrement in volume reabsorption after addition of 10(-4) M luminal enalaprilat is a measure of the role of luminal angiotensin II on transport.	Enalaprilat	72-83	angiotensinogen	Homo sapiens	120-134
11181415-26	2001	These data indicate that renal denervation abolished the luminal enalaprilat-sensitive component of proximal tubule transport, which is consistent with the renal nerves playing a role in the modulation of the intraluminal angiotensin II mediated component of proximal tubule transport.	Enalaprilat	65-76	angiotensinogen	Homo sapiens	222-236
11545137-2	2001	We examined whether the ACE inhibitor, enalaprilat (EN), improves intracellular sodium homeostasis during myocardial ischemia and the relationship of this effect to bradykinin.	Enalaprilat	39-50	angiotensin I converting enzyme	Rattus norvegicus	24-27
11827728-2	2000	In the present study, we have applied recently developed methodologies for assaying pulmonary capillary endothelium-bound (PCEB) ACE activity in man, to estimate the interaction of an ACE inhibitor (enalaprilat) with PCEB ACE in human subjects.	Enalaprilat	199-210	angiotensin I converting enzyme	Homo sapiens	129-132
11139436-4	2000	ACE inhibition or AT(1) receptor blockade attenuated the IGF-I (10(-7) M) induced neonatal rat cardiac fibroblast growth in a concentration-dependent fashion (moexiprilat: 50+/-2%, enalaprilat: 31+/-2%, CV11974; 58+/-1%, all: 10(-7) M).	Enalaprilat	181-192	angiotensin I converting enzyme	Rattus norvegicus	0-3
11139436-4	2000	ACE inhibition or AT(1) receptor blockade attenuated the IGF-I (10(-7) M) induced neonatal rat cardiac fibroblast growth in a concentration-dependent fashion (moexiprilat: 50+/-2%, enalaprilat: 31+/-2%, CV11974; 58+/-1%, all: 10(-7) M).	Enalaprilat	181-192	insulin-like growth factor 1	Rattus norvegicus	57-62
11068029-5	2000	Angiotensin converting enzyme inhibitors, enalaprilat (3 microM), ramiprilat (1 microM) or lisinopril (1 microM), increased the bradykinin-induced renal vasodilation by 40% or more.	Enalaprilat	42-53	angiotensin I converting enzyme	Rattus norvegicus	0-29
11124597-6	2000	Enalaprilat completely reversed the stimulatory effects of CyA on CF collagen synthesis (CyA + enalaprilat 6.40 +/- 0.50% vs. CyA alone 8.33 +/- 0.56% vs. control 6.57 +/- 0.62% vs. enalaprilat alone 5.55 +/- 0.93%, p < 0.05) and PTC secretion of TGFbeta1 (0.71 +/- 0.11, 1.13 +/- 0.09, 0.89 +/- 0.07, and 0.67 +/- 0.09 ng/mg protein/day, respectively, p < 0.05).	Enalaprilat	0-11	transforming growth factor beta 1	Homo sapiens	250-258
11827728-2	2000	In the present study, we have applied recently developed methodologies for assaying pulmonary capillary endothelium-bound (PCEB) ACE activity in man, to estimate the interaction of an ACE inhibitor (enalaprilat) with PCEB ACE in human subjects.	Enalaprilat	199-210	angiotensin I converting enzyme	Homo sapiens	184-187
11827728-2	2000	In the present study, we have applied recently developed methodologies for assaying pulmonary capillary endothelium-bound (PCEB) ACE activity in man, to estimate the interaction of an ACE inhibitor (enalaprilat) with PCEB ACE in human subjects.	Enalaprilat	199-210	angiotensin I converting enzyme	Homo sapiens	184-187
11045389-6	2000	Enalaprilat (200 microg/kg) reduced mean arterial pressure (MAP) by 14+/-10% (mean+/-SD, P=0.006) and RIHP by 18+/-18% (P=0.001), whereas total renal blood flow and medullary PO2 remained unchanged.	Enalaprilat	0-11	PO2	Sus scrofa	175-178
11827728-6	2000	When normalized to predrug (T(0)) activity levels, enalaprilat inhibited PCEB and serum ACE activities at T(15) 74 +/- 6% and 68 +/- 6%, respectively.	Enalaprilat	51-62	angiotensin I converting enzyme	Homo sapiens	88-91
11040233-8	2000	In contrast, after enalaprilat administration a fall in arterial pressure similar to that for dihydralazine was followed by decreased angiotensin II levels and unchanged muscle sympathetic nerve activity, heart rate, and total body norepinephrine spillover, whereas renal norepinephrine spillover increased by 44% (P<0.05).	Enalaprilat	19-30	angiotensinogen	Homo sapiens	134-148
10720592-10	2000	The angiotensin-converting enzyme (ACE) inhibitor enalaprilat (80 ng.	Enalaprilat	50-61	angiotensin I converting enzyme	Homo sapiens	35-38
10948084-3	2000	In the presence of 1 nmol/L of insulin, 1 micromol/L of enalaprilat enhanced insulin-induced glucose uptake from 89.2+/-8.	Enalaprilat	56-67	insulin	Homo sapiens	31-38
10948084-3	2000	In the presence of 1 nmol/L of insulin, 1 micromol/L of enalaprilat enhanced insulin-induced glucose uptake from 89.2+/-8.	Enalaprilat	56-67	insulin	Homo sapiens	77-84
10942157-11	2000	The enzyme cholinesterase was found to be inhibited by enalaprilat, ramiprilat, and fosinopril.	Enalaprilat	55-66	cholinesterase	Oryctolagus cuniculus	11-25
10942157-14	2000	Our data suggest that ACE inhibitors enalaprilat, ramiprilat, and fosinopril produce a significant ocular hypotensive effect in acute and chronic models of ocular hypertension in rabbits.	Enalaprilat	37-48	angiotensin-converting enzyme	Oryctolagus cuniculus	22-25
10881050-5	2000	The specificity of the assay was demonstrated by the inhibition of ACE activity with 3 microM enalaprilat (MK-422).	Enalaprilat	94-105	angiotensin I converting enzyme	Rattus norvegicus	67-70
10881050-5	2000	The specificity of the assay was demonstrated by the inhibition of ACE activity with 3 microM enalaprilat (MK-422).	Enalaprilat	107-113	angiotensin I converting enzyme	Rattus norvegicus	67-70
10852646-1	2000	UNLABELLED: The ACE inhibitor lisinopril is a lysine derivative of enalaprilat, the active metabolite of enalapril.	Enalaprilat	67-78	angiotensin I converting enzyme	Homo sapiens	16-19
10900238-9	2000	Protein kinase C or phosphatase inhibitors, however, blocked the effects of BK on the receptor resensitized by enalaprilat or ramiprilat.	Enalaprilat	111-122	kininogen 1	Homo sapiens	76-78
10874261-4	2000	METHODS: Seven patients with heart failure received a 3-hour infusion of the ACE inhibitor enalaprilat.	Enalaprilat	91-102	angiotensin I converting enzyme	Homo sapiens	77-80
10874261-7	2000	RESULTS: Serum ACE activity was significantly suppressed throughout and after enalaprilat infusion.	Enalaprilat	78-89	angiotensin I converting enzyme	Homo sapiens	15-18
10658731-4	2000	administration of an ACE inhibitor (enalaprilat).	Enalaprilat	36-47	angiotensin I converting enzyme	Homo sapiens	21-24
10710136-8	2000	The ACE-inhibitor enalaprilate inhibited angiotensin I-induced vasoconstriction, but did not significantly affect bradykinin-induced vasodilation.	Enalaprilat	18-30	angiotensin I converting enzyme	Homo sapiens	4-7
10710136-8	2000	The ACE-inhibitor enalaprilate inhibited angiotensin I-induced vasoconstriction, but did not significantly affect bradykinin-induced vasodilation.	Enalaprilat	18-30	angiotensinogen	Homo sapiens	41-54
10714896-5	2000	During reverse microdialysis with bradykinin and enalaprilate a significant decrease in arterial-interstitial-gradient for glucose (AIG(glu)) was observed (from 1.49 +/- 0.08 mM to 0.12 +/- 0.63 mM (p = 0.018) for bradykinin and from 1.5 +/- 0.07 mM to 0.24 +/- 0.67 mM (p = 0.043) for enalaprilate).	Enalaprilat	49-61	kininogen 1	Homo sapiens	214-224
10714896-7	2000	The changes in transcapillary glucose transport during bradykinin and enalaprilate administration were accompanied by significant increases in interstitial lactate levels which was most pronounced for bradykinin (from 0.14 +/- 0.01 mM to 0.40 +/- 0.07 mM, p = 0.018).	Enalaprilat	70-82	kininogen 1	Homo sapiens	201-211
10588480-3	1999	Aortic segments were cultured in medium containing a broad concentration range of the ACE inhibitor enalaprilat (0-100 microM).	Enalaprilat	100-111	angiotensin-converting enzyme	Oryctolagus cuniculus	86-89
10516266-7	1999	Enalaprilat pretreatment in vivo increased renal renin content and basal and stimulated secretion of PR and AR in vitro even in immature animals.	Enalaprilat	0-11	renin	Ovis aries	49-54
10516266-8	1999	Immunohistochemical localization showed that enalaprilat treatment caused an age-related recruitment of renin-containing juxtaglomerular cells.	Enalaprilat	45-56	renin	Ovis aries	104-109
10560789-5	1999	Pulmonary inactivation of BK and conversion of Ang I were determined in conscious enalapril- or vehicle-treated rats before and after intravenous administration of the ACE inhibitor enalaprilat (MK-422, 10 mg/kg).	Enalaprilat	182-193	angiotensin I converting enzyme	Rattus norvegicus	168-171
10560789-9	1999	Acute ACE inhibition with MK-422 reduced BK inactivation to 42.0% +/- 2.7%.	Enalaprilat	26-32	angiotensin I converting enzyme	Rattus norvegicus	6-9
10596866-7	1999	The preincubation of sera with enalaprilat at a concentration inhibiting ACE significantly prevented the rapid degradation of BK and des-Arg9-BK in these four subgroups.	Enalaprilat	31-42	angiotensin I converting enzyme	Homo sapiens	73-76
10532602-4	1999	Tests were performed in the absence and the presence of complete in vitro inhibition of angiotensin-converting enzyme (ACE) activity by enalaprilat.	Enalaprilat	136-147	angiotensin I converting enzyme	Homo sapiens	88-117
10532602-4	1999	Tests were performed in the absence and the presence of complete in vitro inhibition of angiotensin-converting enzyme (ACE) activity by enalaprilat.	Enalaprilat	136-147	angiotensin I converting enzyme	Homo sapiens	119-122
10532602-5	1999	RESULTS: In the presence of ACE inhibition (enalaprilat), the half-life (t1/2) of BK measured in the sera of patients who presented with a severe hypotensive transfusion reaction (361 +/- 90 sec) was not significantly different from that measured in the sera of normal controls (249 +/- 16 sec).	Enalaprilat	44-55	angiotensin I converting enzyme	Homo sapiens	28-31
10532602-6	1999	In the presence of ACE inhibition (enalaprilat), the t1/2 of des-Arg9-BK was significantly greater in patients who presented with a severe hypotensive transfusion reaction (1549 +/- 319 sec) than in normal controls (661 +/- 38 sec) (p < 0.001).	Enalaprilat	35-46	angiotensin I converting enzyme	Homo sapiens	19-22
10532602-6	1999	In the presence of ACE inhibition (enalaprilat), the t1/2 of des-Arg9-BK was significantly greater in patients who presented with a severe hypotensive transfusion reaction (1549 +/- 319 sec) than in normal controls (661 +/- 38 sec) (p < 0.001).	Enalaprilat	35-46	kininogen 1	Homo sapiens	70-72
10596866-7	1999	The preincubation of sera with enalaprilat at a concentration inhibiting ACE significantly prevented the rapid degradation of BK and des-Arg9-BK in these four subgroups.	Enalaprilat	31-42	kininogen 1	Homo sapiens	126-128
10596866-7	1999	The preincubation of sera with enalaprilat at a concentration inhibiting ACE significantly prevented the rapid degradation of BK and des-Arg9-BK in these four subgroups.	Enalaprilat	31-42	kininogen 1	Homo sapiens	142-144
10404842-8	1999	Enalaprilat did not alter femoral vascular tone at rest or vasodilation with sodium nitroprusside, but potentiated bradykinin-mediated vasodilation in patients (p<0.001) and controls (p = 0.02).	Enalaprilat	0-11	kininogen 1	Homo sapiens	115-125
10444586-12	1999	Acute enalaprilat treatment decreased ACE activity in renal intermicrovillar clefts by 90% and in renal endosomes by 84%.	Enalaprilat	6-17	angiotensin I converting enzyme	Rattus norvegicus	38-41
10444586-13	1999	Likewise, intermicrovillar cleft and endosomal ANG II levels decreased by 61% and 52%, respectively, in enalaprilat-treated animals.	Enalaprilat	104-115	angiotensinogen	Rattus norvegicus	47-53
10400051-1	1999	Our objective was to investigate whether the angiotensin converting enzyme inhibitor enalaprilat improves detection of hemodynamically significant renal artery stenoses in dogs.	Enalaprilat	85-96	angiotensin I converting enzyme	Canis lupus familiaris	45-74
10350000-5	1999	With respect to structure-function, ACE inhibitor affinity was strongly correlated with drug lipophilicity (r = 0.944, p < 0.001 for all ACE inhibitors; r = 0.983, p < 0.001 without enalaprilat, quinaprilat and quinapril).	Enalaprilat	188-199	angiotensin-converting enzyme	Oryctolagus cuniculus	36-39
10330262-11	1999	ACE and NEP participate in the degradation of BK since both enalaprilat and omapatrilat have potentiating effects on the t1/2 of BK.	Enalaprilat	60-71	angiotensin I converting enzyme	Rattus norvegicus	0-3
10330262-11	1999	ACE and NEP participate in the degradation of BK since both enalaprilat and omapatrilat have potentiating effects on the t1/2 of BK.	Enalaprilat	60-71	membrane metallo-endopeptidase	Rattus norvegicus	8-11
10359736-6	1999	Cumulative concentration-response curves were constructed for Ang I in the presence of enalaprilat 1 micromol/L, chymostatin 10 micromol/L, or both inhibitors together.	Enalaprilat	87-98	angiotensinogen	Homo sapiens	62-67
10359736-7	1999	In the rabbit, enalaprilat completely inhibited the Ang I response.	Enalaprilat	15-26	angiotensinogen	Homo sapiens	52-57
10359736-8	1999	In human vessels, enalaprilat or chymostatin alone had no effect, but the combination of enalaprilat and chymostatin almost completely inhibited the response to Ang I.	Enalaprilat	89-100	angiotensinogen	Homo sapiens	161-166
10498289-4	1999	A less pronounced effect on cellular proliferation was seen with the ACE inhibitor enalaprilat.	Enalaprilat	83-94	angiotensin I converting enzyme	Rattus norvegicus	69-72
10498289-10	1999	These data show that the ACE inhibitors moexiprilat and enalaprilat inhibit Ang II induced proliferation of cardiac fibroblasts according to their relative potency of ACE inhibition in vitro.	Enalaprilat	56-67	angiotensin I converting enzyme	Rattus norvegicus	25-28
10498289-10	1999	These data show that the ACE inhibitors moexiprilat and enalaprilat inhibit Ang II induced proliferation of cardiac fibroblasts according to their relative potency of ACE inhibition in vitro.	Enalaprilat	56-67	angiotensinogen	Rattus norvegicus	76-82
10498289-10	1999	These data show that the ACE inhibitors moexiprilat and enalaprilat inhibit Ang II induced proliferation of cardiac fibroblasts according to their relative potency of ACE inhibition in vitro.	Enalaprilat	56-67	angiotensin I converting enzyme	Rattus norvegicus	167-170
10326661-2	1999	This study was designed to assess the influence of the activation status of the renin angiotensin system (RAS) on the hemodynamic effects of EXP 3174 (an angiotensin AT1 receptor antagonist) and enalaprilat (an angiotensin converting enzyme inhibitor) in tachycardia-induced heart failure.	Enalaprilat	195-206	renin	Canis lupus familiaris	80-85
10323266-6	1999	Angiotensin-converting enzyme inhibitors (imidaprilat, enalaprilat) inhibited the enzyme activity in bronchial epithelial cells with an IC50 of 0.9-3.6 nM.	Enalaprilat	55-66	angiotensin I converting enzyme	Homo sapiens	0-29
10087051-14	1999	Highly variable enalaprilat trough levels and the fact that adverse effects were more common on high enalaprilat trough levels provide a rationale for individually adjusting ACE-inhibitor dose in case of adverse effects.	Enalaprilat	101-112	angiotensin I converting enzyme	Homo sapiens	174-177
10082496-3	1999	Administration of bradykinin or its ACE-resistant analogue desensitized the receptor, but it was resensitized (arachidonic acid release or [Ca2+]i mobilization) by agents such as enalaprilat (1 micromol/L).	Enalaprilat	179-190	kininogen 1	Homo sapiens	18-28
10096262-2	1999	We investigated whether acute local angiotensin-converting enzyme (ACE) inhibition, achieved by enalaprilat, could influence bradykinin-induced vasodilation in veins of smokers.	Enalaprilat	96-107	angiotensin I converting enzyme	Homo sapiens	36-65
10096262-2	1999	We investigated whether acute local angiotensin-converting enzyme (ACE) inhibition, achieved by enalaprilat, could influence bradykinin-induced vasodilation in veins of smokers.	Enalaprilat	96-107	angiotensin I converting enzyme	Homo sapiens	67-70
10096262-2	1999	We investigated whether acute local angiotensin-converting enzyme (ACE) inhibition, achieved by enalaprilat, could influence bradykinin-induced vasodilation in veins of smokers.	Enalaprilat	96-107	kininogen 1	Homo sapiens	125-135
10082496-10	1999	Enalaprilat potentiated the bradykinin effect in cells expressing a mutant ACE with a single N-domain active site.	Enalaprilat	0-11	kininogen 1	Homo sapiens	28-38
10082496-3	1999	Administration of bradykinin or its ACE-resistant analogue desensitized the receptor, but it was resensitized (arachidonic acid release or [Ca2+]i mobilization) by agents such as enalaprilat (1 micromol/L).	Enalaprilat	179-190	angiotensin I converting enzyme	Homo sapiens	36-39
10082496-10	1999	Enalaprilat potentiated the bradykinin effect in cells expressing a mutant ACE with a single N-domain active site.	Enalaprilat	0-11	angiotensin I converting enzyme	Homo sapiens	75-78
10082496-12	1999	Enalaprilat enhanced signaling via ACE by Galphai in lower concentration than by Galphaq-coupled receptor.	Enalaprilat	0-11	angiotensin I converting enzyme	Homo sapiens	35-38
10082496-6	1999	Enalaprilat resensitized the receptor via ACE to release arachidonic acid by bradykinin at a lower concentration (5 nmol/L) than required to mobilize [Ca2+]i (1 micromol/L).	Enalaprilat	0-11	angiotensin I converting enzyme	Homo sapiens	42-45
10082496-6	1999	Enalaprilat resensitized the receptor via ACE to release arachidonic acid by bradykinin at a lower concentration (5 nmol/L) than required to mobilize [Ca2+]i (1 micromol/L).	Enalaprilat	0-11	kininogen 1	Homo sapiens	77-87
10080484-7	1999	RESULTS: Enalaprilat did not alter either resting coronary vascular tone or dilation with sodium nitroprusside, but potentiated BK-mediated dilation.	Enalaprilat	9-20	kininogen 1	Homo sapiens	128-130
10027827-8	1999	In contrast, when kininase I and II inhibitors (DL-2-mercaptomethyl-3-guanidinoethylthiopropanoic acid and enalaprilat, each 1 microM) were used to prevent the degradation of endogenous BK, NE overflow and reperfusion arrhythmias were enhanced.	Enalaprilat	107-118	kininogen 1	Homo sapiens	186-188
9951431-5	1999	Enalaprilat and captopril increased the sensitivity to bradykinin, decreasing the dose producing half-maximal response (ED50) of bradykinin 18-fold and 5-fold, respectively, without changing the maximal venodilatory response.	Enalaprilat	0-11	kininogen 1	Homo sapiens	55-65
9887083-2	1999	Eight to ten weeks after inducing HF in rats by coronary artery ligation, we administered enalaprilat to suppress ANG II synthesis and studied renal arteriolar function using the in vitro blood-perfused juxtamedullary nephron technique.	Enalaprilat	90-101	angiotensinogen	Rattus norvegicus	114-120
9951431-5	1999	Enalaprilat and captopril increased the sensitivity to bradykinin, decreasing the dose producing half-maximal response (ED50) of bradykinin 18-fold and 5-fold, respectively, without changing the maximal venodilatory response.	Enalaprilat	0-11	kininogen 1	Homo sapiens	129-139
9593073-4	1998	The effect of the ACE inhibitor enalaprilat on intact heart electrophysiology was studied by using multisite optical action-potential recordings with voltage-sensitive dyes.	Enalaprilat	32-43	LOW QUALITY PROTEIN: angiotensin-converting enzyme	Cavia porcellus	18-21
10458510-5	1999	Preincubation of the sera with an ACE inhibitor (enalaprilat) significantly increased the t1/2 of both BK and des-Arg9-BK in both groups.	Enalaprilat	49-60	angiotensin I converting enzyme	Homo sapiens	34-37
10458510-5	1999	Preincubation of the sera with an ACE inhibitor (enalaprilat) significantly increased the t1/2 of both BK and des-Arg9-BK in both groups.	Enalaprilat	49-60	kininogen 1	Homo sapiens	103-105
10458510-5	1999	Preincubation of the sera with an ACE inhibitor (enalaprilat) significantly increased the t1/2 of both BK and des-Arg9-BK in both groups.	Enalaprilat	49-60	kininogen 1	Homo sapiens	119-121
9860785-12	1998	This observation suggests that intrinsic differences exist between quinaprilat and enalaprilat that determine the ability to improve endothelium-mediated vasodilation, ie, their different affinity to tissue ACE.	Enalaprilat	83-94	angiotensin I converting enzyme	Homo sapiens	207-210
9860795-7	1998	This vasodilator effect of exogenous bradykinin was potentiated similarly in both states by enalaprilat, which blocks both angiotensin conversion and bradykinin degradation.	Enalaprilat	92-103	kininogen 1	Canis lupus familiaris	37-47
9860795-7	1998	This vasodilator effect of exogenous bradykinin was potentiated similarly in both states by enalaprilat, which blocks both angiotensin conversion and bradykinin degradation.	Enalaprilat	92-103	kininogen 1	Canis lupus familiaris	150-160
9860795-10	1998	Enalaprilat, however, produced a significant decrease in MAP and a significant increase in CO, which were attributed to the inhibition of bradykinin degradation, because these effects were absent after pretreatment with Hoe 140 (a bradykinin B2 receptor antagonist).	Enalaprilat	0-11	kininogen 1	Canis lupus familiaris	138-148
9860795-10	1998	Enalaprilat, however, produced a significant decrease in MAP and a significant increase in CO, which were attributed to the inhibition of bradykinin degradation, because these effects were absent after pretreatment with Hoe 140 (a bradykinin B2 receptor antagonist).	Enalaprilat	0-11	kininogen 1	Canis lupus familiaris	231-241
9886898-10	1998	The purified ACE were inhibited by enalaprilat and captopril, two potent competitive inhibitors of ACE and by EDTA, using Hippuryl-His-Leu as a substrate.	Enalaprilat	35-46	angiotensin I converting enzyme	Rattus norvegicus	13-16
9886898-10	1998	The purified ACE were inhibited by enalaprilat and captopril, two potent competitive inhibitors of ACE and by EDTA, using Hippuryl-His-Leu as a substrate.	Enalaprilat	35-46	angiotensin I converting enzyme	Rattus norvegicus	99-102
9822455-4	1998	They were allocated on 2 occasions in random order to injection of placebo or 1.25 mg of the ACE inhibitor enalaprilat.	Enalaprilat	107-118	angiotensin I converting enzyme	Homo sapiens	93-96
9781723-11	1998	Soluble thrombomodulin increased in the untreated control patients (from 58 +/- 9 to 79 +/- 14 ng/mL [p < .05]), but significantly decreased in the enalaprilat-treated patients.	Enalaprilat	151-162	thrombomodulin	Homo sapiens	8-22
9802186-1	1998	The objectives of this study were to evaluate the transplacental kinetics and effects on placental function of the angiotensin converting enzyme (ACE) inhibitor, enalaprilat, in the dually perfused human placental lobule system.	Enalaprilat	162-173	angiotensin I converting enzyme	Homo sapiens	115-144
9802186-1	1998	The objectives of this study were to evaluate the transplacental kinetics and effects on placental function of the angiotensin converting enzyme (ACE) inhibitor, enalaprilat, in the dually perfused human placental lobule system.	Enalaprilat	162-173	angiotensin I converting enzyme	Homo sapiens	146-149
9673422-0	1998	Effect of angiotensin II receptor blockade on the interaction between enalaprilat and doxazosin in rat tail arteries.	Enalaprilat	70-81	angiotensinogen	Rattus norvegicus	10-24
9673422-2	1998	Previous work has shown that enalaprilat, an inhibitor of angiotensin-converting enzyme (ACE), potentiated the actions of alpha 1-adrenoceptor antagonists; it was hypothesized that angiotensin II (AngII) modulated the activity of alpha 1-adrenoceptors.	Enalaprilat	29-40	angiotensin I converting enzyme	Rattus norvegicus	58-87
9673422-2	1998	Previous work has shown that enalaprilat, an inhibitor of angiotensin-converting enzyme (ACE), potentiated the actions of alpha 1-adrenoceptor antagonists; it was hypothesized that angiotensin II (AngII) modulated the activity of alpha 1-adrenoceptors.	Enalaprilat	29-40	angiotensin I converting enzyme	Rattus norvegicus	89-92
9673422-2	1998	Previous work has shown that enalaprilat, an inhibitor of angiotensin-converting enzyme (ACE), potentiated the actions of alpha 1-adrenoceptor antagonists; it was hypothesized that angiotensin II (AngII) modulated the activity of alpha 1-adrenoceptors.	Enalaprilat	29-40	angiotensinogen	Rattus norvegicus	181-195
9673422-2	1998	Previous work has shown that enalaprilat, an inhibitor of angiotensin-converting enzyme (ACE), potentiated the actions of alpha 1-adrenoceptor antagonists; it was hypothesized that angiotensin II (AngII) modulated the activity of alpha 1-adrenoceptors.	Enalaprilat	29-40	angiotensinogen	Rattus norvegicus	197-202
10512591-6	1999	Pre-exposure to enalaprilat (24 h) before bFGF reduced ACE mRNA to approximately 50% of that found in the presence of bFGF alone.	Enalaprilat	16-27	angiotensin I converting enzyme	Homo sapiens	55-58
10512591-6	1999	Pre-exposure to enalaprilat (24 h) before bFGF reduced ACE mRNA to approximately 50% of that found in the presence of bFGF alone.	Enalaprilat	16-27	fibroblast growth factor 2	Homo sapiens	118-122
9869501-6	1998	Angiotensin-converting enzyme (ACE) inhibition with enalaprilat revealed a larger, more rapid decrease in MAP in response to omega-CTX (-19 +/- 4 mm Hg from 65 +/- 1 mm Hg after 18 +/- 2 min; n = 6) compared with the control group.	Enalaprilat	52-63	angiotensin-converting enzyme	Oryctolagus cuniculus	0-29
9869501-6	1998	Angiotensin-converting enzyme (ACE) inhibition with enalaprilat revealed a larger, more rapid decrease in MAP in response to omega-CTX (-19 +/- 4 mm Hg from 65 +/- 1 mm Hg after 18 +/- 2 min; n = 6) compared with the control group.	Enalaprilat	52-63	angiotensin-converting enzyme	Oryctolagus cuniculus	31-34
9815869-0	1998	ACE (I/D) genotype as a predictor of the magnitude and duration of the response to an ACE inhibitor drug (enalaprilat) in humans.	Enalaprilat	106-117	angiotensin I converting enzyme	Homo sapiens	0-3
9815869-0	1998	ACE (I/D) genotype as a predictor of the magnitude and duration of the response to an ACE inhibitor drug (enalaprilat) in humans.	Enalaprilat	106-117	angiotensin I converting enzyme	Homo sapiens	86-89
9815869-1	1998	BACKGROUND: We have investigated the possible effects of contrasting ACE (I/D) genotypes on the responses to the ACE inhibitor enalaprilat in normotensive men.	Enalaprilat	127-138	angiotensin I converting enzyme	Homo sapiens	113-116
9815869-2	1998	METHODS AND RESULTS: Subjects with DD (n=12) and II (n=11) ACE genotypes received an intravenous infusion of enalaprilat or placebo.	Enalaprilat	109-120	angiotensin I converting enzyme	Homo sapiens	59-62
9815869-7	1998	CONCLUSIONS: The effect of enalaprilat was significantly greater and lasted longer in normotensive men homozygous for the II ACE genotype.	Enalaprilat	27-38	angiotensin I converting enzyme	Homo sapiens	125-128
9765319-7	1998	A good linear correlation was observed for the inhibitory effect of angiotensin-converting enzyme inhibitors (benazeprilat, cilazaprilat, delaprilat and enalaprilat) between isolated hepatocytes and oatp1-expressing cells.	Enalaprilat	153-164	solute carrier organic anion transporter family, member 1a1	Rattus norvegicus	199-204
9798526-17	1998	), TPR was reduced by 20 +/- 4% compared to only a 6 +/- 3% reduction (p < 0.05) when the enalaprilat was followed 30 min later by a second dose of enalaprilat (1 mg/kg, i.v.).	Enalaprilat	151-162	translocated promoter region, nuclear basket protein	Sus scrofa	3-6
9673444-6	1998	Angiotensin-converting enzyme inhibition was produced in vitro by incubation of enalaprilat or perindoprilat with human serum or cell membranes from rat heart.	Enalaprilat	80-91	angiotensin I converting enzyme	Rattus norvegicus	0-29
9683926-7	1998	The angiotensin-converting enzyme (ACE) inhibitor, enalaprilat (130 nM), reduced BK degradation at all flow rates.	Enalaprilat	51-62	angiotensin I converting enzyme	Rattus norvegicus	4-33
9652356-6	1998	The facilitatory effect of bradykinin also was enhanced by enalaprilat (1 microM) and mergetpa (1 microM), inhibitors of angiotensin-converting enzyme (kininase II) and kininase I, respectively.	Enalaprilat	59-70	angiotensin I converting enzyme (peptidyl-dipeptidase A) 1	Mus musculus	152-163
9652356-6	1998	The facilitatory effect of bradykinin also was enhanced by enalaprilat (1 microM) and mergetpa (1 microM), inhibitors of angiotensin-converting enzyme (kininase II) and kininase I, respectively.	Enalaprilat	59-70	carboxypeptidase N, polypeptide 1	Mus musculus	152-162
9620109-3	1998	Enalaprilat, the intravenous formulation of enalapril, is the only intravenously available ACE inhibitor and can be given to patients with severe liver dysfunction as it is also not a prodrug.	Enalaprilat	0-11	angiotensin I converting enzyme	Homo sapiens	91-94
9683926-7	1998	The angiotensin-converting enzyme (ACE) inhibitor, enalaprilat (130 nM), reduced BK degradation at all flow rates.	Enalaprilat	51-62	angiotensin I converting enzyme	Rattus norvegicus	35-38
9422816-15	1997	These results are more consistent with the antihypertensive effects of enalaprilat or MDL 100,240 in transgenic ((mRen-2)27) rats being due to suppression of angiotensin II production, than due to inhibition of bradykinin degradation.	Enalaprilat	71-82	angiotensinogen	Rattus norvegicus	158-172
9484239-3	1998	The release of the amyloid precursor protein from both SH-SY5Y and IMR-32 neuronal cells by alpha-secretase was blocked by batimastat and other related synthetic hydroxamic acid-based zinc metalloprotease inhibitors, but not by the structurally unrelated zinc metalloprotease inhibitors enalaprilat and phosphoramidon.	Enalaprilat	287-298	amyloid beta precursor protein	Homo sapiens	19-44
9933831-8	1998	CONCLUSION: The functional improvement under the action of enalaprilat suggests that the advantages of the drug may be mediated mainly through an increase in myocardial blood flow and that angiotensin II might be involved in the restricted increase in coronary blood flow during dynamic exercise in hypertensives with coronary microangiopathy.	Enalaprilat	59-70	angiotensinogen	Homo sapiens	189-203
9459339-0	1998	Attenuation of thrombolysis-induced increase of plasminogen activator inhibitor-1 by intravenous enalaprilat.	Enalaprilat	97-108	serpin family E member 1	Homo sapiens	48-81
9459339-1	1998	We examined the effect of intravenous enalaprilat on the course of PAI-1 plasma levels in 23 patients with acute myocardial infarction undergoing thrombolytic therapy.	Enalaprilat	38-49	serpin family E member 1	Homo sapiens	67-72
9459339-5	1998	PAI-1 plasma levels in patients receiving enalaprilat were similar to those of the control patients before thrombolysis (5 ng/ml, 95% confidence interval: 2-10 vs. 7 ng/ml, 95% confidence interval: 2-10; p = 0.5).	Enalaprilat	42-53	serpin family E member 1	Homo sapiens	0-5
9459339-6	1998	The PAI-1AUC was 9 ng/ml/h (95% confidence interval: 5-10) in the enalaprilat group and 19 ng/ml/h (95% confidence interval: 13-26) in the control group (p = 0.0006).	Enalaprilat	66-77	serpin family E member 1	Homo sapiens	4-9
9459339-8	1998	Our study clearly demonstrates that application of intravenous enalaprilat prior to thrombolysis attenuates the thrombolysis-related increase of PAI-1.	Enalaprilat	63-74	serpin family E member 1	Homo sapiens	145-150
9488250-11	1998	In examining the determinants of pHi, the intramucosal-arterial PCO2 difference was improved after enalaprilat administration (27 +/- 6 to 17 +/- 3 mmHg, p = .04) while no difference was observed in arterial bicarbonate (19.5 +/- .7 to 19.7 +/- .8, p = .90).	Enalaprilat	99-110	glucose-6-phosphate isomerase	Homo sapiens	33-36
9488250-12	1998	Additionally, the change in pHi observed with enalaprilat correlated with predrug intramucosal-arterial PCO2 difference (r = .74, r2 = .55, p = .0005).	Enalaprilat	46-57	glucose-6-phosphate isomerase	Homo sapiens	28-31
9374762-5	1997	Enalaprilat, an ACE inhibitor, significantly prevented the rapid degradation of BK and des-Arg9-BK in all species studied, whereas retrothiorphan, a neutral endopeptidase inhibitor, and losartan, an angiotensin II type I receptor antagonist, did not affect this metabolism.	Enalaprilat	0-11	angiotensin I converting enzyme	Homo sapiens	16-19
9374762-5	1997	Enalaprilat, an ACE inhibitor, significantly prevented the rapid degradation of BK and des-Arg9-BK in all species studied, whereas retrothiorphan, a neutral endopeptidase inhibitor, and losartan, an angiotensin II type I receptor antagonist, did not affect this metabolism.	Enalaprilat	0-11	kininogen 1	Homo sapiens	80-82
9374762-5	1997	Enalaprilat, an ACE inhibitor, significantly prevented the rapid degradation of BK and des-Arg9-BK in all species studied, whereas retrothiorphan, a neutral endopeptidase inhibitor, and losartan, an angiotensin II type I receptor antagonist, did not affect this metabolism.	Enalaprilat	0-11	kininogen 1	Homo sapiens	96-98
9351459-6	1997	Enalaprilat decreased the IC50 of [Hyp3-Tyr(Me)8]BK, the BK analogue more resistant to ACE, from 3.2 +/- 0.8 to 0.41 +/- 0.16 nmol/L (P < .05, n = 3).	Enalaprilat	0-11	angiotensin-converting enzyme	Cricetulus griseus	87-90
9466091-2	1997	angiotensin converting enzyme (ACE) inhibitor enalaprilat in 10 critically ill patients, being ventilated with positive end-expiratory pressure (PEEP), on sodium and water excretion was investigated.	Enalaprilat	46-57	angiotensin I converting enzyme	Homo sapiens	0-29
9284425-5	1997	ACE inhibitors can also be classified according to the excretion route of their active moiety, into 2 different excretion route types:(1) excreated mainly through the kidney such as captopril, enalaprilat, lisinopril, benazeprilat, imdaprilat, trandraprilat, etc.	Enalaprilat	193-204	angiotensin I converting enzyme	Homo sapiens	0-3
9321871-7	1997	Intravenous pretreatment with the angiotensin-converting enzyme (ACE) inhibitor enalaprilate (0.7 mg/kg) or the angiotensin II-receptor antagonist losartan (10 mg/kg) altered the response to hypovolemia to a transient one, and alkaline secretion returned to the control level within 40-50 min.	Enalaprilat	80-92	angiotensin I converting enzyme	Rattus norvegicus	34-63
9321871-7	1997	Intravenous pretreatment with the angiotensin-converting enzyme (ACE) inhibitor enalaprilate (0.7 mg/kg) or the angiotensin II-receptor antagonist losartan (10 mg/kg) altered the response to hypovolemia to a transient one, and alkaline secretion returned to the control level within 40-50 min.	Enalaprilat	80-92	angiotensin I converting enzyme	Rattus norvegicus	65-68
9321871-10	1997	However, in enalaprilate-pretreated animals, the inhibition of alkaline secretion due to splanchnic nerve stimulation was transient, a response that became sustained on angiotensin II substitution.	Enalaprilat	12-24	angiotensinogen	Rattus norvegicus	169-183
9331154-0	1997	ACE inhibition by enalaprilate stimulates duodenal mucosal alkaline secretion via a bradykinin pathway in the rat.	Enalaprilat	18-30	angiotensin I converting enzyme	Rattus norvegicus	0-3
9322979-2	1997	In addition, we evaluated the effect of angiotensin-converting enzyme (ACE) inhibition with enalaprilat treatment (10 mg/kg I.V.)	Enalaprilat	92-103	angiotensin I converting enzyme	Rattus norvegicus	71-74
9293966-1	1997	The positive inotropic effects of bradykinin (BK) and 2 analogs resistant to angiotensin I-converting enzyme (ACE) were potentiated on isolated guinea pig atrial preparations by enalaprilat.	Enalaprilat	178-189	LOW QUALITY PROTEIN: angiotensin-converting enzyme	Cavia porcellus	110-113
9239416-5	1997	Acute ACE inhibition (with intrabrachial enalaprilat) enhanced ACh responses in the diabetic patients (P < 0.005), with a further improvement evident after 1 mo of oral therapy with enalapril (P < 0.001) when ACh responses were normalized.	Enalaprilat	41-52	angiotensin I converting enzyme	Homo sapiens	6-9
9239416-7	1997	We conclude that acute administration of the ACE inhibitor, enalaprilat, enhances NO-mediated endothelial function in type I diabetic patients, with further improvement evident after 4 wk of enalapril therapy.	Enalaprilat	60-71	angiotensin I converting enzyme	Homo sapiens	45-48
9207629-7	1997	The BK-induced increases in coronary artery diameter and CBF were significantly reduced (p < 0.01) after pretreatment with NG-monomethyl-L-arginine (200 mumol) and were significantly increased (p < 0.01) after pretreatment with enalaprilat (50 micrograms).	Enalaprilat	234-245	kininogen 1	Homo sapiens	4-6
9249242-7	1997	This response was reduced to 36 +/- 3% (n=8) by the ACE-inhibitor enalaprilat (10 microM), while pretreatment with soybean trypsin inhibitor (STI 200 microg ml(-1)) or CH 5450 (10 microM) had no effect.	Enalaprilat	66-77	angiotensin I converting enzyme	Homo sapiens	52-55
9249242-16	1997	In the presence of enalaprilat (100 microM), carboxypeptidase inhibitor CPI (10 microg ml(-1)) and aprotinin (15 microM), CH 5450 (10 nM-1 microM) caused a concentration-dependent inhibition of AII formation.	Enalaprilat	19-30	NLR family pyrin domain containing 3	Homo sapiens	194-197
9086301-1	1997	This study examined the effect of the angiotensin converting enzyme (ACE) inhibitor, enalaprilat, on mesangial cell (MC) DNA synthesis induced by H2O2, IL-6 and PDGF.	Enalaprilat	85-96	angiotensin I converting enzyme	Homo sapiens	38-67
9086301-1	1997	This study examined the effect of the angiotensin converting enzyme (ACE) inhibitor, enalaprilat, on mesangial cell (MC) DNA synthesis induced by H2O2, IL-6 and PDGF.	Enalaprilat	85-96	angiotensin I converting enzyme	Homo sapiens	69-72
9086301-1	1997	This study examined the effect of the angiotensin converting enzyme (ACE) inhibitor, enalaprilat, on mesangial cell (MC) DNA synthesis induced by H2O2, IL-6 and PDGF.	Enalaprilat	85-96	interleukin 6	Homo sapiens	152-156
9086301-6	1997	Only 2.5 mumol/l enalaprilat effected a significant reduction in IL-6 and PDGF-induced DNA synthesis.	Enalaprilat	17-28	interleukin 6	Homo sapiens	65-69
9086301-8	1997	Addition of enalaprilat with either H2O2 + PDGF or H2O2 + IL-6 effected significant reductions in DNA synthesis over the range 2.5-100 mumol/l.	Enalaprilat	12-23	interleukin 6	Homo sapiens	58-62
8897926-0	1996	Serum interspecies differences in metabolic pathways of bradykinin and [des-Arg9]BK: influence of enalaprilat.	Enalaprilat	98-109	kininogen 1	Homo sapiens	56-66
9087601-7	1997	Intracoronary enalaprilat (0.75 mg) extended the duration of the effect of BK on CBFV without modification of peak responses and induced a further increase in LV posterior EDWT but no change in LV regional myocardial function.	Enalaprilat	14-25	kininogen 1	Canis lupus familiaris	75-77
9062366-5	1997	After acute blockade of ANG II formation by iv enalaprilat injection in sodium-restricted animals, ANG II produced a 40% decrease in renal blood flow, a level between untreated dietary groups and less than high salt diet.	Enalaprilat	47-58	angiotensinogen	Rattus norvegicus	24-30
9062366-5	1997	After acute blockade of ANG II formation by iv enalaprilat injection in sodium-restricted animals, ANG II produced a 40% decrease in renal blood flow, a level between untreated dietary groups and less than high salt diet.	Enalaprilat	47-58	angiotensinogen	Rattus norvegicus	99-105
9061270-2	1997	Lisinopril, the lysine analogue of enalaprilat, is a long-acting angiotensin converting enzyme (ACE) inhibitor which is administered once daily by mouth.	Enalaprilat	35-46	angiotensin I converting enzyme	Homo sapiens	96-99
9175570-4	1997	Non-responders to enalaprilat exhibited significant lower pretreatment levels of PRA, angiotensin-converting enzyme (ACE) and ANG II compared to responders (PRA: 5.5 +/- 3.7 vs 1.1 +/- 2.2 ng/ml/h, P < 0.001; ACE: 12.8 +/- 3.5 vs 8.2 +/- 4.8 U/l, P = 0.003; ANG 11:8.7 +/- 6.2 vs 5.0 +/- 3.8 pg/ml, P = 0.04).	Enalaprilat	18-29	S100 calcium binding protein A6	Homo sapiens	81-84
9175570-4	1997	Non-responders to enalaprilat exhibited significant lower pretreatment levels of PRA, angiotensin-converting enzyme (ACE) and ANG II compared to responders (PRA: 5.5 +/- 3.7 vs 1.1 +/- 2.2 ng/ml/h, P < 0.001; ACE: 12.8 +/- 3.5 vs 8.2 +/- 4.8 U/l, P = 0.003; ANG 11:8.7 +/- 6.2 vs 5.0 +/- 3.8 pg/ml, P = 0.04).	Enalaprilat	18-29	angiotensin I converting enzyme	Homo sapiens	86-115
9175570-4	1997	Non-responders to enalaprilat exhibited significant lower pretreatment levels of PRA, angiotensin-converting enzyme (ACE) and ANG II compared to responders (PRA: 5.5 +/- 3.7 vs 1.1 +/- 2.2 ng/ml/h, P < 0.001; ACE: 12.8 +/- 3.5 vs 8.2 +/- 4.8 U/l, P = 0.003; ANG 11:8.7 +/- 6.2 vs 5.0 +/- 3.8 pg/ml, P = 0.04).	Enalaprilat	18-29	angiotensin I converting enzyme	Homo sapiens	117-120
9175570-4	1997	Non-responders to enalaprilat exhibited significant lower pretreatment levels of PRA, angiotensin-converting enzyme (ACE) and ANG II compared to responders (PRA: 5.5 +/- 3.7 vs 1.1 +/- 2.2 ng/ml/h, P < 0.001; ACE: 12.8 +/- 3.5 vs 8.2 +/- 4.8 U/l, P = 0.003; ANG 11:8.7 +/- 6.2 vs 5.0 +/- 3.8 pg/ml, P = 0.04).	Enalaprilat	18-29	S100 calcium binding protein A6	Homo sapiens	157-160
9175570-4	1997	Non-responders to enalaprilat exhibited significant lower pretreatment levels of PRA, angiotensin-converting enzyme (ACE) and ANG II compared to responders (PRA: 5.5 +/- 3.7 vs 1.1 +/- 2.2 ng/ml/h, P < 0.001; ACE: 12.8 +/- 3.5 vs 8.2 +/- 4.8 U/l, P = 0.003; ANG 11:8.7 +/- 6.2 vs 5.0 +/- 3.8 pg/ml, P = 0.04).	Enalaprilat	18-29	angiotensin I converting enzyme	Homo sapiens	212-215
9175570-6	1997	These data indicate that PRA and ANG II are the major determinants for BP response to enalaprilat.	Enalaprilat	86-97	S100 calcium binding protein A6	Homo sapiens	25-28
8897926-6	1996	Enalaprilat significantly prevented the rapid BK and [des-Arg9]BK degradation in all species except that of [des-Arg9]BK in rat serum.	Enalaprilat	0-11	kininogen 1	Homo sapiens	46-48
8897926-6	1996	Enalaprilat significantly prevented the rapid BK and [des-Arg9]BK degradation in all species except that of [des-Arg9]BK in rat serum.	Enalaprilat	0-11	kininogen 1	Homo sapiens	63-65
8897926-6	1996	Enalaprilat significantly prevented the rapid BK and [des-Arg9]BK degradation in all species except that of [des-Arg9]BK in rat serum.	Enalaprilat	0-11	kininogen 1	Homo sapiens	63-65
8874148-4	1996	Responses to angiotensin I and angiotensin I-(3-10) were decreased by the angiotensin converting enzyme inhibitor enalaprilat in a dose of the angiotensin converting enzyme inhibitor that had no effect on responses to angiotensin II and IV and that enhanced vasodilator responses to bradykinin.	Enalaprilat	114-125	kininogen 1	Homo sapiens	283-293
8876745-1	1996	The aim of the present study was to analyse quantitatively, on a cat gastrocnemius muscle preparation in vivo, the effects of local angiotensin-converting enzyme (ACE) inhibition by enalaprilat on total regional vascular resistance (tone) and its distribution to the large-bore arterial resistance vessels (> 25 microns), the small arterioles (< 25 microns) and the veins.	Enalaprilat	182-193	angiotensin I converting enzyme	Homo sapiens	132-161
8876745-1	1996	The aim of the present study was to analyse quantitatively, on a cat gastrocnemius muscle preparation in vivo, the effects of local angiotensin-converting enzyme (ACE) inhibition by enalaprilat on total regional vascular resistance (tone) and its distribution to the large-bore arterial resistance vessels (> 25 microns), the small arterioles (< 25 microns) and the veins.	Enalaprilat	182-193	angiotensin I converting enzyme	Homo sapiens	163-166
8876745-3	1996	Close-arterial infusion of enalaprilat (0.05-0.20 mg kg muscle tissue min-1) elicited a moderate dilator response in all three consecutive sections of the muscle vascular bed, an increase in capillary pressure and transcapillary fluid filtration.	Enalaprilat	27-38	CD59 molecule (CD59 blood group)	Homo sapiens	70-75
8868976-12	1996	Enalaprilat-treated patients showed the smallest overall changes in standard (CKMB) and new serological markers of myocardial ischaemia (TnT peak: 0.71 (0.1) microgram/1; GPBB peak: 44 (14) ng/ml).	Enalaprilat	0-11	troponin T1, slow skeletal type	Homo sapiens	137-140
8868976-12	1996	Enalaprilat-treated patients showed the smallest overall changes in standard (CKMB) and new serological markers of myocardial ischaemia (TnT peak: 0.71 (0.1) microgram/1; GPBB peak: 44 (14) ng/ml).	Enalaprilat	0-11	glycogen phosphorylase B	Homo sapiens	171-175
8868976-15	1996	Pharmacological interventions, such as the continuous infusion of the ACE inhibitor enalaprilat, before start of CPB may help to protect the heart against ischaemia/reperfusion injury.	Enalaprilat	84-95	angiotensin I converting enzyme	Homo sapiens	70-73
8874148-4	1996	Responses to angiotensin I and angiotensin I-(3-10) were decreased by the angiotensin converting enzyme inhibitor enalaprilat in a dose of the angiotensin converting enzyme inhibitor that had no effect on responses to angiotensin II and IV and that enhanced vasodilator responses to bradykinin.	Enalaprilat	114-125	angiotensinogen	Homo sapiens	13-26
8874148-4	1996	Responses to angiotensin I and angiotensin I-(3-10) were decreased by the angiotensin converting enzyme inhibitor enalaprilat in a dose of the angiotensin converting enzyme inhibitor that had no effect on responses to angiotensin II and IV and that enhanced vasodilator responses to bradykinin.	Enalaprilat	114-125	angiotensinogen	Homo sapiens	31-44
8675701-7	1996	When 10(-11) or 10(-8) M exogenous angiotensin II was added to enalaprilat (10(-4) M) in the luminal perfusate, fluid reabsorption returned to its baseline rate (Jv = 2.78 +/- 0.35 nl/mm.min).	Enalaprilat	63-74	angiotensinogen	Rattus norvegicus	35-49
8764248-0	1996	Bradykinin pathway is involved in acute hemodynamic effects of enalaprilat in dogs with heart failure.	Enalaprilat	63-74	kininogen 1	Canis lupus familiaris	0-10
8764248-7	1996	Bradykinin infusion led to dose-dependent decreases in mean aortic pressure and increases in cardiac output that were not modified by pretreatment with ciprokiren but were potentiated 10-fold by enalaprilat.	Enalaprilat	195-206	kininogen 1	Canis lupus familiaris	0-10
8764248-9	1996	Thus endogenous bradykinin is involved in the acute hemodynamic effects of enalaprilat in experimental heart failure.	Enalaprilat	75-86	kininogen 1	Canis lupus familiaris	16-26
8834708-12	1996	These results also confirm that sympathetic nerve terminal blockade by losartan or the blockade of endogenous angiotensin II formation by enalaprilat are likely to participate in the antihypertensive action of AT1 angiotensin II receptor antagonists and angiotensin converting enzyme.	Enalaprilat	138-149	angiotensinogen	Rattus norvegicus	110-124
8738881-4	1996	We found that pretreatment with aerosolized enalaprilat (1 mM) 3 min prior to a BC10 dose of LBK significantly increased RL as compared to the BC10 dose alone (129 +/- 4.1% vs. 105 +/- 2.4%, P < 0.002, n = 4) and significantly decreased MEF (83 +/- 1.5% vs. 97 +/- 1.4%, P < 0.008, n = 4).	Enalaprilat	44-55	BLCAP, apoptosis inducing factor	Rattus norvegicus	80-84
8738881-4	1996	We found that pretreatment with aerosolized enalaprilat (1 mM) 3 min prior to a BC10 dose of LBK significantly increased RL as compared to the BC10 dose alone (129 +/- 4.1% vs. 105 +/- 2.4%, P < 0.002, n = 4) and significantly decreased MEF (83 +/- 1.5% vs. 97 +/- 1.4%, P < 0.008, n = 4).	Enalaprilat	44-55	BLCAP, apoptosis inducing factor	Rattus norvegicus	143-147
8642232-0	1996	Acute administration of metoprolol and enalaprilat reduces insulin-stimulated thermogenesis and skin blood flow.	Enalaprilat	39-50	insulin	Homo sapiens	59-66
8834708-12	1996	These results also confirm that sympathetic nerve terminal blockade by losartan or the blockade of endogenous angiotensin II formation by enalaprilat are likely to participate in the antihypertensive action of AT1 angiotensin II receptor antagonists and angiotensin converting enzyme.	Enalaprilat	138-149	angiotensinogen	Rattus norvegicus	214-228
8703644-1	1995	administration of the ACE inhibitor enalaprilat in the critically ill. 1.	Enalaprilat	36-47	angiotensin I converting enzyme	Homo sapiens	22-25
8913543-3	1996	In this model, inhibition of ACE with enalapril (given orally) or its active metabolite enalaprilat (given into the brachial artery) influences responses to some, but not all, vasoactive peptides that are substrates of ACE in vitro.	Enalaprilat	88-99	angiotensin I converting enzyme	Homo sapiens	219-222
12013484-0	1996	Studies on the interactions between the angiotensin converting enzyme inhibitor enalaprilat and calcium antagonists in rats.	Enalaprilat	80-91	angiotensin I converting enzyme	Rattus norvegicus	40-69
12013484-2	1996	METHODS: The interactions between the ACE inhibitor enalaprilat and the calcium antagonists diltiazem, cinnarizine, felodipine and verapamil were studied in anesthetized rats for effects on blood pressure and in isolated perfused rat tail arteries for effects at alpha1-adrenoceptors.	Enalaprilat	52-63	angiotensin I converting enzyme	Rattus norvegicus	38-41
8770965-7	1996	Exogenous infusion of angiotensin II completely reversed the blood pressure reduction and renal efferent vasodilatation induced by enalaprilat.	Enalaprilat	131-142	angiotensinogen	Homo sapiens	22-36
8703644-3	1995	administration of the ACE inhibitor enalaprilat were studied.	Enalaprilat	36-47	angiotensin I converting enzyme	Homo sapiens	22-25
8703644-20	1995	Continuous infusion of the ACE inhibitor enalaprilat exerted beneficial cardiorespiratory effects in the critically ill.	Enalaprilat	41-52	angiotensin I converting enzyme	Homo sapiens	27-30
7473177-2	1995	In vitro, moexiprilat exhibited a higher inhibitory potency than enalaprilat against both plasma ACE and purified ACE from rabbit lung.	Enalaprilat	65-76	angiotensin-converting enzyme	Oryctolagus cuniculus	97-100
7473177-2	1995	In vitro, moexiprilat exhibited a higher inhibitory potency than enalaprilat against both plasma ACE and purified ACE from rabbit lung.	Enalaprilat	65-76	angiotensin-converting enzyme	Oryctolagus cuniculus	114-117
8575109-2	1995	Experiments were designed to evaluate the hypothesis that cyclo-oxygenase products modulate the influence of angiotensin II (AII) on the renal juxtamedullary microvasculature of enalaprilat-treated rats.	Enalaprilat	178-189	angiotensinogen	Rattus norvegicus	109-123
7503796-7	1995	When 125I-Ang I was perfused in the presence of ACE inhibitors (enalaprilat, ramiprilat) in concentrations up to 130 microM, the formation of Ang II was only partially inhibited (approximately 50%).	Enalaprilat	64-75	angiotensin I converting enzyme	Rattus norvegicus	48-51
7503796-7	1995	When 125I-Ang I was perfused in the presence of ACE inhibitors (enalaprilat, ramiprilat) in concentrations up to 130 microM, the formation of Ang II was only partially inhibited (approximately 50%).	Enalaprilat	64-75	angiotensinogen	Rattus norvegicus	142-148
8575109-2	1995	Experiments were designed to evaluate the hypothesis that cyclo-oxygenase products modulate the influence of angiotensin II (AII) on the renal juxtamedullary microvasculature of enalaprilat-treated rats.	Enalaprilat	178-189	angiotensinogen	Rattus norvegicus	125-128
8522630-14	1995	Because angiotensin-converting enzyme (ACE) inhibitors generally cause cerebral vasodilatation, enalaprilat may be particularly beneficial for patients who are at high risk of developing cerebral hypotensive episodes secondary to impaired cerebral circulation.	Enalaprilat	96-107	angiotensin I converting enzyme	Homo sapiens	8-37
7657820-9	1995	In the presence of 1 microM enalaprilat, ACE activity was reduced by 85%, to 7.3 +/- 1.4 fmol/min/mg in the failing group and to 4.6 +/- 1.3 fmol/min/mg in the nonfailing group (P < 0.001).	Enalaprilat	28-39	angiotensin I converting enzyme	Homo sapiens	41-44
8522630-14	1995	Because angiotensin-converting enzyme (ACE) inhibitors generally cause cerebral vasodilatation, enalaprilat may be particularly beneficial for patients who are at high risk of developing cerebral hypotensive episodes secondary to impaired cerebral circulation.	Enalaprilat	96-107	angiotensin I converting enzyme	Homo sapiens	39-42
7864430-6	1995	Although there were no significant differences in catecholamine levels, plasma renin activity was significantly increased at postincision in the preoperative-enalaprilat group versus the placebo group.	Enalaprilat	158-169	renin	Homo sapiens	79-84
7768559-4	1995	The effect of renin on junctional conductance seems to be mainly due to the synthesis of Ang II because enalaprilat (10(-9) mol/L) dialyzed into the cell caused an appreciable reduction in the effect of renin.	Enalaprilat	104-115	renin	Rattus norvegicus	14-19
7768559-4	1995	The effect of renin on junctional conductance seems to be mainly due to the synthesis of Ang II because enalaprilat (10(-9) mol/L) dialyzed into the cell caused an appreciable reduction in the effect of renin.	Enalaprilat	104-115	renin	Rattus norvegicus	203-208
7768559-5	1995	The intracellular administration of renin (0.2 pmol/L) plus angiotensinogen (0.4 pmol/L) produced a faster and stronger fall in junctional conductance (84.3 +/- 1.35%, P < .05), and the effect was greatly reduced by enalaprilat.	Enalaprilat	219-230	renin	Rattus norvegicus	36-41
7768559-8	1995	Moreover, renin dialyzed into just one cell of the pair induced rectification of the junctional membrane, which was prevented by enalaprilat.	Enalaprilat	129-140	renin	Rattus norvegicus	10-15
7714339-8	1995	The conversion of BK into des-Arg9-BK was generally efficient, and the persistence and concentration of both peptides were increased in the presence of enalaprilat an inhibitor of the angiotensin converting enzyme (ACEI).	Enalaprilat	152-163	angiotensin-converting enzyme	Oryctolagus cuniculus	184-213
7714339-8	1995	The conversion of BK into des-Arg9-BK was generally efficient, and the persistence and concentration of both peptides were increased in the presence of enalaprilat an inhibitor of the angiotensin converting enzyme (ACEI).	Enalaprilat	152-163	angiotensin-converting enzyme	Oryctolagus cuniculus	215-219
7477443-0	1995	Potentiation by enalaprilat of fenoldopam-evoked natriuresis is due to blockade of intrarenal production of angiotensin-II in rats.	Enalaprilat	16-27	angiotensinogen	Rattus norvegicus	108-122
7864411-3	1995	administration of the angiotensin-converting enzyme (ACE) inhibitor enalaprilat (0.06 mg/kg) on important controllers of the circulation was investigated in 14 patients undergoing aortocoronary bypass grafting with a mean arterial blood pressure (MAP) > 85 mm Hg after induction of anesthesia.	Enalaprilat	68-79	angiotensin I converting enzyme	Homo sapiens	22-51
7864411-3	1995	administration of the angiotensin-converting enzyme (ACE) inhibitor enalaprilat (0.06 mg/kg) on important controllers of the circulation was investigated in 14 patients undergoing aortocoronary bypass grafting with a mean arterial blood pressure (MAP) > 85 mm Hg after induction of anesthesia.	Enalaprilat	68-79	angiotensin I converting enzyme	Homo sapiens	53-56
7859389-6	1995	Furthermore, (1) when the half-life of bradykinin was prolonged with the kininase II/angiotensin-converting enzyme inhibitors captopril and enalaprilat, anaphylactic coronary vasoconstriction was attenuated and reversed, and arrhythmias were alleviated; (2) the bradykinin B2-receptor antagonist HOE 140 prevented these effects; and (3) HOE 140 exacerbated both anaphylactic coronary vasoconstriction and arrhythmias.	Enalaprilat	140-151	B2 bradykinin receptor	Cavia porcellus	262-284
7769807-12	1995	Angiotensin-II plasma concentrations significantly decreased during enalaprilat infusion (0.25 mg/h: from 53.1 +/- 11.3 to 22.1 +/- 9.3 pg/ml; 0.50 mg/h: 62.1 +/- 14.4 to 17.9 +/- 7.9 pg/ml), but they remained significantly elevated in the untreated control patients.	Enalaprilat	68-79	angiotensinogen	Homo sapiens	0-14
7890486-5	1995	However, enalaprilat or benazepril enhanced the relaxation of ciliary arteries to bradykinin (P < 0.02).	Enalaprilat	9-20	kininogen 1	Homo sapiens	82-92
7890486-6	1995	In the perfused porcine eye, enalaprilat (10(-5) M) augmented vasodilation to bradykinin (P < 0.02).	Enalaprilat	29-40	kininogen 1	Homo sapiens	78-88
7769807-1	1995	administration of the angiotensin-converting enzyme inhibitor enalaprilat in the critically ill: effects on regulators of circulatory homeostasis.	Enalaprilat	62-73	angiotensin I converting enzyme	Homo sapiens	22-51
7769807-5	1995	administration of the ACE inhibitor enalaprilat on regulators of circulation was studied in 45 critically ill patients.	Enalaprilat	36-47	angiotensin I converting enzyme	Homo sapiens	22-25
7769807-13	1995	Vasopressin plasma level increased only in the control group (p < 0.01) and decreased in the patients in whom 0.50 mg/h of enalaprilat was infused.	Enalaprilat	126-137	arginine vasopressin	Homo sapiens	0-11
7599749-8	1995	Almost complete suppression of plasma ACE activity was achieved within 30 min in 48 patients treated with intravenous enalaprilat, initiated within 24 h from the onset of infarction.	Enalaprilat	118-129	angiotensin I converting enzyme	Homo sapiens	38-41
7718754-0	1995	Cardiorespiratory response of intravenous angiotensin-converting enzyme inhibitor enalaprilat in hypertensive cardiac surgery patients.	Enalaprilat	82-93	angiotensin I converting enzyme	Homo sapiens	42-71
7994817-7	1994	Effective inhibition of the renin-angiotensin system by remikiren and enalaprilat was indicated by increases of plasma immunoreactive renin together with rapid and complete inhibition of renin activity after remikiren and an increase after enalaprilat (all P < or = .05).	Enalaprilat	70-81	renin	Homo sapiens	28-33
8665992-0	1995	Polymorphic inhibition of human angiotensin I-converting enzyme by enalaprilat.	Enalaprilat	67-78	angiotensin I converting enzyme	Homo sapiens	32-63
8665992-4	1995	This paper reports the possible polymorphic response of ACE to the ACE inhibitor enalaprilat in 54 normal Chinese subjects that is independent of the I/D polymorphism.	Enalaprilat	81-92	angiotensin I converting enzyme	Homo sapiens	56-59
8665992-4	1995	This paper reports the possible polymorphic response of ACE to the ACE inhibitor enalaprilat in 54 normal Chinese subjects that is independent of the I/D polymorphism.	Enalaprilat	81-92	angiotensin I converting enzyme	Homo sapiens	67-70
8665992-5	1995	The kinetics of ACE inhibition with enalaprilat was studied in serum from 54 normal Chinese subjects.	Enalaprilat	36-47	angiotensin I converting enzyme	Homo sapiens	16-19
7994817-7	1994	Effective inhibition of the renin-angiotensin system by remikiren and enalaprilat was indicated by increases of plasma immunoreactive renin together with rapid and complete inhibition of renin activity after remikiren and an increase after enalaprilat (all P < or = .05).	Enalaprilat	70-81	renin	Homo sapiens	134-139
7994817-7	1994	Effective inhibition of the renin-angiotensin system by remikiren and enalaprilat was indicated by increases of plasma immunoreactive renin together with rapid and complete inhibition of renin activity after remikiren and an increase after enalaprilat (all P < or = .05).	Enalaprilat	70-81	renin	Homo sapiens	134-139
7994817-7	1994	Effective inhibition of the renin-angiotensin system by remikiren and enalaprilat was indicated by increases of plasma immunoreactive renin together with rapid and complete inhibition of renin activity after remikiren and an increase after enalaprilat (all P < or = .05).	Enalaprilat	240-251	renin	Homo sapiens	28-33
7994817-8	1994	Remikiren and enalaprilat rapidly and to a similar extent reduced resting blood pressure through a reduction of systemic vascular resistance, and these changes were significantly correlated to baseline plasma renin activity.	Enalaprilat	14-25	renin	Homo sapiens	209-214
7522595-2	1994	Preincubation with captopril, enalaprilat, enalapril, or ramiprilat for 40 min significantly reduced the angiotensin II-induced transplasma membrane calcium influx but did not influence the angiotension II-induced calcium release from internal stores.	Enalaprilat	30-41	angiotensinogen	Rattus norvegicus	105-119
7882177-7	1994	Because resetting is angiotensin II dependent, the converting enzyme inhibitor Enalaprilat was used to provide angiotensin II blockade.	Enalaprilat	79-90	angiotensinogen	Rattus norvegicus	21-35
7882177-7	1994	Because resetting is angiotensin II dependent, the converting enzyme inhibitor Enalaprilat was used to provide angiotensin II blockade.	Enalaprilat	79-90	angiotensinogen	Rattus norvegicus	111-125
8092321-2	1994	In the present study we hypothesized that N-acetyl-L-cysteine (NAC), by increasing the availability of reduced sulfhydryl groups, would enhance the antihypertensive response to the ACEIs captopril and enalaprilat by a mechanism dependent on nitric oxide.	Enalaprilat	201-212	X-linked Kx blood group	Homo sapiens	63-66
8092321-7	1994	However, when the SHRs were pretreated with NAC, the same dose of enalaprilat significantly reduced blood pressure from 176 +/- 5 to 151 +/- 5 mmHg (n = 6).	Enalaprilat	66-77	X-linked Kx blood group	Homo sapiens	44-47
8092321-9	1994	The results of this study suggest that NAC, a donor of sulfhydryl groups, potentiates the antihypertensive response to captopril and enalaprilat in SHR by a nitric oxide-dependent mechanism.	Enalaprilat	133-144	X-linked Kx blood group	Homo sapiens	39-42
8067439-6	1994	Decreases in systemic arterial pressure and in hindquarters perfusion pressure in response to bradykinin were enhanced by the angiotensin-converting enzyme inhibitors captopril and enalaprilat.	Enalaprilat	181-192	kininogen 1	Homo sapiens	94-104
7946937-8	1994	The chemotactic response of human neutrophils to fMLP was reduced by 27.6% with MPG (n = 8; P < 0.05), by 13.2% with enalaprilat (n = 8; P = 0.075) and by 5.2% with captopril (n = 8; P = 0.66) at 5 microM (therapeutic concentration.)	Enalaprilat	120-131	formyl peptide receptor 1	Homo sapiens	49-53
11835078-0	1994	Electrophysiologic Changes in the Human Heart Produced by Enalaprilat (Angiotensin-Converting Enzyme Inhibitor).	Enalaprilat	58-69	angiotensin I converting enzyme	Homo sapiens	71-100
8023980-1	1994	This study investigates the effect of angiotensin-converting-enzyme inhibition by intravenous enalaprilat (100 micrograms/kg) on splanchnic vascular capacitance during acute left ventricular failure induced by coronary microembolization in alpha-chloralose/urethan anesthetized dogs.	Enalaprilat	94-105	angiotensin I converting enzyme	Canis lupus familiaris	38-67
8024040-4	1994	The contractile response to ANG I (1 microM) was depressed by enalaprilat from 66 +/- 22 (mean +/- SD) to 39 +/- 13% of the K+ (124 mM)-induced response (P < 0.01, n = 11), and the combination of enalaprilat and STI resulted in a further reduction in contractile amplitude to 25 +/- 14% (P < 0.01 vs. K+, and P < 0.05 vs. enalaprilat alone) and a significantly slower developing contraction with a time to peak of 3.7 +/- 1.7 vs. 1.1 +/- 0.3 min for ANG I alone (P < 0.01).	Enalaprilat	62-73	angiotensinogen	Homo sapiens	28-33
8024040-4	1994	The contractile response to ANG I (1 microM) was depressed by enalaprilat from 66 +/- 22 (mean +/- SD) to 39 +/- 13% of the K+ (124 mM)-induced response (P < 0.01, n = 11), and the combination of enalaprilat and STI resulted in a further reduction in contractile amplitude to 25 +/- 14% (P < 0.01 vs. K+, and P < 0.05 vs. enalaprilat alone) and a significantly slower developing contraction with a time to peak of 3.7 +/- 1.7 vs. 1.1 +/- 0.3 min for ANG I alone (P < 0.01).	Enalaprilat	199-210	angiotensinogen	Homo sapiens	28-33
8024040-4	1994	The contractile response to ANG I (1 microM) was depressed by enalaprilat from 66 +/- 22 (mean +/- SD) to 39 +/- 13% of the K+ (124 mM)-induced response (P < 0.01, n = 11), and the combination of enalaprilat and STI resulted in a further reduction in contractile amplitude to 25 +/- 14% (P < 0.01 vs. K+, and P < 0.05 vs. enalaprilat alone) and a significantly slower developing contraction with a time to peak of 3.7 +/- 1.7 vs. 1.1 +/- 0.3 min for ANG I alone (P < 0.01).	Enalaprilat	199-210	angiotensinogen	Homo sapiens	28-33
8070480-1	1994	In this study, the acute haemodynamic effects of angiotensin converting enzyme (ACE) inhibition with intravenous enalaprilat alone or in combination with preload restoration were determined in patients with severe heart failure complicating acute myocardial infarction.	Enalaprilat	113-124	angiotensin I converting enzyme	Homo sapiens	49-78
8192653-6	1994	Captopril, lisinopril, fosinoprilat and enalaprilat, all selective inhibitors of mammalian ACE, were also good inhibitors of the insect enzyme with IC50 values of 400 nM, 130 nM, 16 nM and 290 nM respectively.	Enalaprilat	40-51	angiotensin I converting enzyme	Homo sapiens	91-94
8179016-5	1994	Captopril and enalaprilat, ANG II-converting enzyme inhibitors, decreased the pressor response to ANG I while increasing the pressor response to ANG II and III.	Enalaprilat	14-25	angiotensinogen	Rattus norvegicus	27-33
8179016-5	1994	Captopril and enalaprilat, ANG II-converting enzyme inhibitors, decreased the pressor response to ANG I while increasing the pressor response to ANG II and III.	Enalaprilat	14-25	angiotensinogen	Rattus norvegicus	145-151
8018455-0	1994	Isolated circulatory response to intravenous administration of the ACE inhibitor enalaprilat.	Enalaprilat	81-92	angiotensin I converting enzyme	Homo sapiens	67-70
8018455-1	1994	The isolated vascular effects of intravenous administration of the angiotensin converting enzyme (ACE) inhibitor enalaprilat were investigated.	Enalaprilat	113-124	angiotensin I converting enzyme	Homo sapiens	67-96
8018455-1	1994	The isolated vascular effects of intravenous administration of the angiotensin converting enzyme (ACE) inhibitor enalaprilat were investigated.	Enalaprilat	113-124	angiotensin I converting enzyme	Homo sapiens	98-101
8070480-4	1994	Enalaprilat alone (median dose 0.9 mg) reduced significantly the PAWP (from 25 to 17 mmHg; P = 0.004), the mean arterial pressure (from 87 to 83 mmHg; P = 0.008), the mean pulmonary arterial pressure and the right atrial pressure.	Enalaprilat	0-11	WBP2 N-terminal like	Homo sapiens	65-69
8379924-4	1993	We have shown this to be due to formation of a fragment, CPP-A-A, the structure of which is closely related to ACE inhibitors such as enalaprilat.	Enalaprilat	134-145	angiotensin-converting enzyme	Sus scrofa	111-114
7700846-1	1994	Objectives of this study were to determine if aerosolized bradykinin causes bronchoconstriction in anesthetized, mechanically ventilated rats, and if pretreatment with enalaprilat, an inhibitor of angiotensin-converting enzyme (ACE), or phosphoramidon, an inhibitor of endopeptidase 24.11 (EP 24.11), alters the response.	Enalaprilat	168-179	angiotensin I converting enzyme	Rattus norvegicus	197-226
8205376-3	1994	The inhibition of ACE activity paralleled enalaprilat concentrations following both single and multiple dosing and the time of maximum inhibition of ACE activity was associated on both occasions with maximum concentration of enalaprilat.	Enalaprilat	42-53	angiotensin I converting enzyme	Homo sapiens	18-21
8205376-3	1994	The inhibition of ACE activity paralleled enalaprilat concentrations following both single and multiple dosing and the time of maximum inhibition of ACE activity was associated on both occasions with maximum concentration of enalaprilat.	Enalaprilat	225-236	angiotensin I converting enzyme	Homo sapiens	149-152
8304523-3	1994	In the newborn, administration of the ACE inhibitor enalaprilat produced significant (P < 0.05) decreases in baseline RSNA (69 +/- 5 vs. 47 +/- 7% maximum) and HR (81 +/- 3 vs. 59 +/- 4% max), as well as in the baroreflex curve midpoints for RSNA (93 +/- 4 vs. 87 +/- 3 mmHg) and HR (95 +/- 4 vs. 81 +/- 5 mmHg); no change in the sensitivities (gains) of the baroreflex responses were seen.	Enalaprilat	52-63	angiotensin-converting enzyme	Ovis aries	38-41
8282342-2	1994	Enalaprilat (2 mg IV) was administered to anesthetized rats to reduce endogenous Ang II levels.	Enalaprilat	0-11	angiotensinogen	Rattus norvegicus	81-87
7527095-3	1994	However, comparison of ACE inhibitory activities of the diacid forms of trandolapril and enalapril, i.e., trandolaprilat and enalaprilat, measured in vitro on various tissues, showed that trandolaprilat was only three- to fivefold more active than enalaprilat.	Enalaprilat	125-136	angiotensin I converting enzyme	Homo sapiens	23-26
7827189-11	1994	Plasma angiotensin converting enzyme (ACE) activity was suppressed below detectable limits at four hours following intraperitoneal enalaprilat, and remained suppressed throughout all sampling time points following oral enalapril treatment.	Enalaprilat	131-142	angiotensin I converting enzyme	Homo sapiens	7-36
7827189-11	1994	Plasma angiotensin converting enzyme (ACE) activity was suppressed below detectable limits at four hours following intraperitoneal enalaprilat, and remained suppressed throughout all sampling time points following oral enalapril treatment.	Enalaprilat	131-142	angiotensin I converting enzyme	Homo sapiens	38-41
7827189-13	1994	CONCLUSION: This study demonstrates that intraperitoneal administration of enalaprilat is a rapidly effective route of administration of this ACE inhibitor.	Enalaprilat	75-86	angiotensin I converting enzyme	Homo sapiens	142-145
8244513-7	1993	Enalaprilat similarly decreased the Ang II-induced contraction.	Enalaprilat	0-11	angiotensinogen	Rattus norvegicus	36-42
8261712-2	1993	The conventional pharmacokinetic profile of the angiotensin converting enzyme (ACE) inhibitor, enalapril, is a lipid-soluble and relatively inactive prodrug with good oral absorption (60 to 70%), a rapid peak plasma concentration (1 hour) and rapid clearance (undetectable by 4 hours) by de-esterification in the liver to a primary active diacid metabolite, enalaprilat.	Enalaprilat	358-369	angiotensin I converting enzyme	Homo sapiens	48-77
8261712-2	1993	The conventional pharmacokinetic profile of the angiotensin converting enzyme (ACE) inhibitor, enalapril, is a lipid-soluble and relatively inactive prodrug with good oral absorption (60 to 70%), a rapid peak plasma concentration (1 hour) and rapid clearance (undetectable by 4 hours) by de-esterification in the liver to a primary active diacid metabolite, enalaprilat.	Enalaprilat	358-369	angiotensin I converting enzyme	Homo sapiens	79-82
8261712-8	1993	Conventional pharmacokinetic approaches have recently been extended by more detailed descriptions of the nonlinear binding of enalaprilat to ACE in plasma and tissue sites.	Enalaprilat	126-137	angiotensin I converting enzyme	Homo sapiens	141-144
8408241-5	1993	Angiotensin converting enzyme (ACE) activity detected in IVEC cells was present but lower than ACE activity in primary endothelial cells and was completely blocked by enalaprilat (1 microM), a specific ACE inhibitor.	Enalaprilat	167-178	angiotensin I converting enzyme	Homo sapiens	0-29
8408241-5	1993	Angiotensin converting enzyme (ACE) activity detected in IVEC cells was present but lower than ACE activity in primary endothelial cells and was completely blocked by enalaprilat (1 microM), a specific ACE inhibitor.	Enalaprilat	167-178	angiotensin I converting enzyme	Homo sapiens	31-34
8408241-5	1993	Angiotensin converting enzyme (ACE) activity detected in IVEC cells was present but lower than ACE activity in primary endothelial cells and was completely blocked by enalaprilat (1 microM), a specific ACE inhibitor.	Enalaprilat	167-178	angiotensin I converting enzyme	Homo sapiens	95-98
8408241-5	1993	Angiotensin converting enzyme (ACE) activity detected in IVEC cells was present but lower than ACE activity in primary endothelial cells and was completely blocked by enalaprilat (1 microM), a specific ACE inhibitor.	Enalaprilat	167-178	angiotensin I converting enzyme	Homo sapiens	95-98
8394914-6	1993	Enalaprilat (6 x 10(-8) M), an inhibitor of ACE, also enhanced BK-induced contraction.	Enalaprilat	0-11	angiotensin I converting enzyme	Rattus norvegicus	44-47
8394785-9	1993	The positive inotropic effect of angiotensin I could be blocked by enalaprilate (10(-5) mol/L).	Enalaprilat	67-79	angiotensinogen	Homo sapiens	33-46
8397997-0	1993	Effects of enalaprilat on hemodynamics and ventricular activation duration in hypertensive patients with left ventricular hypertrophy: clinical evidence of improved excitation-contraction coupling with angiotensin converting enzyme inhibition in human hypertension.	Enalaprilat	11-22	angiotensin I converting enzyme	Homo sapiens	202-231
8397997-3	1993	The angiotensin converting enzyme inhibitor enalaprilat has been found to improve electromechanical coupling of heart cells in animal models.	Enalaprilat	44-55	angiotensin I converting enzyme	Homo sapiens	4-33
8231461-1	1993	We previously demonstrated the dependency of serum angiotensin converting enzyme (ACE) inhibition by the inhibitor enalaprilat in vitro on the concentration of substrate and enzyme present in the assay, according to a competitive tight-binding mechanism.	Enalaprilat	115-126	angiotensin I converting enzyme	Homo sapiens	82-85
7690096-8	1993	Thus, these results indicate that blockade of the AT1 receptor of AII by EXP3174 induces hemodynamic modifications similar to those evoked by the ACE inhibitor enalaprilat.	Enalaprilat	160-171	angiotensin I converting enzyme	Canis lupus familiaris	146-149
8383016-7	1993	The maximal effect of the ACE inhibitor enalaprilat (5 mg) was an increase in CSA from 7.7 +/- 0.7 to 8.4 +/- 0.8 mm2 and an increase in APV from 36 +/- 10 to 53 +/- 20 cm/sec, with an increase in coronary blood flow from 82 +/- 25 to 122 +/- 41 mL/min.	Enalaprilat	40-51	angiotensin I converting enzyme	Canis lupus familiaris	26-29
8231461-1	1993	We previously demonstrated the dependency of serum angiotensin converting enzyme (ACE) inhibition by the inhibitor enalaprilat in vitro on the concentration of substrate and enzyme present in the assay, according to a competitive tight-binding mechanism.	Enalaprilat	115-126	angiotensin I converting enzyme	Homo sapiens	51-80
8504625-5	1993	The AUC of enalapril diacid increased 13-fold at CLCR values < 30 ml/min, but that of temocapril diacid increased only 2-fold.	Enalaprilat	11-27	chymotrypsin C	Homo sapiens	49-53
8391949-13	1993	Results of this study indicate that enalaprilat enhances baroreflex control of renal and total NA spillover in rabbits with CHF and further support the view that activation of the renin-angiotensin system contributes significantly to the attenuated baroreflex responses in CHF.	Enalaprilat	36-47	LOW QUALITY PROTEIN: renin	Oryctolagus cuniculus	180-185
7683421-1	1993	The pharmacological potency of angiotensin-converting enzyme (ACE) inhibitors (lisinopril and enalaprilat) on the transcription of low density lipoprotein receptor and 3-hydroxy-3-methylglutaryl-CoA reductase genes was examined in human vascular smooth muscle cells and compared with the action of Ca(2+)-channel blockers (manidipine, verapamil, and diltiazem).	Enalaprilat	94-105	angiotensin I converting enzyme	Homo sapiens	31-60
7683421-1	1993	The pharmacological potency of angiotensin-converting enzyme (ACE) inhibitors (lisinopril and enalaprilat) on the transcription of low density lipoprotein receptor and 3-hydroxy-3-methylglutaryl-CoA reductase genes was examined in human vascular smooth muscle cells and compared with the action of Ca(2+)-channel blockers (manidipine, verapamil, and diltiazem).	Enalaprilat	94-105	angiotensin I converting enzyme	Homo sapiens	62-65
7683421-1	1993	The pharmacological potency of angiotensin-converting enzyme (ACE) inhibitors (lisinopril and enalaprilat) on the transcription of low density lipoprotein receptor and 3-hydroxy-3-methylglutaryl-CoA reductase genes was examined in human vascular smooth muscle cells and compared with the action of Ca(2+)-channel blockers (manidipine, verapamil, and diltiazem).	Enalaprilat	94-105	low density lipoprotein receptor	Homo sapiens	131-163
7683421-2	1993	Analogous to Ca(2+)-channel blockers, nanomolar concentrations of enalaprilat or lisinopril stimulated the synthesis of low density lipoprotein receptor mRNA and amplified the transcription induced by recombinant platelet-derived growth factor BB.	Enalaprilat	66-77	low density lipoprotein receptor	Homo sapiens	120-152
8479122-9	1993	In vivo pretreatment of rats with simultaneous administration of the angiotensin-converting enzyme inhibitor, enalaprilat, and the thromboxane synthase inhibitor, OKY-046, maintained the amount of G alpha s and G alpha q/11 in rats with BUO at the levels seen in SOC rats.	Enalaprilat	110-121	G protein subunit alpha q	Rattus norvegicus	211-220
8384414-12	1993	Blockade of ANG II by enalaprilat or by the AT1-receptor blocker losartan potassium significantly inhibited regulatory vasodilatation and vasoconstriction at low RPP.	Enalaprilat	22-33	angiotensinogen	Rattus norvegicus	12-18
8383028-7	1993	This study supports the use of IV enalaprilat, a parenteral angiotensin-converting enzyme (ACE) inhibitor, as an effective and rapidly acting vasodilator in the management of selected patients with chronic heart failure and MR who require immediate hemodynamic improvement.	Enalaprilat	34-45	angiotensin I converting enzyme	Homo sapiens	60-89
8383028-7	1993	This study supports the use of IV enalaprilat, a parenteral angiotensin-converting enzyme (ACE) inhibitor, as an effective and rapidly acting vasodilator in the management of selected patients with chronic heart failure and MR who require immediate hemodynamic improvement.	Enalaprilat	34-45	angiotensin I converting enzyme	Homo sapiens	91-94
7508047-2	1993	The angiotensin-converting enzyme (ACE) inhibitor enalaprilat (10(-7) M) markedly augmented endothelium-dependent relaxations to bradykinin in SV (concentration shift: 10-fold; n = 6; p < 0.005), but not in IMA; in both blood vessels, it had no effect on endothelium-dependent relaxations to acetylcholine.	Enalaprilat	50-61	angiotensin I converting enzyme	Homo sapiens	4-33
7508047-2	1993	The angiotensin-converting enzyme (ACE) inhibitor enalaprilat (10(-7) M) markedly augmented endothelium-dependent relaxations to bradykinin in SV (concentration shift: 10-fold; n = 6; p < 0.005), but not in IMA; in both blood vessels, it had no effect on endothelium-dependent relaxations to acetylcholine.	Enalaprilat	50-61	angiotensin I converting enzyme	Homo sapiens	35-38
7508047-2	1993	The angiotensin-converting enzyme (ACE) inhibitor enalaprilat (10(-7) M) markedly augmented endothelium-dependent relaxations to bradykinin in SV (concentration shift: 10-fold; n = 6; p < 0.005), but not in IMA; in both blood vessels, it had no effect on endothelium-dependent relaxations to acetylcholine.	Enalaprilat	50-61	kininogen 1	Homo sapiens	129-139
7508047-3	1993	The contractions to angiotensin I (Ang I; 10(-7) M) were markedly inhibited by enalaprilat (10(-7) M) in SV (control: 34 +/- 6% of 100 mM KCl; treatment: 18 +/- 6%; n = 7; p < 0.05) but not in IMA (control: 33 +/- 4%; treatment: 30 +/- 6%; n = 7; NS) and abolished by the Ang II receptor antagonist DuP 753 (10(-7) M) in both blood vessels.	Enalaprilat	79-90	angiotensinogen	Homo sapiens	20-33
7508047-3	1993	The contractions to angiotensin I (Ang I; 10(-7) M) were markedly inhibited by enalaprilat (10(-7) M) in SV (control: 34 +/- 6% of 100 mM KCl; treatment: 18 +/- 6%; n = 7; p < 0.05) but not in IMA (control: 33 +/- 4%; treatment: 30 +/- 6%; n = 7; NS) and abolished by the Ang II receptor antagonist DuP 753 (10(-7) M) in both blood vessels.	Enalaprilat	79-90	angiotensinogen	Homo sapiens	35-40
1363432-7	1992	Enalaprilat (an inhibitor of kininase II) blocked the formation of BK1-7 and BK1-5 and increased the recovery of BK4-9.	Enalaprilat	0-11	angiotensin I converting enzyme	Rattus norvegicus	29-40
1337458-11	1992	The data suggest that angiotensin converting enzyme inhibition with enalaprilat reduces conduction velocity delay in hypertensive patients with LVH.	Enalaprilat	68-79	angiotensin I converting enzyme	Homo sapiens	22-51
1363432-7	1992	Enalaprilat (an inhibitor of kininase II) blocked the formation of BK1-7 and BK1-5 and increased the recovery of BK4-9.	Enalaprilat	0-11	potassium voltage-gated channel subfamily A member 2	Rattus norvegicus	67-72
1363432-7	1992	Enalaprilat (an inhibitor of kininase II) blocked the formation of BK1-7 and BK1-5 and increased the recovery of BK4-9.	Enalaprilat	0-11	potassium voltage-gated channel subfamily A member 2	Rattus norvegicus	77-82
1363433-8	1992	When kininase II was inhibited with enalaprilat, the recovery of bradykinin increased from 10 to 43% in SHR and from 23 to 58% in NWR, whereas about 90% of the higher bradykinin homologues were recovered in both SHR and NWR.	Enalaprilat	36-47	angiotensin I converting enzyme	Rattus norvegicus	5-16
1336190-9	1992	The hydrolysis of Ang I into Ang II by pulmonary ACE was inhibited to a similar extent by both cFP-A-A-F-pAB and the ACE inhibitor MK 422.	Enalaprilat	131-137	angiotensinogen	Homo sapiens	18-23
1282072-7	1992	Potencies of all these agonists were not significantly different (P > 0.05) when experiments were carried out in the presence of the neutral endopeptidase inhibitor, phosphoramidon, and the kininase II inhibitor, enalaprilat (both 1 microM).	Enalaprilat	216-227	angiotensin I converting enzyme	Rattus norvegicus	193-204
1336190-9	1992	The hydrolysis of Ang I into Ang II by pulmonary ACE was inhibited to a similar extent by both cFP-A-A-F-pAB and the ACE inhibitor MK 422.	Enalaprilat	131-137	angiogenin	Homo sapiens	18-21
1336190-9	1992	The hydrolysis of Ang I into Ang II by pulmonary ACE was inhibited to a similar extent by both cFP-A-A-F-pAB and the ACE inhibitor MK 422.	Enalaprilat	131-137	angiotensin I converting enzyme	Homo sapiens	49-52
1336190-9	1992	The hydrolysis of Ang I into Ang II by pulmonary ACE was inhibited to a similar extent by both cFP-A-A-F-pAB and the ACE inhibitor MK 422.	Enalaprilat	131-137	angiotensin I converting enzyme	Homo sapiens	117-120
1381019-7	1992	Balanced vasodilatation after selective alpha-adrenoceptor blockade (doxazosin) and angiotensin-converting enzyme (ACE) inhibition (enalaprilat) without increase in heart rate (HR) suggests that these therapies may have definite haemodynamic advantages over the hydralazine/ISDN combination.	Enalaprilat	132-143	angiotensin I converting enzyme	Homo sapiens	84-113
1381019-7	1992	Balanced vasodilatation after selective alpha-adrenoceptor blockade (doxazosin) and angiotensin-converting enzyme (ACE) inhibition (enalaprilat) without increase in heart rate (HR) suggests that these therapies may have definite haemodynamic advantages over the hydralazine/ISDN combination.	Enalaprilat	132-143	angiotensin I converting enzyme	Homo sapiens	115-118
1328628-7	1992	Enalaprilat inhibited in a dose-dependent manner the increases in stromal cell alkaline phosphatase activity and media PGE concentration that occurred in the control cultures; these effects were fully reversed by concurrent treatment with angiotensin II.	Enalaprilat	0-11	angiotensinogen	Rattus norvegicus	239-253
1328628-8	1992	The inhibition of stromal alkaline phosphatase activity was also reversed by PGE2; conversely, the ability of angiotensin II to reverse the effect of enalaprilat was lost in the presence of indomethacin.	Enalaprilat	150-161	angiotensinogen	Rattus norvegicus	110-124
1352511-3	1992	Captopril (0.5 mg/kg/hr) and enalaprilat (300 micrograms/kg/hr) significantly reduced the response to ANG I, but not ANG II or NE.	Enalaprilat	29-40	angiogenin-4	Alligator mississippiensis	102-105
1331222-4	1992	The ACE inhibitor, enalaprilat, was infused i.c.v.	Enalaprilat	19-30	angiotensin I converting enzyme	Rattus norvegicus	4-7
1330581-5	1992	Enalaprilat inhibited the activity of purified ACE, whereas KPP was completely devoid of such an effect.	Enalaprilat	0-11	angiotensin I converting enzyme	Rattus norvegicus	47-50
1317352-4	1992	Pretreatment with the angiotensin converting enzyme inhibitor enalaprilat (2 mg/kg) eliminated angiotensin II formation and augmented circulating levels of angiotensin I and angiotensin-(1-7) in spontaneously hypertensive and Wistar-Kyoto rats.	Enalaprilat	62-73	angiotensinogen	Rattus norvegicus	95-109
1314526-3	1992	It was found that the required hypotension (51 (SEM 1) mmHg) could be obtained and maintained at much lower isoflurane concentrations (less than 1%) after blockade of the angiotensin converting enzyme activity by enalaprilat (2.5 mg i.v.)	Enalaprilat	213-224	SEM1 26S proteasome subunit	Homo sapiens	48-53
1317125-8	1992	In rats fed normal chow, infusion of enalaprilat for 1 h abolished plasma ACE activity but decreased renal ACE activity by only 58%.	Enalaprilat	37-48	angiotensin I converting enzyme	Rattus norvegicus	74-77
1317125-8	1992	In rats fed normal chow, infusion of enalaprilat for 1 h abolished plasma ACE activity but decreased renal ACE activity by only 58%.	Enalaprilat	37-48	angiotensin I converting enzyme	Rattus norvegicus	107-110
1312853-0	1992	The effect of saturation of ACE binding sites on the pharmacokinetics of enalaprilat in man.	Enalaprilat	73-84	angiotensin I converting enzyme	Homo sapiens	28-31
1315824-1	1992	OBJECTIVE AND DESIGN: This study was designed to test whether previous work, which showed that the angiotensin converting enzyme (ACE) inhibitor enalaprilat potentiated the alpha 1-adrenoceptor antagonist activity of doxazosin in isolated rat tail arteries, could be extended to demonstrate a synergistic hypotensive effect of these two drugs.	Enalaprilat	145-156	angiotensin I converting enzyme	Rattus norvegicus	99-128
1315824-1	1992	OBJECTIVE AND DESIGN: This study was designed to test whether previous work, which showed that the angiotensin converting enzyme (ACE) inhibitor enalaprilat potentiated the alpha 1-adrenoceptor antagonist activity of doxazosin in isolated rat tail arteries, could be extended to demonstrate a synergistic hypotensive effect of these two drugs.	Enalaprilat	145-156	angiotensin I converting enzyme	Rattus norvegicus	130-133
1312513-4	1992	The most potent converting enzyme inhibitors toward aminopeptidase P were the carboxylalkyl compounds, cilazaprilat, enalaprilat, and ramiprilat (I50 values of 3-12 microM).	Enalaprilat	117-128	X-prolyl aminopeptidase 2	Sus scrofa	52-68
1312853-6	1992	The pharmacokinetics of enalaprilat were best described by a one compartment model with zero order input incorporating saturable binding to plasma and tissue ACE.	Enalaprilat	24-35	angiotensin I converting enzyme	Homo sapiens	158-161
1741993-8	1991	The acute blood pressure decrease initiated in normotensive rats by an ACE-inhibitor (enalaprilat) was abolished in medullectomized rats, indicating an interaction between the renin-angiotensin and the renomedullary antihypertensive systems.	Enalaprilat	86-97	angiotensin I converting enzyme	Rattus norvegicus	71-74
1310484-11	1992	When human umbilical endothelial cells were incubated in the presence of the angiotensin converting enzyme inhibitor enalaprilat (1 microM), generation of angiotensin II was undetectable.	Enalaprilat	117-128	angiotensinogen	Homo sapiens	155-169
1327596-8	1992	The potency of the active diacids in inhibiting plasma ACE activity was perindoprilat greater than cilazaprilat greater than enalaprilat.	Enalaprilat	125-136	angiotensin I converting enzyme	Homo sapiens	55-58
1656995-0	1991	The role of enzyme and substrate concentration in the evaluation of serum angiotensin converting enzyme (ACE) inhibition by enalaprilat in vitro.	Enalaprilat	124-135	angiotensin I converting enzyme	Homo sapiens	74-103
1656995-0	1991	The role of enzyme and substrate concentration in the evaluation of serum angiotensin converting enzyme (ACE) inhibition by enalaprilat in vitro.	Enalaprilat	124-135	angiotensin I converting enzyme	Homo sapiens	105-108
1656995-1	1991	The relationship between serum angiotensin converting enzyme (ACE) activity and concentration of the ACE inhibitor enalaprilat was determined in vitro in the presence of different concentrations (S = 4-200 mM) of the substrate Hip-Gly-Gly.	Enalaprilat	115-126	angiotensin I converting enzyme	Homo sapiens	31-60
1656995-1	1991	The relationship between serum angiotensin converting enzyme (ACE) activity and concentration of the ACE inhibitor enalaprilat was determined in vitro in the presence of different concentrations (S = 4-200 mM) of the substrate Hip-Gly-Gly.	Enalaprilat	115-126	angiotensin I converting enzyme	Homo sapiens	62-65
1656995-1	1991	The relationship between serum angiotensin converting enzyme (ACE) activity and concentration of the ACE inhibitor enalaprilat was determined in vitro in the presence of different concentrations (S = 4-200 mM) of the substrate Hip-Gly-Gly.	Enalaprilat	115-126	angiotensin I converting enzyme	Homo sapiens	101-104
1656995-2	1991	From Henderson plots, a competitive tight-binding relationship between enalaprilat and serum ACE was found yielding a value of approximately 5 nM for serum ACE concentration (Et) and an inhibition constant (Ki) for enalaprilat of approximately 0.1 nM.	Enalaprilat	71-82	angiotensin I converting enzyme	Homo sapiens	93-96
1656995-2	1991	From Henderson plots, a competitive tight-binding relationship between enalaprilat and serum ACE was found yielding a value of approximately 5 nM for serum ACE concentration (Et) and an inhibition constant (Ki) for enalaprilat of approximately 0.1 nM.	Enalaprilat	71-82	angiotensin I converting enzyme	Homo sapiens	156-159
1656995-2	1991	From Henderson plots, a competitive tight-binding relationship between enalaprilat and serum ACE was found yielding a value of approximately 5 nM for serum ACE concentration (Et) and an inhibition constant (Ki) for enalaprilat of approximately 0.1 nM.	Enalaprilat	215-226	angiotensin I converting enzyme	Homo sapiens	93-96
1281378-2	1992	Enalaprilat, moexiprilat and ramiprilat similarly potentiated the increase in [Ca2+]i elicited by bradykinin and caused an increase in resting [Ca2+]i when given alone.	Enalaprilat	0-11	kininogen 1	Homo sapiens	98-108
1330574-4	1992	The relationships between serum enalaprilat and serum ACE activity were similar after both treatments, both consistent with a value for Ki of enalaprilat of about 0.1 nmol.l-1.	Enalaprilat	32-43	angiotensin I converting enzyme	Homo sapiens	54-57
1330574-5	1992	Thus, serum ACE activity was not affected by hydrochlorothiazide but completely reflected the pharmacokinetics of enalaprilat in both treatments.	Enalaprilat	114-125	angiotensin I converting enzyme	Homo sapiens	12-15
1777188-2	1991	ACE inhibition (10 mg enalaprilic acid, intravenously) markedly improved the sensitivity of [123I]hippuran renography in 10 renovascular hypertensive dogs with a mild to moderate unilateral renal artery stenosis from 50 to 100%.	Enalaprilat	22-38	angiotensin I converting enzyme	Canis lupus familiaris	0-3
1665404-0	1991	Endothelin-1-induced renal vasoconstriction is blunted by enalaprilat and enhanced by EDRF antagonist in awake normotensive rats.	Enalaprilat	58-69	endothelin 1	Rattus norvegicus	0-12
1657799-0	1991	Enalaprilat in acute myocardial infarction: tolerability and effects on the renin-angiotensin system.	Enalaprilat	0-11	renin	Homo sapiens	76-81
1720843-2	1991	In contrast, the effect of concomitant administration of enalaprilat only slightly increased the effect of bradykinin on coronary flow.	Enalaprilat	57-68	kininogen 1	Homo sapiens	107-117
1652204-2	1991	This increase was abolished by the angiotensin-converting enzyme (ACE) inhibitor, enalaprilat, given in vivo.	Enalaprilat	82-93	angiotensin I converting enzyme	Rattus norvegicus	35-64
1652204-2	1991	This increase was abolished by the angiotensin-converting enzyme (ACE) inhibitor, enalaprilat, given in vivo.	Enalaprilat	82-93	angiotensin I converting enzyme	Rattus norvegicus	66-69
1827206-10	1991	Although the radionuclide renogram is no longer adequate as a radiographic screening tool, stimulation with an ACE inhibitor, such as captopril or enalaprilat, may produce excellent results.	Enalaprilat	147-158	angiotensin I converting enzyme	Homo sapiens	111-114
1663586-2	1991	The ACE inhibitors ramiprilat and enalaprilat (0.3 microM) enhanced the increase in [Ca2+]i elicited by bradykinin (3 nM) and also caused an increase in resting [Ca2+]i when given alone.	Enalaprilat	34-45	angiotensin I converting enzyme	Homo sapiens	4-7
1663586-2	1991	The ACE inhibitors ramiprilat and enalaprilat (0.3 microM) enhanced the increase in [Ca2+]i elicited by bradykinin (3 nM) and also caused an increase in resting [Ca2+]i when given alone.	Enalaprilat	34-45	kininogen 1	Homo sapiens	104-114
1646164-6	1991	After enalaprilat, norepinephrine venoarterial difference increased in the renin-secreting kidney (from 264 to 396, SED = 57 pg/ml, p less than 0.05), whereas it increased only slightly in the contralateral kidney (from 149 to 256, SED = 72 pg/ml, NS).	Enalaprilat	6-17	renin	Homo sapiens	75-80
1649762-3	1991	[3H]Ramiprilat binding was completely inhibited by specific inhibitors of ACE: ramiprilat, ramipril, enalaprilat, enalapril and captopril.	Enalaprilat	101-112	angiotensin I converting enzyme	Rattus norvegicus	74-77
1709269-3	1991	However other inhibitors of these two enzymes, kelatorphan for endopeptidase-24.11 and enalaprilat for angiotensin I converting enzyme were essentially inactive, indicating that both enzymes are probably not involved in the degradation of endogenous substance P. Instead, the non-additive protecting effect of bacitracin, captopril and thiorphan might be due to the blockade of some "bacitracin-sensitive enzyme" playing a key role in the catabolism of SP within the rat spinal cord.	Enalaprilat	87-98	angiotensin I converting enzyme	Rattus norvegicus	103-134
1846840-7	1991	Administration of MK-422 led to the disappearance of circulating angiotensin II and its fragments both before and after a second injection of the same dose of renin.	Enalaprilat	18-24	renin	Canis lupus familiaris	159-164
1848958-1	1991	The angiotensin-converting enzyme inhibitor enalapril is available for intravenous administration in the form of enalaprilat.	Enalaprilat	113-124	angiotensin I converting enzyme	Homo sapiens	4-33
2088853-2	1990	In this study we have shown that SH-containing ACE inhibitors (captopril, epicaptopril, zofenopril) are potent FR scavengers at a concentration of 4 x 10(-5) M whereas non-SH ACE inhibitors (enalaprilat, quinaprilat and perindoprilat) have no FR-scavenging activity at this concentration.	Enalaprilat	191-202	angiotensin I converting enzyme	Homo sapiens	47-50
1708041-1	1991	Using paired isolated perfused rat tail artery segments, it was found that enalaprilat, an ACE inhibitor, augmented 1.6-fold the contractile responses to phenylephrine (PE), an alpha 1-adrenoceptor agonist.	Enalaprilat	75-86	angiotensin I converting enzyme	Rattus norvegicus	91-94
1712272-6	1991	Enalaprilat, applied locally, but not cilazaprilat, enhanced the inflammatory reactions caused by intradermal injections of allergen and substance P. Both angiotensin converting enzyme (ACE) inhibitors enhanced the inflammatory skin response evoked by bradykinin.	Enalaprilat	0-11	LOW QUALITY PROTEIN: angiotensin-converting enzyme	Cavia porcellus	186-189
1646895-12	1991	The small but significant inhibition found with Enalaprilat for the larger arterioles suggests that the local angiotensin II level may affect the response to cocaine.	Enalaprilat	48-59	angiotensinogen	Rattus norvegicus	110-124
1849639-9	1991	Enalaprilat may compensate for the reduction of mucosal blood flow by limiting formation of angiotensin II and/or preventing degradation of bradykinin.	Enalaprilat	0-11	angiotensinogen	Homo sapiens	92-106
1849639-9	1991	Enalaprilat may compensate for the reduction of mucosal blood flow by limiting formation of angiotensin II and/or preventing degradation of bradykinin.	Enalaprilat	0-11	kininogen 1	Homo sapiens	140-150
2165184-6	1990	The potent angiotensin converting enzyme (ACE) inhibitor, enalaprilic acid [MK-422] (10(-6) M) increased the contractile response to the prostate to bradykinin two-fold while having no effect on bradykinin-induced contractions in the bladder.	Enalaprilat	58-74	angiotensin I converting enzyme	Canis lupus familiaris	11-40
2172161-7	1990	A close linear relation was found between plasma angiotensin II and the angiotensin I/drug level ratio (r = 0.91 for benazeprilat and r = 0.88 for enalaprilat, p less than 0.001).	Enalaprilat	147-158	angiotensinogen	Homo sapiens	49-63
2172161-7	1990	A close linear relation was found between plasma angiotensin II and the angiotensin I/drug level ratio (r = 0.91 for benazeprilat and r = 0.88 for enalaprilat, p less than 0.001).	Enalaprilat	147-158	angiotensinogen	Homo sapiens	49-62
2282472-11	1990	Enalaprilic acid, the active metabolite of the converting enzyme inhibitor enalapril (300 nM), attenuated responses to angiotensin I but failed to inhibit those to angiotensinogen up to 1 microM.	Enalaprilat	0-16	angiotensinogen	Homo sapiens	119-132
2165184-6	1990	The potent angiotensin converting enzyme (ACE) inhibitor, enalaprilic acid [MK-422] (10(-6) M) increased the contractile response to the prostate to bradykinin two-fold while having no effect on bradykinin-induced contractions in the bladder.	Enalaprilat	58-74	angiotensin I converting enzyme	Canis lupus familiaris	42-45
2165184-6	1990	The potent angiotensin converting enzyme (ACE) inhibitor, enalaprilic acid [MK-422] (10(-6) M) increased the contractile response to the prostate to bradykinin two-fold while having no effect on bradykinin-induced contractions in the bladder.	Enalaprilat	58-74	kininogen 1	Canis lupus familiaris	149-159
2165184-6	1990	The potent angiotensin converting enzyme (ACE) inhibitor, enalaprilic acid [MK-422] (10(-6) M) increased the contractile response to the prostate to bradykinin two-fold while having no effect on bradykinin-induced contractions in the bladder.	Enalaprilat	76-82	angiotensin I converting enzyme	Canis lupus familiaris	11-40
2165184-6	1990	The potent angiotensin converting enzyme (ACE) inhibitor, enalaprilic acid [MK-422] (10(-6) M) increased the contractile response to the prostate to bradykinin two-fold while having no effect on bradykinin-induced contractions in the bladder.	Enalaprilat	76-82	angiotensin I converting enzyme	Canis lupus familiaris	42-45
2165184-6	1990	The potent angiotensin converting enzyme (ACE) inhibitor, enalaprilic acid [MK-422] (10(-6) M) increased the contractile response to the prostate to bradykinin two-fold while having no effect on bradykinin-induced contractions in the bladder.	Enalaprilat	76-82	kininogen 1	Canis lupus familiaris	149-159
2165184-11	1990	The activity of enalaprilic acid to amplify the bradykinin-induced contractions in the canine prostate is consistent with high levels of ACE in the tissue.	Enalaprilat	16-32	kininogen 1	Canis lupus familiaris	48-58
2165184-11	1990	The activity of enalaprilic acid to amplify the bradykinin-induced contractions in the canine prostate is consistent with high levels of ACE in the tissue.	Enalaprilat	16-32	angiotensin I converting enzyme	Canis lupus familiaris	137-140
1696659-0	1990	Enalaprilat effects renin-angiotensin and adrenergic response to induced hypotension in the rabbit.	Enalaprilat	0-11	LOW QUALITY PROTEIN: renin	Oryctolagus cuniculus	20-25
2159506-5	1990	All renin inhibitors lowered blood pressure significantly beyond the maximal response to enalaprilat.	Enalaprilat	89-100	renin	Macaca mulatta	4-9
2166521-2	1990	AB-47 was slightly more potent than enalaprilat in inhibiting rabbit lung ACE.	Enalaprilat	36-47	angiotensin-converting enzyme	Oryctolagus cuniculus	74-77
2166521-3	1990	The ACE inhibition and bradykinin (BK) potentiation by AB-47 in guinea-pig ileal longitudinal muscle were as potent as with enalaprilat.	Enalaprilat	124-135	LOW QUALITY PROTEIN: angiotensin-converting enzyme	Cavia porcellus	4-7
2160492-2	1990	In addition, we also examined the chronic effects on renal function and blood pressure of the angiotensin converting enzyme (ACE) inhibitor enalaprilat.	Enalaprilat	140-151	angiotensin I converting enzyme	Canis lupus familiaris	94-123
2160492-2	1990	In addition, we also examined the chronic effects on renal function and blood pressure of the angiotensin converting enzyme (ACE) inhibitor enalaprilat.	Enalaprilat	140-151	angiotensin I converting enzyme	Canis lupus familiaris	125-128
2162536-7	1990	Although the converting enzyme inhibitor enalaprilat (MK-422) significantly reduced Ang II formation, it had no effect on the levels of Ang-(1-7).	Enalaprilat	41-52	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	84-90
2162536-7	1990	Although the converting enzyme inhibitor enalaprilat (MK-422) significantly reduced Ang II formation, it had no effect on the levels of Ang-(1-7).	Enalaprilat	54-60	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	84-90
35455696-1	2022	The angiotensin-converting enzyme inhibitor enalapril is hydrolysed to an active metabolite, enalaprilat, in the liver via carboxylesterase 1 (CES1).	Enalaprilat	93-104	angiotensin I converting enzyme	Homo sapiens	4-33
1967591-7	1990	The addition of angiotensin II after enalaprilic acid (10(-4) M) did not normalize the response in +T and -T. Enalaprilic acid diminishes the contractile response of the papillary muscle to beta-adrenergic stimulation.	Enalaprilat	110-126	angiotensinogen	Rattus norvegicus	16-30
34775060-1	2022	Formulations on the base of an inhibitor of angiotensin-converting enzyme, enalaprilat, were prepared by the inclusion of the drug into calcium phosphate (CaP)-particles in situ, followed by the covering of the particles with 5 kDa chitosan or 72 kDa glycol chitosan and cross-linking with sodium tripolyphosphate.	Enalaprilat	75-86	angiotensin-converting enzyme	Oryctolagus cuniculus	44-73
2154128-4	1990	Administration of an ACE inhibitor, enalaprilat, given in vivo returned basal prostanoid production by isolated glomeruli of BUO rats to levels seen in glomeruli of control rats.	Enalaprilat	36-47	angiotensin I converting enzyme	Rattus norvegicus	21-24
2147879-3	1990	The in vitro affinity for ACE is 7 times higher than for enalaprilat and 47 times higher than for captopril.	Enalaprilat	57-68	angiotensin I converting enzyme	Homo sapiens	26-29
34651661-11	2021	In particular, DAS showed advantages in terms of improved chamber dilation and dysfunction in model mice, and the improvement occurred in the early stage of the treatment compared with enalaprilat, an angiotensin-converting enzyme inhibitor that has been widely used in the clinical treatment of DCM and HF.	Enalaprilat	185-196	angiotensin I converting enzyme (peptidyl-dipeptidase A) 1	Mus musculus	201-230
35455696-1	2022	The angiotensin-converting enzyme inhibitor enalapril is hydrolysed to an active metabolite, enalaprilat, in the liver via carboxylesterase 1 (CES1).	Enalaprilat	93-104	carboxylesterase 1	Homo sapiens	123-141
35455696-1	2022	The angiotensin-converting enzyme inhibitor enalapril is hydrolysed to an active metabolite, enalaprilat, in the liver via carboxylesterase 1 (CES1).	Enalaprilat	93-104	carboxylesterase 1	Homo sapiens	143-147
35455696-6	2022	Mean peak and trough enalaprilat concentrations, adjusted by clinical variables, were significantly lower in CES1 rs2244613 heterozygotes (by 16.6% and 19.6%) and in CC homozygotes (by 32.7% and 41.4%) vs. the AA genotype.	Enalaprilat	21-32	carboxylesterase 1	Homo sapiens	109-113
2556057-4	1989	Complete inhibition of angiotensin converting enzyme occurred with all doses of enalaprilat, which allowed the four different treatment groups to be considered as one large treated group.	Enalaprilat	80-91	angiotensin I converting enzyme	Homo sapiens	23-52
35088420-2	2022	It was recently reported that febuxostat inhibited organic anion transporter 3 (OAT3)-mediated uptake of enalaprilat.	Enalaprilat	105-116	solute carrier family 22 member 8	Homo sapiens	51-78
35088420-2	2022	It was recently reported that febuxostat inhibited organic anion transporter 3 (OAT3)-mediated uptake of enalaprilat.	Enalaprilat	105-116	solute carrier family 22 member 8	Homo sapiens	80-84
2559850-0	1989	Coronary vasodilation induced by intracoronary enalaprilat: an argument for the role of a local renin-angiotensin system in patients with dilated cardiomyopathy.	Enalaprilat	47-58	renin	Homo sapiens	96-101
2559850-5	1989	Despite these steady haemodynamic conditions, intracoronary enalaprilat provoked a significant elevation of coronary sinus blood flow (181 +/- 73 to 214 +/- 79 ml min-1, P less than 0.001) with a reduction of coronary resistance (0.51 +/- 0.17 to 0.41 +/- 0.15 mmHg ml-1 min, P less than 0.001), and no significant alteration in plasma renin activity or plasma aldosterone.	Enalaprilat	60-71	CD59 molecule (CD59 blood group)	Homo sapiens	163-168
2559850-5	1989	Despite these steady haemodynamic conditions, intracoronary enalaprilat provoked a significant elevation of coronary sinus blood flow (181 +/- 73 to 214 +/- 79 ml min-1, P less than 0.001) with a reduction of coronary resistance (0.51 +/- 0.17 to 0.41 +/- 0.15 mmHg ml-1 min, P less than 0.001), and no significant alteration in plasma renin activity or plasma aldosterone.	Enalaprilat	60-71	renin	Homo sapiens	336-341
2559850-6	1989	The results of this intracoronary infusion of enalaprilat demonstrate that this angiotensin converting-enzyme inhibitor has significant coronary vasodilator properties, which can be evidenced without stimulating the peripheral renin-angiotensin system.	Enalaprilat	46-57	angiotensin I converting enzyme	Homo sapiens	80-109
9118114-2	1989	In vitro, equine serum ACE was sensitive to the following inhibitors (IC50): enalapril (570 nM or 215 ng/ml), captopril (190 nM or 41.3 ng/ml), and enalaprilat (6 nM or 2.1 ng/ml).	Enalaprilat	148-159	angiotensin I converting enzyme	Equus caballus	23-26
19210444-7	1989	However, following treatment with ovarian steroids, infusion of saralasin or injection of enalaprilat resulted in a significant increase in plasma prolactin tilers.	Enalaprilat	90-101	prolactin	Rattus norvegicus	147-156
19210444-9	1989	After enalaprilat administration, prolactin levels did not rise significantly until 90 min and then remained elevated up to 120 min post-injection.	Enalaprilat	6-17	prolactin	Rattus norvegicus	34-43
2476598-6	1989	At doses greater than 78 ng/min, cilazaprilat and enalaprilat completely inhibited angiotensin I-induced venoconstriction.	Enalaprilat	50-61	angiotensinogen	Homo sapiens	83-96
2476598-10	1989	We conclude that cilazaprilat and enalaprilat are inhibitors of ACE associated with the vein wall, but there is no evidence for either drug of direct, ACE-independent, prostaglandin-mediated vasodilation.	Enalaprilat	34-45	angiotensin I converting enzyme	Homo sapiens	64-67
2547465-7	1989	The observations in these studies with lisinopril are similar to those reported for enalaprilat, the active metabolite of the ACE inhibitor, enalapril maleate.	Enalaprilat	84-95	angiotensin I converting enzyme	Homo sapiens	126-129
2543535-7	1989	Serum enalaprilat concentration correlated (p less than 0.001) with the percentage of inhibition of ACE activity.	Enalaprilat	6-17	angiotensin I converting enzyme	Homo sapiens	100-103
2545578-4	1989	The IC50 values of MK-421 and MK-422 against ACE were 2,000 nM and 3.5 nM, respectively.	Enalaprilat	30-36	angiotensin I converting enzyme	Rattus norvegicus	45-48
2557432-10	1989	Enalaprilat (13 nmol min-1) inhibited converting enzyme in the infused arm, in which it caused approximately a 100-fold reduction in sensitivity to angiotensin I, while having no effect on the vasoconstriction caused by angiotensin II.	Enalaprilat	0-11	CD59 molecule (CD59 blood group)	Homo sapiens	21-26
2557432-10	1989	Enalaprilat (13 nmol min-1) inhibited converting enzyme in the infused arm, in which it caused approximately a 100-fold reduction in sensitivity to angiotensin I, while having no effect on the vasoconstriction caused by angiotensin II.	Enalaprilat	0-11	angiotensinogen	Homo sapiens	148-161
2557432-11	1989	Enalaprilat increased vasodilatation caused by bradykinin.	Enalaprilat	0-11	kininogen 1	Homo sapiens	47-57
2645758-3	1989	Because several ACE inhibitors, including captopril and enalaprilat, are eliminated by the kidneys, there are predictable age-related effects on pharmacokinetics.	Enalaprilat	56-67	angiotensin I converting enzyme	Homo sapiens	16-19
2474098-5	1989	Binding of [3H]ramiprilat was also inhibited by increasing concentrations of enalaprilat, another ACE inhibitor.	Enalaprilat	77-88	angiotensin I converting enzyme	Homo sapiens	98-101
2474161-2	1989	Intradermally evoked wheal and flare reactions to ovalbumin, capsaicin and bradykinin, in ovalbumin sensitized guinea pigs, was previously demonstrated to be enhanced by pretreatment with the ACE-inhibitor MK 422 (the active parent diacid of enalapril).	Enalaprilat	206-212	LOW QUALITY PROTEIN: angiotensin-converting enzyme	Cavia porcellus	192-195
2854218-2	1988	The competitive bradykinin B1-receptor antagonist, des-Arg9-Leu8-bradykinin antagonized venous responses to both bradykinin and enalaprilic acid effectively and with similar potency whereas the bradykinin B2-receptor antagonist Thi5,8,D-Phe7-bradykinin was about 100 times less potent when tested against bradykinin.	Enalaprilat	128-144	kininogen 1	Canis lupus familiaris	65-75
2852237-1	1988	Inhibition of the action of endothelially-located angiotensin converting enzyme (ACE) in blood vessels of the human forearm was studied using enalaprilat, the active metabolite of the prodrug enalapril.	Enalaprilat	142-153	angiotensin I converting enzyme	Homo sapiens	81-84
2852237-2	1988	In a dose of 5 micrograms/min enalaprilat inhibits arteriolar vasoconstriction in response to angiotensin I (Ang I) and enhances vasodilation in response to bradykinin.	Enalaprilat	30-41	angiotensinogen	Homo sapiens	94-107
2854218-2	1988	The competitive bradykinin B1-receptor antagonist, des-Arg9-Leu8-bradykinin antagonized venous responses to both bradykinin and enalaprilic acid effectively and with similar potency whereas the bradykinin B2-receptor antagonist Thi5,8,D-Phe7-bradykinin was about 100 times less potent when tested against bradykinin.	Enalaprilat	128-144	kininogen 1	Canis lupus familiaris	16-26
2854218-2	1988	The competitive bradykinin B1-receptor antagonist, des-Arg9-Leu8-bradykinin antagonized venous responses to both bradykinin and enalaprilic acid effectively and with similar potency whereas the bradykinin B2-receptor antagonist Thi5,8,D-Phe7-bradykinin was about 100 times less potent when tested against bradykinin.	Enalaprilat	128-144	kininogen 1	Canis lupus familiaris	65-75
2852237-2	1988	In a dose of 5 micrograms/min enalaprilat inhibits arteriolar vasoconstriction in response to angiotensin I (Ang I) and enhances vasodilation in response to bradykinin.	Enalaprilat	30-41	angiotensinogen	Homo sapiens	109-114
2852237-2	1988	In a dose of 5 micrograms/min enalaprilat inhibits arteriolar vasoconstriction in response to angiotensin I (Ang I) and enhances vasodilation in response to bradykinin.	Enalaprilat	30-41	kininogen 1	Homo sapiens	157-167
2854218-2	1988	The competitive bradykinin B1-receptor antagonist, des-Arg9-Leu8-bradykinin antagonized venous responses to both bradykinin and enalaprilic acid effectively and with similar potency whereas the bradykinin B2-receptor antagonist Thi5,8,D-Phe7-bradykinin was about 100 times less potent when tested against bradykinin.	Enalaprilat	128-144	kininogen 1	Canis lupus familiaris	65-75
2854218-2	1988	The competitive bradykinin B1-receptor antagonist, des-Arg9-Leu8-bradykinin antagonized venous responses to both bradykinin and enalaprilic acid effectively and with similar potency whereas the bradykinin B2-receptor antagonist Thi5,8,D-Phe7-bradykinin was about 100 times less potent when tested against bradykinin.	Enalaprilat	128-144	kininogen 1	Canis lupus familiaris	65-75
2854218-2	1988	The competitive bradykinin B1-receptor antagonist, des-Arg9-Leu8-bradykinin antagonized venous responses to both bradykinin and enalaprilic acid effectively and with similar potency whereas the bradykinin B2-receptor antagonist Thi5,8,D-Phe7-bradykinin was about 100 times less potent when tested against bradykinin.	Enalaprilat	128-144	kininogen 1	Canis lupus familiaris	65-75
2854218-9	1988	In contrast, venous responses to enalaprilic acid were unchanged by thromboxane A2 receptor blockade and enhanced after dazoxiben.	Enalaprilat	33-49	thromboxane A2 receptor	Canis lupus familiaris	68-91
2851680-2	1988	Its active form, CS-622 diacid, was slightly more potent than enalaprilat in inhibiting ACE isolated from rabbit lung.	Enalaprilat	62-73	angiotensin-converting enzyme	Oryctolagus cuniculus	88-91
2831145-5	1988	In the presence of MK 422 (50 microM), Ang-(1-7) was still generated, while the production of Ang-(1-8) was inhibited.	Enalaprilat	19-25	angiopoietin 1	Canis lupus familiaris	39-47
2843688-1	1988	The effectiveness of 2 angiotensin converting enzyme inhibitors, intravenous enalaprilat and oral captopril, in stimulating renin secretion was compared in 47 hypertensive patients with suspected renovascular hypertension.	Enalaprilat	77-88	renin	Homo sapiens	124-129
2843688-9	1988	Plasma renin activity increased by 5 and 15 minutes with enalaprilat and captopril, respectively.	Enalaprilat	57-68	renin	Homo sapiens	7-12
3412207-5	1988	Thus it is hypothesized that treatment of both MS and AIDS patients with a synthetic polymer containing the amino acids EAL might eliminate the antibodies to vasopressin-neurophysin and thus alleviate some of the clinical symptoms.	Enalaprilat	120-123	arginine vasopressin	Rattus norvegicus	158-169
2834938-0	1988	Unrelated responses of brachial artery hemodynamics and renin-angiotensin system to acute converting enzyme inhibition by enalaprilat in essential hypertension.	Enalaprilat	122-133	renin	Homo sapiens	56-61
2834938-1	1988	The simultaneous acute effects of converting enzyme inhibition by intravenous enalaprilat on the circulating renin-angiotensin system and on the brachial artery were studied in 12 hypertensive patients by a double-blind comparison with saline effects in 14 hypertensive patients.	Enalaprilat	78-89	renin	Homo sapiens	109-114
2834938-4	1988	Compared with the saline vehicle, enalaprilat significantly decreased angiotensin enzyme converting activity (p less than 0.001), increased plasma renin activity (p less than 0.01) and decreased plasma aldosterone concentrations (p less than 0.01).	Enalaprilat	34-45	renin	Homo sapiens	147-152
2827913-3	1988	To minimize peripheral effects, a bilateral intracoronary infusion of enalaprilat (0.05 mg.min-1, 1 ml.min-1 in each coronary artery) was performed in 16 patients with dilated cardiomyopathy.	Enalaprilat	70-81	CD59 molecule (CD59 blood group)	Homo sapiens	91-96
2827913-3	1988	To minimize peripheral effects, a bilateral intracoronary infusion of enalaprilat (0.05 mg.min-1, 1 ml.min-1 in each coronary artery) was performed in 16 patients with dilated cardiomyopathy.	Enalaprilat	70-81	CD59 molecule (CD59 blood group)	Homo sapiens	103-108
3416869-4	1988	The data indicate that the C-2 hydroxyl group of galactose is involved in weak interactions as a hydrogen-bond acceptor with uncharged groups of EIL and EAL.	Enalaprilat	153-156	complement C2	Homo sapiens	27-30
2831145-5	1988	In the presence of MK 422 (50 microM), Ang-(1-7) was still generated, while the production of Ang-(1-8) was inhibited.	Enalaprilat	19-25	angiopoietin 1	Canis lupus familiaris	94-102
2831146-7	1988	Similarly, topical application of MK 422 prevented the pressor effect of Ang I.	Enalaprilat	34-40	angiotensinogen	Homo sapiens	73-78
2833190-14	1987	The data illustrate that the ACE inhibitors spiraprilic and enalaprilic acids not only lower blood pressure but also enhance large artery compliance.	Enalaprilat	60-77	angiotensin I converting enzyme	Canis lupus familiaris	29-32
2468049-6	1988	Serum enalaprilat concentration correlated significantly (p less than 0.001) with percentage of inhibition of ACE activity.	Enalaprilat	6-17	angiotensin I converting enzyme	Homo sapiens	110-113
2466391-4	1988	In this thesis the ACE-inhibitor MK 422 (active parent diacid of enalapril) was demonstrated to potentiate wheal and flare reactions induced by allergens, bradykinin or capsaicin, and to increase infiltration of "inflammatory cells", like eosinophils and neutrophils, into inflammatory dermal test sites in sensitized guinea pigs.	Enalaprilat	33-39	LOW QUALITY PROTEIN: angiotensin-converting enzyme	Cavia porcellus	19-22
2821209-6	1987	Enalaprilat or captopril administered to rats caused a decrease in mean arterial blood pressure that lasted for over 24 h. In mesenteric preparations taken from animals 24 h after treatment with ACE inhibitors, kininase activity was inhibited whereas converting activity was unchanged.	Enalaprilat	0-11	angiotensin I converting enzyme	Rattus norvegicus	195-198
2822902-5	1987	Finally, the effect of pH in the perfusing solution on ACE inhibition by enalaprilat was studied.	Enalaprilat	73-84	angiotensin I converting enzyme	Rattus norvegicus	55-58
3027262-5	1987	Enzyme activity was inhibited by classical angiotensin converting enzyme inhibitors, including captopril, enalaprilat (MK422), and lisinopril (MK521).	Enalaprilat	106-117	angiotensin-converting enzyme	Sus scrofa	43-72
3036166-2	1987	125I MK351A, a tyrosyl derivative of enalaprilic acid, and a potent ACE inhibitor, bound in a concentration and time dependent manner to ACE.	Enalaprilat	37-53	angiotensin I converting enzyme	Homo sapiens	137-140
24233338-6	1987	Captopril (1 x 10(-6) M) and MK-422 (1 x 10(-6) M) blocked trout gill ACE activity, however, EDTA was inhibitory only at high concentrations (1 x 10(-3) M).	Enalaprilat	29-35	angiotensin I converting enzyme	Homo sapiens	70-73
3315334-11	1987	Replacement with AIII did not correct the hypotension but completely reversed the renal and renin responses to enalaprilat and restored GT balance without affecting FF.	Enalaprilat	111-122	renin	Rattus norvegicus	92-97
2437401-0	1987	Dilation of epicardial arteries in conscious dogs induced by angiotensin-converting enzyme inhibition with enalaprilat.	Enalaprilat	107-118	angiotensin I converting enzyme	Canis lupus familiaris	61-90
2437401-2	1987	Therefore, we analyzed in conscious dogs the effect of angiotensin-converting enzyme (ACE) inhibition by enalaprilat on parameters potentially important to provocation of myocardial ischemia, such as sympathetic activity, myocardial oxygen consumption, and vascular tone in coronary conduit and resistance vessels.	Enalaprilat	105-116	angiotensin I converting enzyme	Canis lupus familiaris	55-84
2437401-2	1987	Therefore, we analyzed in conscious dogs the effect of angiotensin-converting enzyme (ACE) inhibition by enalaprilat on parameters potentially important to provocation of myocardial ischemia, such as sympathetic activity, myocardial oxygen consumption, and vascular tone in coronary conduit and resistance vessels.	Enalaprilat	105-116	angiotensin I converting enzyme	Canis lupus familiaris	86-89
3027262-5	1987	Enzyme activity was inhibited by classical angiotensin converting enzyme inhibitors, including captopril, enalaprilat (MK422), and lisinopril (MK521).	Enalaprilat	119-124	angiotensin-converting enzyme	Sus scrofa	43-72
2455152-1	1987	The acute blood pressure response to an angiotensin converting enzyme inhibitor (enalaprilat) was compared in patients with uncomplicated essential hypertension with that obtained under similar conditions with a calcium entry blocker (nifedipine).	Enalaprilat	81-92	angiotensin I converting enzyme	Homo sapiens	40-69
3029438-3	1987	Renin-angiotensin system blockade with the converting enzyme inhibitor, MK422, resulted in restoration of baseline renal blood flow and glomerular filtration 30 minutes after cross-clamp release.	Enalaprilat	72-77	renin	Canis lupus familiaris	0-5
3033782-1	1987	Anesthetized dogs in acute left ventricular failure were treated with the ACE-inhibitor enalaprilat (MK-422).	Enalaprilat	88-99	angiotensin I converting enzyme	Canis lupus familiaris	74-77
3503919-7	1987	Other ACE inhibitors such as captopril (0.1%) and enalaprilic acid (0.01%) also reduced IOP by 4.0 +/- 0.4 and 4.7 +/- 0.4 mmHg, respectively.	Enalaprilat	50-66	angiotensin-converting enzyme	Oryctolagus cuniculus	6-9
3033782-1	1987	Anesthetized dogs in acute left ventricular failure were treated with the ACE-inhibitor enalaprilat (MK-422).	Enalaprilat	101-107	angiotensin I converting enzyme	Canis lupus familiaris	74-77
3021948-7	1986	The bullfrog renal HHL hydrolyzing activity was completely inhibited by typical ACE inhibitors, ethylenediamine tetraacetic acid (10(-3) M), captopril (10(-5) M), SA-466 (10(-5) M) and MK-422 (10(-6) M).	Enalaprilat	185-191	angiotensin I converting enzyme	Homo sapiens	80-83
3029219-1	1986	Angiotensin converting enzyme (ACE) was measured in rat plasma and tissues by analysis of the binding of the radio-inhibitor 125I-MK351A, a tyrosyl derivative of enalaprilic acid.	Enalaprilat	162-178	angiotensin I converting enzyme	Rattus norvegicus	0-29
3029219-1	1986	Angiotensin converting enzyme (ACE) was measured in rat plasma and tissues by analysis of the binding of the radio-inhibitor 125I-MK351A, a tyrosyl derivative of enalaprilic acid.	Enalaprilat	162-178	angiotensin I converting enzyme	Rattus norvegicus	31-34
3020993-10	1986	The effect of ANG I on absorption could be prevented by prior treatment of the animals with the converting enzyme inhibitor MK 422.	Enalaprilat	124-130	angiogenin	Rattus norvegicus	14-17
3023555-6	1986	Intravenous enalaprilat stimulated plasma renin activity and decreased immunoreactive plasma angiotensin II and plasma aldosterone concentrations.	Enalaprilat	12-23	renin	Homo sapiens	42-47
3023555-6	1986	Intravenous enalaprilat stimulated plasma renin activity and decreased immunoreactive plasma angiotensin II and plasma aldosterone concentrations.	Enalaprilat	12-23	angiotensinogen	Homo sapiens	93-107
3011046-0	1986	Age and the pharmacokinetics of angiotensin converting enzyme inhibitors enalapril and enalaprilat.	Enalaprilat	87-98	angiotensin I converting enzyme	Homo sapiens	32-61
3017276-1	1986	MK351A, a tyrosyl analogue of enalaprilic acid (MK422) is a potent inhibitor of angiotensin-converting enzyme (ACE).	Enalaprilat	30-46	angiotensin I converting enzyme	Homo sapiens	80-109
3017276-1	1986	MK351A, a tyrosyl analogue of enalaprilic acid (MK422) is a potent inhibitor of angiotensin-converting enzyme (ACE).	Enalaprilat	30-46	angiotensin I converting enzyme	Homo sapiens	111-114
3017276-1	1986	MK351A, a tyrosyl analogue of enalaprilic acid (MK422) is a potent inhibitor of angiotensin-converting enzyme (ACE).	Enalaprilat	48-53	angiotensin I converting enzyme	Homo sapiens	80-109
3017276-1	1986	MK351A, a tyrosyl analogue of enalaprilic acid (MK422) is a potent inhibitor of angiotensin-converting enzyme (ACE).	Enalaprilat	48-53	angiotensin I converting enzyme	Homo sapiens	111-114
3011047-0	1986	Age and the pharmacodynamics of angiotensin converting enzyme inhibitors enalapril and enalaprilat.	Enalaprilat	87-98	angiotensin I converting enzyme	Homo sapiens	32-61
3005777-15	1986	The resumption of normal renal cortical blood flow after the administration of the converting enzyme inhibitor MK422 suggests that elevated plasma renin activity may contribute to renal dysfunction after thoracic aortic occlusion.	Enalaprilat	111-116	renin	Canis lupus familiaris	147-152
3005569-2	1986	In this study the alanylproline portion of the potent ACE inhibitor enalaprilat (2) is replaced by a series of monocyclic lactams containing the required recognition and binding elements.	Enalaprilat	68-79	angiotensin I converting enzyme	Homo sapiens	54-57
3028059-1	1986	Heretofore, carboxyalkyl peptide inhibitors of kininase II (e.g. N-[1-carboxy-3-phenylpropyl]-Ala-Pro, "enalaprilic acid") have been synthesized by means that yield racemic product.	Enalaprilat	104-120	angiotensin I converting enzyme	Homo sapiens	47-58
3005826-8	1986	The affinity of ACE for both [3H] captopril and enalaprilat is greater at 37 degrees than at 0 degree, demonstrating that these interactions are entropically driven, perhaps by an isomerization of the enzyme molecule.	Enalaprilat	48-59	angiotensin I converting enzyme	Rattus norvegicus	16-19
2438497-16	1986	With MK422 i.v.t., there was a decrease in brain ANG II.	Enalaprilat	5-10	angiotensinogen	Rattus norvegicus	49-55
2422495-3	1986	Enalapril (MK-421) is an esterified prodrug, which in man is converted by the liver to the bioactive potent ACE inhibitor enalaprilate (enalaprilic acid, MK-422).	Enalaprilat	122-134	angiotensin I converting enzyme	Homo sapiens	108-111
2422495-3	1986	Enalapril (MK-421) is an esterified prodrug, which in man is converted by the liver to the bioactive potent ACE inhibitor enalaprilate (enalaprilic acid, MK-422).	Enalaprilat	136-152	angiotensin I converting enzyme	Homo sapiens	108-111
2422495-3	1986	Enalapril (MK-421) is an esterified prodrug, which in man is converted by the liver to the bioactive potent ACE inhibitor enalaprilate (enalaprilic acid, MK-422).	Enalaprilat	154-160	angiotensin I converting enzyme	Homo sapiens	108-111
2996575-7	1985	Plasma concentrations of the active drug, enalaprilate, were dose related and log enalaprilate correlated significantly with percentage of plasma angiotensin converting enzyme activity (r = -0.66).	Enalaprilat	42-54	angiotensin I converting enzyme	Homo sapiens	146-175
3001497-4	1985	The angiotensin-converting enzyme (ACE) inhibitors, MK-422 and captopril, potently inhibited the formation of YGGFM and RF with IC50 values of 8 nM and 95 nM, respectively.	Enalaprilat	52-58	angiotensin I converting enzyme (peptidyl-dipeptidase A) 1	Mus musculus	35-38
3001497-7	1985	However, when subanalgesic doses of inhibitors were co-administered with a subanalgesic dose of YGGFMRF, only the ACE inhibitors, MK-422 and captopril, potentiated the analgesic response of the peptide.	Enalaprilat	130-136	angiotensin I converting enzyme (peptidyl-dipeptidase A) 1	Mus musculus	114-117
3005681-0	1985	Pharmacological comparison of captopril and MK-422 by a new method for measuring activity of angiotensin converting enzyme (ACE).	Enalaprilat	44-50	angiotensin-converting enzyme	Sus scrofa	93-122
3005681-0	1985	Pharmacological comparison of captopril and MK-422 by a new method for measuring activity of angiotensin converting enzyme (ACE).	Enalaprilat	44-50	angiotensin-converting enzyme	Sus scrofa	124-127
3005681-5	1985	In the in vitro system (cultured aortic endothelial cells), the ACE inhibitory activities of the two drugs were compared in terms of the 50%-inhibition point on the dose response curve, and it was found that MK-422 was about 100 times more potent than captopril.	Enalaprilat	208-214	angiotensin-converting enzyme	Sus scrofa	64-67
2998676-1	1985	Enalapril maleate (MK-421), a nonmercapto-containing angiotensin converting enzyme (ACE) inhibitor, is converted in vivo to enalaprilat (MK-422), the active diacid.	Enalaprilat	124-135	angiotensin I converting enzyme	Homo sapiens	53-82
2998676-1	1985	Enalapril maleate (MK-421), a nonmercapto-containing angiotensin converting enzyme (ACE) inhibitor, is converted in vivo to enalaprilat (MK-422), the active diacid.	Enalaprilat	124-135	angiotensin I converting enzyme	Homo sapiens	84-87
2998676-1	1985	Enalapril maleate (MK-421), a nonmercapto-containing angiotensin converting enzyme (ACE) inhibitor, is converted in vivo to enalaprilat (MK-422), the active diacid.	Enalaprilat	137-143	angiotensin I converting enzyme	Homo sapiens	53-82
2998676-1	1985	Enalapril maleate (MK-421), a nonmercapto-containing angiotensin converting enzyme (ACE) inhibitor, is converted in vivo to enalaprilat (MK-422), the active diacid.	Enalaprilat	137-143	angiotensin I converting enzyme	Homo sapiens	84-87
2996575-7	1985	Plasma concentrations of the active drug, enalaprilate, were dose related and log enalaprilate correlated significantly with percentage of plasma angiotensin converting enzyme activity (r = -0.66).	Enalaprilat	82-94	angiotensin I converting enzyme	Homo sapiens	146-175
3012004-7	1985	All the renal effects of MK 422 could be reversed by infusion with angiotensin II.	Enalaprilat	25-31	angiotensinogen	Homo sapiens	67-81
2992838-0	1985	Comparative systemic and renal effects of dopamine and angiotensin-converting enzyme inhibition with enalaprilat in patients with heart failure.	Enalaprilat	101-112	angiotensin I converting enzyme	Homo sapiens	55-84
2989171-6	1985	Administration of the vasopressin antagonist after enalaprilat further reduced blood pressure only in Long-Evans rats.	Enalaprilat	51-62	arginine vasopressin	Rattus norvegicus	22-33
2410713-2	1985	Intrarenal ACE inhibition was achieved by infusing the potent ACE inhibitor MK-422 into the renal artery in a dose (0.32 micrograms/kg/min) that in dogs fed a normal sodium (n = 11) and low sodium (n = 10) diet markedly attenuated the renal blood flow response to intrarenal arterial angiotensin I (0.4 and 0.8 micrograms, respectively).	Enalaprilat	76-82	angiotensin I converting enzyme	Canis lupus familiaris	11-14
2989171-9	1985	Plasma angiotensin II levels were increased by the vasopressin antagonist and decreased by enalaprilat.	Enalaprilat	91-102	angiotensinogen	Rattus norvegicus	7-21
2410713-2	1985	Intrarenal ACE inhibition was achieved by infusing the potent ACE inhibitor MK-422 into the renal artery in a dose (0.32 micrograms/kg/min) that in dogs fed a normal sodium (n = 11) and low sodium (n = 10) diet markedly attenuated the renal blood flow response to intrarenal arterial angiotensin I (0.4 and 0.8 micrograms, respectively).	Enalaprilat	76-82	angiotensin I converting enzyme	Canis lupus familiaris	62-65
2987127-7	1985	Infusion of a maximally effective dose of a statine-containing renin inhibitor (SCRIP) with the high dose of enalaprilat produced no further fall in blood pressure (68 +/- 7 mm Hg), but immunoreactive angiotensin II levels fell to essentially zero in four of five dogs.	Enalaprilat	109-120	renin	Canis lupus familiaris	63-68
2410713-5	1985	This dose of MK-422 maximally inhibited systemic ACE, as evidenced by the complete abolition of the renal blood flow response to intravenous angiotensin I; the responses were decreased by 95 and 96% in the normal and low sodium groups, respectively.	Enalaprilat	13-19	angiotensin I converting enzyme	Canis lupus familiaris	49-52
2983065-3	1985	Hydrolysis of BPAP (4.2 microM) was 64.1 +/- 3.3% at 37 degrees C and was significantly decreased (P less than .01) to 10.1 +/- 8.7% by the addition of the ACE inhibitor, MK422 (10(-6) M).	Enalaprilat	171-176	angiotensin-converting enzyme	Oryctolagus cuniculus	156-159
2982830-10	1985	The formation of YGG, YGGF, and YGGFM by synaptic membranes could be stimulated 3-fold by the addition of 30 mM NaCl and inhibited by MK-422, an ACE inhibitor, with an IC50 of 3 nM.	Enalaprilat	134-140	angiotensin I converting enzyme	Rattus norvegicus	145-148
2982541-2	1985	Enalapril is rapidly converted by ester hydrolysis to enalaprilat, a potent ACE inhibitor; enalapril itself is only a weak ACE inhibitor.	Enalaprilat	54-65	angiotensin I converting enzyme	Homo sapiens	76-79
2994984-1	1985	Enalapril, an orally-active, long-acting, nonsulphydryl angiotensin-converting enzyme (ACE) inhibitor, is extensively hydrolysed in vivo to enalaprilat, its bioactive form.	Enalaprilat	140-151	angiotensin I converting enzyme	Homo sapiens	56-85
2994984-1	1985	Enalapril, an orally-active, long-acting, nonsulphydryl angiotensin-converting enzyme (ACE) inhibitor, is extensively hydrolysed in vivo to enalaprilat, its bioactive form.	Enalaprilat	140-151	angiotensin I converting enzyme	Homo sapiens	87-90
2994984-5	1985	Peak serum enalaprilat concentrations are reached 4 hours post-dose, and the profile is polyphasic with a prolonged terminal half-life (greater than 30 hours) due to the binding of enalaprilat to ACE.	Enalaprilat	181-192	angiotensin I converting enzyme	Homo sapiens	196-199
6100874-1	1984	Enalapril is administered as the ethyl ester of the potent angiotensin converting enzyme (ACE) inhibitor enalaprilat.	Enalaprilat	105-116	angiotensin I converting enzyme	Homo sapiens	59-88
3005181-1	1985	The di-acid metabolite of enalapril, enalaprilat, and its lysine analogue lisinopril are potent inhibitors of angiotensin converting enzyme (ACE); they do not contain sulphydryl groups.	Enalaprilat	37-48	angiotensin I converting enzyme	Homo sapiens	110-139
3005181-1	1985	The di-acid metabolite of enalapril, enalaprilat, and its lysine analogue lisinopril are potent inhibitors of angiotensin converting enzyme (ACE); they do not contain sulphydryl groups.	Enalaprilat	37-48	angiotensin I converting enzyme	Homo sapiens	141-144
6094795-6	1984	Moreover, enalaprilic acid blunted the marked rise in plasma cathepsin D (P less than .01) and myocardial depressant factor activities (P less than .01), and plasma amino-nitrogen concentrations (P less than .05) observed in the untreated hemorrhaged cats.	Enalaprilat	10-26	cathepsin D	Felis catus	61-72
6100756-15	1984	In conclusion, both captopril and MK-422 prevent the development of hypertension in SHR, presumably by blocking angiotensin-converting enzyme, suggesting that the brain renin-angiotensin system contributes to the pathogenesis of hypertension in that model.	Enalaprilat	34-40	renin	Rattus norvegicus	169-174
6100874-1	1984	Enalapril is administered as the ethyl ester of the potent angiotensin converting enzyme (ACE) inhibitor enalaprilat.	Enalaprilat	105-116	angiotensin I converting enzyme	Homo sapiens	90-93
6150096-1	1984	A simple in-vitro enzyme system has been used to demonstrate that human angiotensin I interacts competitively with the two non-thiol converting enzyme inhibitors CGS 13934 and MK-422 to inhibit the hydrolysis of a synthetic substrate by human plasma ACE.	Enalaprilat	176-182	angiotensinogen	Homo sapiens	72-85
6150096-0	1984	Human angiotensin I competes with two non-thiol converting enzyme inhibitors (CGS 13934 & MK-422) to inhibit the angiotensin-converting enzyme activity of human plasma.	Enalaprilat	94-100	angiotensinogen	Homo sapiens	6-19
6150096-1	1984	A simple in-vitro enzyme system has been used to demonstrate that human angiotensin I interacts competitively with the two non-thiol converting enzyme inhibitors CGS 13934 and MK-422 to inhibit the hydrolysis of a synthetic substrate by human plasma ACE.	Enalaprilat	176-182	angiotensin I converting enzyme	Homo sapiens	250-253
6320208-5	1984	Enalaprilic acid at 0.5 to 1.0 microgram/ml also blocked the angiotensin II response by 94 +/- 5%.	Enalaprilat	0-16	angiotensinogen	Homo sapiens	61-75
6097377-6	1984	Increasing serum MK422 was correlated with reducing serum ACE activity (P less than 0.001, r = 0.8, n = 104).	Enalaprilat	17-22	angiotensin I converting enzyme	Homo sapiens	58-61
6097377-9	1984	ID50 for serum ACE was 32 ng MK422/ml following the single 10 mg dose of MK421 and 70 ng MK422/ml during chronic treatment.	Enalaprilat	29-34	angiotensin I converting enzyme	Homo sapiens	15-18
6097377-9	1984	ID50 for serum ACE was 32 ng MK422/ml following the single 10 mg dose of MK421 and 70 ng MK422/ml during chronic treatment.	Enalaprilat	89-94	angiotensin I converting enzyme	Homo sapiens	15-18
6099390-4	1984	Serum angiotensin-converting enzyme (ACE) activity was inhibited maximally at 4 h (by 57 +/- 4% of control activity) and had a similar time course to the serum MK-422 level.	Enalaprilat	160-166	angiotensin I converting enzyme	Homo sapiens	6-35
6099390-4	1984	Serum angiotensin-converting enzyme (ACE) activity was inhibited maximally at 4 h (by 57 +/- 4% of control activity) and had a similar time course to the serum MK-422 level.	Enalaprilat	160-166	angiotensin I converting enzyme	Homo sapiens	37-40
6199659-4	1984	This hydrolysis is inhibited by the angiotensin-converting enzyme inhibitors captopril, MK-422, and EDTA, and is dependent on the concentration of chloride ion.	Enalaprilat	88-94	angiotensin-converting enzyme	Oryctolagus cuniculus	36-65
6099738-3	1984	During long-term administration of enalapril, a similar relationship between the plasma enalaprilic acid level, ACE inhibition and the hypotensive effect was shown, although the dose-response curve for plasma enalaprilic acid to ACE inhibition was displaced to the right compared to the acute dose-response curve.	Enalaprilat	209-225	angiotensin I converting enzyme	Homo sapiens	229-232
6326700-6	1984	Captopril and MK-421, and to a much lesser extent MK-422, inhibited the amidolysis of a fluorogenic synthetic substrate by human plasmin; the inhibition was ameliorated by increasing the substrate concentration.	Enalaprilat	50-56	plasminogen	Homo sapiens	129-136
6100610-1	1983	Enalapril, a long-acting, non-sulfhydryl, angiotensin converting enzyme (ACE) inhibitor, is well absorbed after oral administration, and hydrolised to its bioactive form, enalaprilic acid (EA).	Enalaprilat	171-187	angiotensin I converting enzyme	Homo sapiens	42-71
6199136-3	1984	After a single dose of enalapril (MK421), a new ACE inhibitor, in patients with essential hypertension a close linear relationship between the plasma level of enalaprilic acid (MK422) and the degree of ACE inhibition could be demonstrated.	Enalaprilat	159-175	angiotensin I converting enzyme	Homo sapiens	48-51
6199136-3	1984	After a single dose of enalapril (MK421), a new ACE inhibitor, in patients with essential hypertension a close linear relationship between the plasma level of enalaprilic acid (MK422) and the degree of ACE inhibition could be demonstrated.	Enalaprilat	159-175	angiotensin I converting enzyme	Homo sapiens	202-205
6199136-3	1984	After a single dose of enalapril (MK421), a new ACE inhibitor, in patients with essential hypertension a close linear relationship between the plasma level of enalaprilic acid (MK422) and the degree of ACE inhibition could be demonstrated.	Enalaprilat	177-182	angiotensin I converting enzyme	Homo sapiens	48-51
6199136-3	1984	After a single dose of enalapril (MK421), a new ACE inhibitor, in patients with essential hypertension a close linear relationship between the plasma level of enalaprilic acid (MK422) and the degree of ACE inhibition could be demonstrated.	Enalaprilat	177-182	angiotensin I converting enzyme	Homo sapiens	202-205
6199136-6	1984	As in the acute study there was also a linear relationship between the plasma level of MK422 and the degree of ACE inhibition.	Enalaprilat	87-92	angiotensin I converting enzyme	Homo sapiens	111-114
6199136-7	1984	However, the plasma enalaprilic acid level-ACE inhibition dose response curve after chronic administration was shifted to the right, compared to the dose response curve after acute administration suggesting that ACE had been induced during chronic administration of enalapril in humans.	Enalaprilat	20-36	angiotensin I converting enzyme	Homo sapiens	43-46
6199136-7	1984	However, the plasma enalaprilic acid level-ACE inhibition dose response curve after chronic administration was shifted to the right, compared to the dose response curve after acute administration suggesting that ACE had been induced during chronic administration of enalapril in humans.	Enalaprilat	20-36	angiotensin I converting enzyme	Homo sapiens	212-215
6199136-8	1984	There were direct linear relationships between both the degree of ACE inhibition the plasma and enalaprilic acid (MK422) level to the fall in mean arterial pressure.	Enalaprilat	96-112	angiotensin I converting enzyme	Homo sapiens	66-69
6199136-8	1984	There were direct linear relationships between both the degree of ACE inhibition the plasma and enalaprilic acid (MK422) level to the fall in mean arterial pressure.	Enalaprilat	114-119	angiotensin I converting enzyme	Homo sapiens	66-69
6100610-1	1983	Enalapril, a long-acting, non-sulfhydryl, angiotensin converting enzyme (ACE) inhibitor, is well absorbed after oral administration, and hydrolised to its bioactive form, enalaprilic acid (EA).	Enalaprilat	171-187	angiotensin I converting enzyme	Homo sapiens	73-76
6100611-2	1983	A close relationship between serum MK-422 levels and percentage ACE inhibition could be demonstrated and the acute fall in blood pressure showed a good correlation with either measurement.	Enalaprilat	35-41	angiotensin I converting enzyme	Homo sapiens	64-67
6100611-4	1983	As in the acute study, close relationships between the serum MK-422 level and ACE inhibition, and between either measurement and the fall in blood pressure, could be demonstrated after chronic enalapril administration.	Enalaprilat	61-67	angiotensin I converting enzyme	Homo sapiens	78-81
6124377-1	1982	N-[1-(S)-carboxy-3-phenylpropyl]-L-alanyl-L-proline (MK-422), is a potent angiotensin I-converting enzyme (ACE) inhibitor, but as a diacid is poorly absorbed in laboratory animals.	Enalaprilat	0-51	angiotensin I converting enzyme	Canis lupus familiaris	74-105
6175573-7	1982	We conclude that captopril and MK-421 diacid decreases vascular reactivity in the rat isolated kidney by a mechanism independent of ACE inhibition and unrelated to a prostaglandin-dependent vascular mechanism.	Enalaprilat	31-44	angiotensin I converting enzyme	Rattus norvegicus	132-135
6295819-2	1983	The parent diacid (MK-422) N-[(S)-1-carboxy-3-phenylpropyl]-L-Ala-L-Pro of MK-421 inhibited hog plasma ACE with an I50 of 1.2 nM.	Enalaprilat	19-25	angiotensin I converting enzyme	Rattus norvegicus	103-106
6295819-4	1983	However, both enalapril and MK-422 were potent inhibitors of ACE by the i.v.	Enalaprilat	28-34	angiotensin I converting enzyme	Rattus norvegicus	61-64
6124377-1	1982	N-[1-(S)-carboxy-3-phenylpropyl]-L-alanyl-L-proline (MK-422), is a potent angiotensin I-converting enzyme (ACE) inhibitor, but as a diacid is poorly absorbed in laboratory animals.	Enalaprilat	0-51	angiotensin I converting enzyme	Canis lupus familiaris	107-110
6124377-1	1982	N-[1-(S)-carboxy-3-phenylpropyl]-L-alanyl-L-proline (MK-422), is a potent angiotensin I-converting enzyme (ACE) inhibitor, but as a diacid is poorly absorbed in laboratory animals.	Enalaprilat	53-59	angiotensin I converting enzyme	Canis lupus familiaris	74-105
6124377-1	1982	N-[1-(S)-carboxy-3-phenylpropyl]-L-alanyl-L-proline (MK-422), is a potent angiotensin I-converting enzyme (ACE) inhibitor, but as a diacid is poorly absorbed in laboratory animals.	Enalaprilat	53-59	angiotensin I converting enzyme	Canis lupus familiaris	107-110
6124377-8	1982	A procedure was developed for the quantitation of MK-422 and enalapril in plasma and urine by their inhibition of purified ACE.	Enalaprilat	50-56	angiotensin I converting enzyme	Canis lupus familiaris	123-126
33520633-0	2021	In-silico drug repurposing study: Amprenavir, enalaprilat, and plerixafor, potential drugs for destabilizing the SARS-CoV-2 S-protein-angiotensin-converting enzyme 2 complex.	Enalaprilat	46-57	vitronectin	Homo sapiens	124-133
33520633-0	2021	In-silico drug repurposing study: Amprenavir, enalaprilat, and plerixafor, potential drugs for destabilizing the SARS-CoV-2 S-protein-angiotensin-converting enzyme 2 complex.	Enalaprilat	46-57	angiotensin converting enzyme 2	Homo sapiens	134-165
33520633-7	2021	Using umbrella sampling molecular dynamics simulations, the binding energy of SP with ACE2 (-29.58 kcal/mol) without ligands, and in complex with amprenavir (-20.13 kcal/mol), enalaprilat (-23.84 kcal/mol), and plerixafor (-19.72 kcal/mol) were calculated.	Enalaprilat	176-187	angiotensin converting enzyme 2	Homo sapiens	86-90
33218024-6	2020	Among them, enalaprilat, an ACE inhibitor, showed a Kd value of 1.5 nM against the ACE2.	Enalaprilat	12-23	angiotensin I converting enzyme	Homo sapiens	28-31
33270074-3	2020	In this case-control study, we investigated the relationship between EAL and genetic variants of the nonhomologous end-joining (XRCC6 rs5751129, XRCC4 rs6869366 and rs28360071), since they might affect DNA repair capacity, leading to KMT2A-r and leukemogenesis.	Enalaprilat	69-72	X-ray repair cross complementing 6	Homo sapiens	128-133
33218024-6	2020	Among them, enalaprilat, an ACE inhibitor, showed a Kd value of 1.5 nM against the ACE2.	Enalaprilat	12-23	angiotensin converting enzyme 2	Homo sapiens	83-87
33007874-8	2020	RESULTS: Uptake of enalaprilat into cells expressing OAT3 as well as OAT4 was significantly higher compared to control cells.	Enalaprilat	19-30	solute carrier family 22 member 8	Homo sapiens	53-57
33007874-9	2020	The enalaprilat affinity for OAT3 was 640 (95% CI: 520-770) microM.	Enalaprilat	4-15	solute carrier family 22 member 8	Homo sapiens	29-33
33007874-12	2020	CONCLUSION: The affinity of enalaprilat for OAT3 and OAT4 was notably low compared to other substrates.	Enalaprilat	28-39	solute carrier family 22 member 8	Homo sapiens	44-48
32766265-3	2020	The half-life of BK (100 nM) added to normal plasma was 34 s, a value that was increased ~12-fold when the angiotensin converting enzyme (ACE) inhibitor enalaprilat (130 nM) was added (enzyme immunoassay measurements).	Enalaprilat	153-164	kininogen 1	Homo sapiens	17-19
33007874-12	2020	CONCLUSION: The affinity of enalaprilat for OAT3 and OAT4 was notably low compared to other substrates.	Enalaprilat	28-39	solute carrier family 22 member 9	Homo sapiens	53-57
32494933-7	2020	These consistent changes were also observed by treating the H19-7 fetal hippocampal cell line with dexamethasone and were reversed by GR inhibitor (RU486) and ACE inhibitor (enalaprilat).	Enalaprilat	174-185	angiotensin I converting enzyme	Rattus norvegicus	159-162
32766265-3	2020	The half-life of BK (100 nM) added to normal plasma was 34 s, a value that was increased ~12-fold when the angiotensin converting enzyme (ACE) inhibitor enalaprilat (130 nM) was added (enzyme immunoassay measurements).	Enalaprilat	153-164	angiotensin I converting enzyme	Homo sapiens	107-136
32766265-3	2020	The half-life of BK (100 nM) added to normal plasma was 34 s, a value that was increased ~12-fold when the angiotensin converting enzyme (ACE) inhibitor enalaprilat (130 nM) was added (enzyme immunoassay measurements).	Enalaprilat	153-164	angiotensin I converting enzyme	Homo sapiens	138-141
25832562-3	2015	Enalapril, a carboxyl ester prodrug, is reported to be metabolized by human carboxylesterase-1 (CES1) but not by carboxylesterase-2 (CES2) to its active metabolite enalaprilat.	Enalaprilat	164-175	carboxylesterase 1	Homo sapiens	96-100
32547398-0	2020	Identification of Structural Features for the Inhibition of OAT3-Mediated Uptake of Enalaprilat by Selected Drugs and Flavonoids.	Enalaprilat	84-95	solute carrier family 22 member 8	Homo sapiens	60-64
32547398-4	2020	In the present study, OAT3-mediated uptake of enalaprilat was first characterized, and the inhibition of OAT3 transport activity was then examined for a number of flavonoid and drug molecules with diverse structures.	Enalaprilat	46-57	solute carrier family 22 member 8	Homo sapiens	22-26
32547398-6	2020	In addition, commonly used drugs such as urate transporter 1 (URAT1) inhibitors also displayed potent inhibition on OAT3-mediated enalaprilat uptake.	Enalaprilat	130-141	solute carrier family 22 member 12	Homo sapiens	41-60
32547398-6	2020	In addition, commonly used drugs such as urate transporter 1 (URAT1) inhibitors also displayed potent inhibition on OAT3-mediated enalaprilat uptake.	Enalaprilat	130-141	solute carrier family 22 member 12	Homo sapiens	62-67
32547398-6	2020	In addition, commonly used drugs such as urate transporter 1 (URAT1) inhibitors also displayed potent inhibition on OAT3-mediated enalaprilat uptake.	Enalaprilat	130-141	solute carrier family 22 member 8	Homo sapiens	116-120
32547398-10	2020	Taken together, the present study identified OAT3-mediated uptake of enalaprilat as an important mechanism for its renal clearance, which may be liable for drug-drug and herb-drug interactions.	Enalaprilat	69-80	solute carrier family 22 member 8	Homo sapiens	45-49
32547398-12	2020	The clinical relevance of the inhibition of OAT3-mediated enalaprilat uptake warrants further investigation, particularly in populations where herbal remedies and drugs are used concomitantly.	Enalaprilat	58-69	solute carrier family 22 member 8	Homo sapiens	44-48
30531841-9	2019	Enalaprilat decreased MAP more in RD BPH/2J compared to sham (-12 vs -3 mmHg, P < 0.001) but had no effect in BPN/3J.	Enalaprilat	0-11	GLI-Kruppel family member GLI3	Mus musculus	37-40
30113034-6	2018	Using a surface plasmon resonance biosensor and nuclear magnetic resonance spectroscopy, we have found that the ACE inhibitor enalaprilat effectively inhibits zinc-dependent dimerization of the metal-binding domains of intact Abeta and Abeta with isomerized Asp7 (isoAbeta).	Enalaprilat	126-137	angiotensin I converting enzyme	Homo sapiens	112-115
30113034-6	2018	Using a surface plasmon resonance biosensor and nuclear magnetic resonance spectroscopy, we have found that the ACE inhibitor enalaprilat effectively inhibits zinc-dependent dimerization of the metal-binding domains of intact Abeta and Abeta with isomerized Asp7 (isoAbeta).	Enalaprilat	126-137	amyloid beta precursor protein	Homo sapiens	226-231
30113034-6	2018	Using a surface plasmon resonance biosensor and nuclear magnetic resonance spectroscopy, we have found that the ACE inhibitor enalaprilat effectively inhibits zinc-dependent dimerization of the metal-binding domains of intact Abeta and Abeta with isomerized Asp7 (isoAbeta).	Enalaprilat	126-137	amyloid beta precursor protein	Homo sapiens	236-241
30113034-8	2018	The results confirm the role of zincdependent oligomerization of Abeta in AD pathogenesis and make it possible one to consider enalaprilat as a prototype of antiaggregation agents for treating AD.	Enalaprilat	127-138	amyloid beta precursor protein	Homo sapiens	65-70
26793104-8	2015	These effects were potentiated ~15-fold by the angiotensin converting enzyme (ACE) inhibitor, enalaprilat, but extensively inhibited by icatibant (a B2R antagonist) and not influenced by the Arg-carboxypeptidase (CP) inhibitor (Plummer"s inhibitor).	Enalaprilat	94-105	angiotensin I converting enzyme	Rattus norvegicus	47-76
26793104-8	2015	These effects were potentiated ~15-fold by the angiotensin converting enzyme (ACE) inhibitor, enalaprilat, but extensively inhibited by icatibant (a B2R antagonist) and not influenced by the Arg-carboxypeptidase (CP) inhibitor (Plummer"s inhibitor).	Enalaprilat	94-105	angiotensin I converting enzyme	Rattus norvegicus	78-81
25919042-4	2015	The amount of enalaprilat excreted into the urine was 35% smaller in subjects with the CES1 c.428G/A genotype than in those with the c.428G/G genotype (P = 0.044).	Enalaprilat	14-25	carboxylesterase 1	Homo sapiens	87-91
25919042-7	2015	CONCLUSIONS: The CES1 c.428G > A SNV decreased enalaprilat concentrations, probably by reducing the hydrolysis of enalapril, but had no observable effect on the pharmacokinetics of quinapril.	Enalaprilat	50-61	carboxylesterase 1	Homo sapiens	17-21
30782069-5	2019	VEGF stimulation significantly promoted cell proliferation and migration of HUVECs, knockdown of MIAT dramatically reversed the effects of VEGF, while cells co-transfected with miR-1246 inhibitor obviously abolished the effect of VEGF+si-MIAT, however, enalaprilat abolished the effects of VEGF+si-MIAT+miR-1246 inhibitor.	Enalaprilat	253-264	vascular endothelial growth factor A	Rattus norvegicus	0-4
30333824-6	2018	The angiotensin converting enzyme inhibitor enalaprilat, without any effect per se, increased immunoreactive BK (iBK) concentration under active stimulation of blood.	Enalaprilat	44-55	kininogen 1	Homo sapiens	109-111
28356668-4	2017	We report two pediatric cases of atypical HUS with severe refractory malignant hypertension, in which we targeted the renin-angiotensin system by using intravenous (IV) enalaprilat, oral aliskiren, and oral enalapril with quick and dramatic response of blood pressure.	Enalaprilat	169-180	renin	Homo sapiens	118-123
25663023-0	2015	Upregulation of SERCA2a following short-term ACE inhibition (by enalaprilat) alters contractile performance and arrhythmogenicity of healthy myocardium in rat.	Enalaprilat	64-75	angiotensin I converting enzyme	Rattus norvegicus	45-48
25772062-8	2015	The exposure of the cells to 0.5 mM enalapril and enalaprilat contributed to increase in IGF-IR and alpha2beta1 integrin receptor as well as TGF-beta1 and NF-kappaB p65 expressions.	Enalaprilat	50-61	insulin like growth factor 1 receptor	Homo sapiens	89-95
25772062-8	2015	The exposure of the cells to 0.5 mM enalapril and enalaprilat contributed to increase in IGF-IR and alpha2beta1 integrin receptor as well as TGF-beta1 and NF-kappaB p65 expressions.	Enalaprilat	50-61	transforming growth factor beta 1	Homo sapiens	141-150
25772062-8	2015	The exposure of the cells to 0.5 mM enalapril and enalaprilat contributed to increase in IGF-IR and alpha2beta1 integrin receptor as well as TGF-beta1 and NF-kappaB p65 expressions.	Enalaprilat	50-61	RELA proto-oncogene, NF-kB subunit	Homo sapiens	155-168
25772062-9	2015	Enalapril- and enalaprilat-dependent increase of collagen biosynthesis in fibroblasts results from increase of prolidase activity and expression, which may undergo through activation of alpha2beta1 integrin and IGF-IR signaling as well as upregulation of TGF-beta1 and NF-kappaB p65, the inhibitor of collagen gene expression.	Enalaprilat	15-26	peptidase D	Homo sapiens	111-120
25772062-9	2015	Enalapril- and enalaprilat-dependent increase of collagen biosynthesis in fibroblasts results from increase of prolidase activity and expression, which may undergo through activation of alpha2beta1 integrin and IGF-IR signaling as well as upregulation of TGF-beta1 and NF-kappaB p65, the inhibitor of collagen gene expression.	Enalaprilat	15-26	insulin like growth factor 1 receptor	Homo sapiens	211-217
25772062-9	2015	Enalapril- and enalaprilat-dependent increase of collagen biosynthesis in fibroblasts results from increase of prolidase activity and expression, which may undergo through activation of alpha2beta1 integrin and IGF-IR signaling as well as upregulation of TGF-beta1 and NF-kappaB p65, the inhibitor of collagen gene expression.	Enalaprilat	15-26	transforming growth factor beta 1	Homo sapiens	255-264
25772062-9	2015	Enalapril- and enalaprilat-dependent increase of collagen biosynthesis in fibroblasts results from increase of prolidase activity and expression, which may undergo through activation of alpha2beta1 integrin and IGF-IR signaling as well as upregulation of TGF-beta1 and NF-kappaB p65, the inhibitor of collagen gene expression.	Enalaprilat	15-26	RELA proto-oncogene, NF-kB subunit	Homo sapiens	269-282
24958844-0	2014	Role of multidrug resistance-associated protein 4 in the basolateral efflux of hepatically derived enalaprilat.	Enalaprilat	99-110	ATP binding cassette subfamily C member 4	Homo sapiens	8-49
24958844-6	2014	ATP-dependent uptake of enalaprilat into vesicles expressing multidrug resistance-associated protein (MRP) 4 was significantly greater (~3.8-fold) than in control vesicles.	Enalaprilat	24-35	ATP binding cassette subfamily C member 4	Homo sapiens	61-108
24958844-8	2014	The functional importance of MRP4 in the basolateral excretion of derived enalaprilat was evaluated using a novel basolateral efflux protocol developed in human sandwich-cultured hepatocytes.	Enalaprilat	74-85	ATP binding cassette subfamily C member 4	Homo sapiens	29-33
24958844-9	2014	Under normal culture conditions, the mean intrinsic basolateral efflux clearance (CLint ,basolateral) of enalaprilat was 0.026 +- 0.012 microl/min; enalaprilat CLint,basolateral was significantly reduced to 0.009 +- 0.009 microl/min by pretreatment with the pan-MRP inhibitor MK-571.	Enalaprilat	105-116	ATP binding cassette subfamily C member 1	Homo sapiens	262-265
24958844-10	2014	Results suggest that hepatically derived enalaprilat is excreted across the hepatic basolateral membrane by MRP4.	Enalaprilat	41-52	ATP binding cassette subfamily C member 4	Homo sapiens	108-112
23404365-4	2013	Enalapril and its metabolite enalaprilat are potent inhibitors of the angiotensin-converting-enzyme (ACE).	Enalaprilat	29-40	angiotensin I converting enzyme	Homo sapiens	70-99
25224238-18	2014	Enalaprilat treatment may attenuate lung injury by interventing local RAS in lung tissue with decreased ratio of ACE mRNA to ACE2 mRNA and lung AngII concentration.	Enalaprilat	0-11	angiotensin-converting enzyme	Oryctolagus cuniculus	113-116
25224238-18	2014	Enalaprilat treatment may attenuate lung injury by interventing local RAS in lung tissue with decreased ratio of ACE mRNA to ACE2 mRNA and lung AngII concentration.	Enalaprilat	0-11	angiotensin-converting enzyme 2	Oryctolagus cuniculus	125-129
24342267-0	2014	Chronic infusion of enalaprilat into hypothalamic paraventricular nucleus attenuates angiotensin II-induced hypertension and cardiac hypertrophy by restoring neurotransmitters and cytokines.	Enalaprilat	20-31	angiotensinogen	Rattus norvegicus	85-99
24342267-3	2014	Rats underwent subcutaneous infusions of ANG II or saline and bilateral PVN infusions of ACE inhibitor enalaprilat (ENL, 2.5mug/h) or vehicle for 4weeks.	Enalaprilat	103-114	angiotensin I converting enzyme	Rattus norvegicus	89-92
23834779-0	2013	Enalaprilat increases PPARbeta/delta expression, without influence on PPARalpha and PPARgamma, and modulate cardiac function in sub-acute model of daunorubicin-induced cardiomyopathy.	Enalaprilat	0-11	peroxisome proliferator-activated receptor delta	Rattus norvegicus	22-30
24583339-9	2014	The IOP-lowering effect of enalaprilat seems to be attributed to reduced angiotensin II type 1 receptor stimulation and modulation of MMP and cytokines activities.	Enalaprilat	27-38	angiotensin II receptor, type 1b	Rattus norvegicus	73-103
24516103-8	2014	Enalaprilat increased bradykinin-stimulated vasodilation and tissue plasminogen activator release; sitagliptin did not affect these responses to bradykinin.	Enalaprilat	0-11	kininogen 1	Homo sapiens	22-32
24516103-10	2014	In women, sitagliptin diminished tissue plasminogen activator release in response to substance P both alone and during enalaprilat.	Enalaprilat	119-130	tachykinin precursor 1	Homo sapiens	85-96
24639651-4	2014	Of three BK sequences extended by a C-terminal dipeptide, BK-His-Leu had the most desirable profile, exhibiting little direct affinity for the receptor but a significant one for ACE (as shown by competition of [(3)H]BK binding to B2R-GFP or of [(3)H]enalaprilat to recombinant ACE, respectively).	Enalaprilat	250-261	kininogen 1	Homo sapiens	58-60
24639651-4	2014	Of three BK sequences extended by a C-terminal dipeptide, BK-His-Leu had the most desirable profile, exhibiting little direct affinity for the receptor but a significant one for ACE (as shown by competition of [(3)H]BK binding to B2R-GFP or of [(3)H]enalaprilat to recombinant ACE, respectively).	Enalaprilat	250-261	kininogen 1	Homo sapiens	58-60
24639651-5	2014	The potency of the contractile effect of this analog on the vein was reduced 18-fold by the ACE inhibitor enalaprilat, pharmacologically evidencing BK regeneration in situ.	Enalaprilat	106-117	angiotensin I converting enzyme	Homo sapiens	92-95
24639651-5	2014	The potency of the contractile effect of this analog on the vein was reduced 18-fold by the ACE inhibitor enalaprilat, pharmacologically evidencing BK regeneration in situ.	Enalaprilat	106-117	kininogen 1	Homo sapiens	148-150
24639651-7	2014	B2R-GFP internalization in response to 100 nM of the extended peptides recapitulated these findings, as enalaprilat selectively inhibited the effect of BK-His-Leu and Plummer"s inhibitor, that of BK-Arg.	Enalaprilat	104-115	bradykinin receptor B2	Homo sapiens	0-3
24639651-7	2014	B2R-GFP internalization in response to 100 nM of the extended peptides recapitulated these findings, as enalaprilat selectively inhibited the effect of BK-His-Leu and Plummer"s inhibitor, that of BK-Arg.	Enalaprilat	104-115	kininogen 1	Homo sapiens	152-154
23949641-6	2013	The ACE-I enalaprilat was given transanally at a dose of 6.25 mg/kg for 21 days.	Enalaprilat	10-21	angiotensin I converting enzyme (peptidyl-dipeptidase A) 1	Mus musculus	4-7
23949641-10	2013	RESULTS: Enalaprilat exhibited better survival (91 %) versus other treatment groups (PSL: 85.7 %, PSL + ACE-I: 71.4 %, placebo: 66.6 %).	Enalaprilat	9-20	angiotensin I converting enzyme (peptidyl-dipeptidase A) 1	Mus musculus	104-107
23404365-4	2013	Enalapril and its metabolite enalaprilat are potent inhibitors of the angiotensin-converting-enzyme (ACE).	Enalaprilat	29-40	angiotensin I converting enzyme	Homo sapiens	101-104
20015194-12	2011	Angiotensin converting enzyme inhibitor enalaprilat also directly activated B1Rs to generate high output nitric oxide via the same pathway.	Enalaprilat	40-51	angiotensin I converting enzyme	Homo sapiens	0-29
23647543-2	2013	MD simulations and interaction energy calculations for docking and crystal structures were performed to investigate the correct conformation of the ACE with enalaprilat and nanopepetide.	Enalaprilat	157-168	angiotensin I converting enzyme	Homo sapiens	148-151
23903258-1	2013	Enalaprilat (H2L), which is the active metabolite of the pro-drug enalapril, is an angiotensin-converting enzyme inhibitor.	Enalaprilat	0-11	angiotensin I converting enzyme	Homo sapiens	83-112
21986309-2	2012	To identify cytokine-dependent or -independent mechanisms for the latter phenomenon, the ACE inhibitor enalaprilat and several peptides potentiated in vivo by ACE blockade were applied either directly to human umbilical artery smooth muscle cells (hUA-SMCs) or to differentiated monoblastoid U937 cells to produce a conditioned medium (CM) that was later transferred to hUA-SMCs.	Enalaprilat	103-114	angiotensin I converting enzyme	Homo sapiens	89-92
22542537-7	2012	PVAT attenuated the relaxation response to thiopental, and this attenuation effect was reduced by both angiotensin II (Ang II) type 1 receptor antagonists CV-11974 (2-n-butyl-4-choloro-5-hydroxymethyl-1-[2"-(1H-tetrazol-5-yl)biphenyl-methyl]-imidazole) or losartan and the angiotensin-converting enzyme inhibitor enalaprilat.	Enalaprilat	313-324	angiotensin II receptor, type 1b	Rattus norvegicus	103-142
21646245-0	2011	Acute effects of the ACE inhibitor enalaprilat on the pulmonary, cerebral and systemic blood flow and resistance after the bidirectional cavopulmonary connection.	Enalaprilat	35-46	angiotensin I converting enzyme	Homo sapiens	21-24
22395404-0	2012	Inhibitory effects of enalaprilat on rat cardiac fibroblast proliferation via ROS/P38MAPK/TGF-beta1 signaling pathway.	Enalaprilat	22-33	transforming growth factor, beta 1	Rattus norvegicus	90-99
22395404-5	2012	It could be concluded that enalaprilat can inhibit the cardiac fibroblast proliferation induced by Ang II via blocking ROS/P38MAPK/TGF-beta(1) signaling pathways and the study provides a theoretical proof for the application of ACEIs in treating myocardial fibrosis and discovering the primary mechanism through which ACEIs inhibit CFb proliferation.	Enalaprilat	27-38	angiotensinogen	Rattus norvegicus	99-105
22395404-5	2012	It could be concluded that enalaprilat can inhibit the cardiac fibroblast proliferation induced by Ang II via blocking ROS/P38MAPK/TGF-beta(1) signaling pathways and the study provides a theoretical proof for the application of ACEIs in treating myocardial fibrosis and discovering the primary mechanism through which ACEIs inhibit CFb proliferation.	Enalaprilat	27-38	transforming growth factor, beta 1	Rattus norvegicus	131-142
23166630-5	2012	The "short" ACE inhibitor enalaprilat (tripeptide analog) and "long" inhibitor teprotide (nonapeptide) produced strikingly different mAb 1G12 binding with enalaprilat strongly increasing mAb 1G12 binding and teprotide decreasing binding.	Enalaprilat	26-37	angiotensin I converting enzyme	Homo sapiens	12-15
23166630-5	2012	The "short" ACE inhibitor enalaprilat (tripeptide analog) and "long" inhibitor teprotide (nonapeptide) produced strikingly different mAb 1G12 binding with enalaprilat strongly increasing mAb 1G12 binding and teprotide decreasing binding.	Enalaprilat	155-166	angiotensin I converting enzyme	Homo sapiens	12-15
21864683-7	2011	Venous tissue treatment with the ACE inhibitor enalaprilat reduced the apparent potency of Met-Lys-BK-Ser-Ser by 15-fold, while not affecting that of BK.	Enalaprilat	47-58	angiotensin I converting enzyme	Homo sapiens	33-36
21864683-7	2011	Venous tissue treatment with the ACE inhibitor enalaprilat reduced the apparent potency of Met-Lys-BK-Ser-Ser by 15-fold, while not affecting that of BK.	Enalaprilat	47-58	kininogen 1	Homo sapiens	99-101
21795644-2	2011	Using cultured nephritic glomeruli from rats with anti-Thy-1-induced glomerulonephritis, the maximally effective dose of enalaprilate was determined to be 10(-4) M, which reduced mRNAs for transforming growth factor (TGF)-beta1, fibronectin (FN), and plasminogen activator inhibitor-1 (PAI-1) by 49, 65, and 56% and production of TGF-beta1 and FN proteins by 60 and 49%, respectively.	Enalaprilat	121-133	transforming growth factor, beta 1	Rattus norvegicus	189-227
21795644-2	2011	Using cultured nephritic glomeruli from rats with anti-Thy-1-induced glomerulonephritis, the maximally effective dose of enalaprilate was determined to be 10(-4) M, which reduced mRNAs for transforming growth factor (TGF)-beta1, fibronectin (FN), and plasminogen activator inhibitor-1 (PAI-1) by 49, 65, and 56% and production of TGF-beta1 and FN proteins by 60 and 49%, respectively.	Enalaprilat	121-133	fibronectin 1	Rattus norvegicus	229-240
21795644-2	2011	Using cultured nephritic glomeruli from rats with anti-Thy-1-induced glomerulonephritis, the maximally effective dose of enalaprilate was determined to be 10(-4) M, which reduced mRNAs for transforming growth factor (TGF)-beta1, fibronectin (FN), and plasminogen activator inhibitor-1 (PAI-1) by 49, 65, and 56% and production of TGF-beta1 and FN proteins by 60 and 49%, respectively.	Enalaprilat	121-133	fibronectin 1	Rattus norvegicus	242-244
21795644-2	2011	Using cultured nephritic glomeruli from rats with anti-Thy-1-induced glomerulonephritis, the maximally effective dose of enalaprilate was determined to be 10(-4) M, which reduced mRNAs for transforming growth factor (TGF)-beta1, fibronectin (FN), and plasminogen activator inhibitor-1 (PAI-1) by 49, 65, and 56% and production of TGF-beta1 and FN proteins by 60 and 49%, respectively.	Enalaprilat	121-133	serpin family E member 1	Rattus norvegicus	251-284
21795644-2	2011	Using cultured nephritic glomeruli from rats with anti-Thy-1-induced glomerulonephritis, the maximally effective dose of enalaprilate was determined to be 10(-4) M, which reduced mRNAs for transforming growth factor (TGF)-beta1, fibronectin (FN), and plasminogen activator inhibitor-1 (PAI-1) by 49, 65, and 56% and production of TGF-beta1 and FN proteins by 60 and 49%, respectively.	Enalaprilat	121-133	serpin family E member 1	Rattus norvegicus	286-291
21795644-2	2011	Using cultured nephritic glomeruli from rats with anti-Thy-1-induced glomerulonephritis, the maximally effective dose of enalaprilate was determined to be 10(-4) M, which reduced mRNAs for transforming growth factor (TGF)-beta1, fibronectin (FN), and plasminogen activator inhibitor-1 (PAI-1) by 49, 65, and 56% and production of TGF-beta1 and FN proteins by 60 and 49%, respectively.	Enalaprilat	121-133	transforming growth factor, beta 1	Rattus norvegicus	330-339
21795644-2	2011	Using cultured nephritic glomeruli from rats with anti-Thy-1-induced glomerulonephritis, the maximally effective dose of enalaprilate was determined to be 10(-4) M, which reduced mRNAs for transforming growth factor (TGF)-beta1, fibronectin (FN), and plasminogen activator inhibitor-1 (PAI-1) by 49, 65, and 56% and production of TGF-beta1 and FN proteins by 60 and 49%, respectively.	Enalaprilat	121-133	fibronectin 1	Rattus norvegicus	344-346
21795644-4	2011	In contrast, two- and threefold disease-induced increases in renin mRNA and activity were further increased 2- and 3.7-fold with 10(-4) M enalaprilate treatment.	Enalaprilat	138-150	renin	Homo sapiens	61-66
21795644-5	2011	Depressing the renin receptor by 80% with small interfering (si) RNA alone reduced fibrotic markers in a manner remarkably similar to enalaprilate alone but had no effect on glomerular renin expression.	Enalaprilat	134-146	renin	Homo sapiens	15-20
21665049-3	2011	OBJECTIVE: The purpose of this study was to investigate the functional significance of the OATP1B1 genetic polymorphism on the pharmacokinetics of enalapril and its active metabolite enalaprilat in healthy Chinese adult male participants.	Enalaprilat	183-194	solute carrier organic anion transporter family member 1B1	Homo sapiens	91-98
20637368-7	2010	Enalaprilat and valsartan partly lowered overproduction of TGF-beta1 mRNA and excreted protein of podocytes, whereas enalaprilat plus valsartan completely restored them to the level as control.	Enalaprilat	0-11	transforming growth factor beta 1	Homo sapiens	59-68
20452384-10	2010	The [(3)H]enalaprilat binding assay applied to HUVECs supports that ACE is a particularly active kininase and that endothelial ACE expression is dynamically and specifically regulated.	Enalaprilat	10-21	angiotensin I converting enzyme	Homo sapiens	68-71
20452384-10	2010	The [(3)H]enalaprilat binding assay applied to HUVECs supports that ACE is a particularly active kininase and that endothelial ACE expression is dynamically and specifically regulated.	Enalaprilat	10-21	angiotensin I converting enzyme	Homo sapiens	127-130
20156432-5	2010	In rat mesenteric arteries, treatment of the vessels with an ACE inhibitor (enalaprilat) or angiotensin II type 1 receptor antagonist (candesartan) reduced PVAT-mediated potentiation of EFS-induced contraction.	Enalaprilat	76-87	angiotensin I converting enzyme	Rattus norvegicus	61-64
18816584-5	2009	In this work, we attempted to elucidate the possible mode of interaction between the peptides and ACE, including mechanisms of binding to the cofactor Zn2+, and further contrast this with the known mode of inhibition exerted by synthetic drugs (Captopril, Enalaprilat and Lisinopril).	Enalaprilat	256-267	angiotensin I converting enzyme	Homo sapiens	98-101
20048199-3	2010	We investigated the hypothesis that the acute administration of drugs to inhibit reactive oxygen species (Tempol), angiotensin II type 1 receptors (candesartan), or angiotensin-converting enzyme (enalaprilat) lowers mean arterial pressure and increases kidney blood flow and oxygenation in the clipped kidney of chronic 2K,1C rats in contrast to sham controls.	Enalaprilat	196-207	angiotensin I converting enzyme	Rattus norvegicus	165-194
19481149-2	2009	Here we investigated RAS signaling in retinas explanted from adult rats exposed for 48 h to high glucose (HG), with or without the Angiotensin Converting Enzyme inhibitor enalaprilat, which blocks RAS.	Enalaprilat	171-182	angiotensin I converting enzyme	Rattus norvegicus	131-160
19481149-4	2009	In the presence of enalaprilat, tyrosine phosphorylation signal and AT(1)R upregulation decreased and activation of PLCgamma1 and CREB reverted, showing their relation to RAS signaling.	Enalaprilat	19-30	angiotensin II receptor, type 1a	Rattus norvegicus	68-74
19481149-4	2009	In the presence of enalaprilat, tyrosine phosphorylation signal and AT(1)R upregulation decreased and activation of PLCgamma1 and CREB reverted, showing their relation to RAS signaling.	Enalaprilat	19-30	phospholipase C, gamma 1	Rattus norvegicus	116-125
19481149-4	2009	In the presence of enalaprilat, tyrosine phosphorylation signal and AT(1)R upregulation decreased and activation of PLCgamma1 and CREB reverted, showing their relation to RAS signaling.	Enalaprilat	19-30	cAMP responsive element binding protein 1	Rattus norvegicus	130-134
19397686-7	2009	Enalaprilat or valsartan partly improved nephrin expression when compared with that by podocytes exposed to the mesangial medium (P<0.05), while the nephrin expression of podocytes with enalaprilat or valsartan was lower than that of podocytes exposed to medium of mesangial cells stimulated by aIgA1 from healthy control (P<0.05).	Enalaprilat	0-11	NPHS1 adhesion molecule, nephrin	Homo sapiens	41-48
19397686-7	2009	Enalaprilat or valsartan partly improved nephrin expression when compared with that by podocytes exposed to the mesangial medium (P<0.05), while the nephrin expression of podocytes with enalaprilat or valsartan was lower than that of podocytes exposed to medium of mesangial cells stimulated by aIgA1 from healthy control (P<0.05).	Enalaprilat	189-200	NPHS1 adhesion molecule, nephrin	Homo sapiens	152-159
18399693-1	2008	Studies that allow computing values of aqueous proton dissociation constants (pKa), gas phase proton affinities, and the free energy of solvation have been performed for six members of angiotensin-I-converting enzyme (ACE) inhibitor family (captopril, enalaprilat, imidaprilat, ramiprilat, perindoprilat, and spiraprilat).	Enalaprilat	252-263	angiotensin I converting enzyme	Homo sapiens	218-221
19088803-5	2008	Ten patients were given 50 microg x min-1 enalaprilat in an intracoronary infusion between the balloon inflations, whereas the others received an infusion of saline.	Enalaprilat	42-53	CD59 molecule (CD59 blood group)	Homo sapiens	36-41
18182236-5	2008	Kinin B1 and B2 receptors were detected by immunofluorescence and showed to be activated by BK and DesR9 BK, increasing the acidification rate which was enhanced in the presence of enalaprilat.	Enalaprilat	181-192	bradykinin receptor, beta 1	Mus musculus	0-8
18594743-3	2008	MATERIALS AND METHODS: We evaluated the effects of the angiotensin converting enzyme inhibitor, Enalaprilat, and the AT-1 receptor antagonist, Losartan, on mRNA fibronectin and laminin synthesis by glomerular epithelial cells, in conditions mimicking hyperglycemia.	Enalaprilat	96-107	fibronectin 1	Homo sapiens	161-172
18594743-4	2008	RESULTS: In high glucose conditions, Enalaprilat reduced significantly the mRNA expression of fibronectin (p 0.03), but not significantly that of laminin.	Enalaprilat	37-48	fibronectin 1	Homo sapiens	94-105
18329669-6	2008	The presence of angiotensin I-converting enzyme (ACE) inhibitor (50 nM enalaprilat) did not affect the WH-induced vasodilating effect, though WH showed a slight ACE inhibitory activity (IC50: 93 microM).	Enalaprilat	71-82	angiotensin I converting enzyme	Rattus norvegicus	49-52
18201802-4	2008	We used the tritiated form of an ACE inhibitor previously proposed to activate the B1R, enalaprilat, to address these questions using recombinant human B1Rs and naturally expressed or recombinant ACE.	Enalaprilat	88-99	angiotensin I converting enzyme	Homo sapiens	33-36
18201802-4	2008	We used the tritiated form of an ACE inhibitor previously proposed to activate the B1R, enalaprilat, to address these questions using recombinant human B1Rs and naturally expressed or recombinant ACE.	Enalaprilat	88-99	bradykinin receptor B1	Homo sapiens	83-86
18201802-6	2008	[3H]Enalaprilat (0.25-10 nM) did not bind to cells expressing recombinant human B1R, but bound with a subnanomolar affinity to recombinant ACE or to naturally expressed ACE in human umbilical vein endothelial cells.	Enalaprilat	4-15	angiotensin I converting enzyme	Homo sapiens	139-142
18201802-6	2008	[3H]Enalaprilat (0.25-10 nM) did not bind to cells expressing recombinant human B1R, but bound with a subnanomolar affinity to recombinant ACE or to naturally expressed ACE in human umbilical vein endothelial cells.	Enalaprilat	4-15	angiotensin I converting enzyme	Homo sapiens	169-172
18259028-7	2008	Enalaprilat significantly increased basal net t-PA antigen release (from -0.8+/-1.0 to 3.2+/-1.2 ng/min/100 mL, P=0.012), but not the release of active t-PA, during either placebo or 17beta-estradiol.	Enalaprilat	0-11	plasminogen activator, tissue type	Homo sapiens	46-50
18259028-8	2008	Enalaprilat potentiated bradykinin-stimulated vasodilation and t-PA antigen and activity release similarly during placebo and 17beta-estradiol treatment.	Enalaprilat	0-11	kininogen 1	Homo sapiens	24-34
18259028-8	2008	Enalaprilat potentiated bradykinin-stimulated vasodilation and t-PA antigen and activity release similarly during placebo and 17beta-estradiol treatment.	Enalaprilat	0-11	plasminogen activator, tissue type	Homo sapiens	63-67
18093879-8	2008	HgCl2 increased the angiotensin converting enzyme (ACE) activity explaining the result obtained with enalaprilate.	Enalaprilat	101-113	angiotensin I converting enzyme	Rattus norvegicus	20-49
18093879-8	2008	HgCl2 increased the angiotensin converting enzyme (ACE) activity explaining the result obtained with enalaprilate.	Enalaprilat	101-113	angiotensin I converting enzyme	Rattus norvegicus	51-54
18180402-6	2008	Enalaprilat enhanced the effect of bradykinin on forearm blood flow, forearm vascular resistance, and t-PA release (all P<0.001).	Enalaprilat	0-11	kininogen 1	Homo sapiens	35-45
18180402-6	2008	Enalaprilat enhanced the effect of bradykinin on forearm blood flow, forearm vascular resistance, and t-PA release (all P<0.001).	Enalaprilat	0-11	plasminogen activator, tissue type	Homo sapiens	102-106
17653597-3	2007	The use of enalaprilat inhibited the changes in urine output, blood pressure, serum concentration of urea, p0(2), and tissue activity of MPO and MDA in the pancreas and lungs.	Enalaprilat	11-22	myeloperoxidase	Rattus norvegicus	137-140
17716647-5	2007	The bradykinin/angiotensin I selectivity ratios calculated from double displacement experiments were: perindoprilat, 1.44; ramiprilat, 1.16; quinaprilat, 1.09; trandolaprilat, 1.08; enalaprilat, 1.00.	Enalaprilat	182-193	kininogen 1	Homo sapiens	4-14
17716647-5	2007	The bradykinin/angiotensin I selectivity ratios calculated from double displacement experiments were: perindoprilat, 1.44; ramiprilat, 1.16; quinaprilat, 1.09; trandolaprilat, 1.08; enalaprilat, 1.00.	Enalaprilat	182-193	angiotensinogen	Homo sapiens	15-28
15992826-6	2005	Parallel groups were treated with the ACE inhibitor Enalaprilat (200 mg/kg/day).	Enalaprilat	52-63	angiotensin I converting enzyme	Rattus norvegicus	38-41
17342403-4	2007	We hypothesized that ACE-I, using enalaprilat, would decrease colonic epithelial cell apoptosis and reduce colitis severity in the dextran sulfate sodium (DSS)-induced colitis model in mice.	Enalaprilat	34-45	angiotensin I converting enzyme (peptidyl-dipeptidase A) 1	Mus musculus	21-24
17241184-11	2007	CONCLUSION: Enalaprilat as adjunct to primary angioplasty might be a protective approach to prevent leucocyte adhesion and the release of ET-1, thereby improving coronary blood flow.	Enalaprilat	12-23	endothelin 1	Homo sapiens	138-142
16650303-8	2006	CONCLUSION: We have concluded that enalaprilat interferes in this alteration of permeability, suggesting that angiotensin II is involved in the loss of selectivity of the glomerular membrane.	Enalaprilat	35-46	angiotensinogen	Rattus norvegicus	110-124
16282523-4	2006	In cytokine-treated human lung microvascular endothelial cells, B1 receptor activation by ACE inhibitors (enalaprilat, quinaprilat) or peptide ligands (des-Arg10-Lys1-bradykinin, des-Arg9-bradykinin) inhibited PKC epsilon with an IC50 = 7 x 10(-9) M. Despite the reported differences in binding affinity to receptor, the two peptide ligands were equally active, even when inhibitor blocked the cleavage of Lys(1), thus the conversion by aminopeptidase.	Enalaprilat	106-117	angiotensin I converting enzyme	Homo sapiens	90-93
16282523-5	2006	The synthetic undecapeptide (LLPHEAWHFAR) representing the binding site for ACE inhibitors on human B(1) receptors reduced PKC epsilon inhibition by enalaprilat but not by peptide agonist.	Enalaprilat	149-160	angiotensin I converting enzyme	Homo sapiens	76-79
16282523-5	2006	The synthetic undecapeptide (LLPHEAWHFAR) representing the binding site for ACE inhibitors on human B(1) receptors reduced PKC epsilon inhibition by enalaprilat but not by peptide agonist.	Enalaprilat	149-160	protein kinase C epsilon	Homo sapiens	123-134
17523052-4	2007	This cleavage could be inhibited by EDTA and the ACE inhibitor, enalaprilat, the de-esterified acid derivative of enalapril.	Enalaprilat	64-75	angiotensin I converting enzyme	Rattus norvegicus	49-52
17218981-6	2006	The angiotensin-converting enzyme (ACE) inhibitor enalaprilat enhanced responses to BK and the BK analog HT-BK without altering responses to PA-BK and inhibited responses to Ang I.	Enalaprilat	50-61	angiotensin I converting enzyme	Rattus norvegicus	4-33
17218981-6	2006	The angiotensin-converting enzyme (ACE) inhibitor enalaprilat enhanced responses to BK and the BK analog HT-BK without altering responses to PA-BK and inhibited responses to Ang I.	Enalaprilat	50-61	angiotensin I converting enzyme	Rattus norvegicus	35-38
17218981-11	2006	These data suggest that ACE inhibitor-potentiated responses to BK are not mediated by an A-779-sensitive mechanism and are consistent with the hypothesis that enalaprilat-induced BK potentiation is due to decreased BK inactivation.	Enalaprilat	159-170	angiotensin I converting enzyme	Rattus norvegicus	24-27
17004021-0	2006	The effect of sublingual captopril versus intravenous enalaprilat on angiotensin II plasma levels.	Enalaprilat	54-65	angiotensinogen	Homo sapiens	69-83
15992826-10	2005	Concurrent treatment with Enalaprilat reversed the hypertension induced by ANG II infusion (98 +/- 3 versus 155 +/- 4 mmHg; P < 0.001).	Enalaprilat	26-37	angiotensinogen	Rattus norvegicus	75-81
15992826-12	2005	Enalaprilat significantly decreased renal ACE activity in ANG II-treated rats, compared to ANG II alone (11.4 +/- 1.0 versus 59.2 +/- 11.9 units/mg protein; P < 0.001).	Enalaprilat	0-11	angiotensin I converting enzyme	Rattus norvegicus	42-45
15992826-12	2005	Enalaprilat significantly decreased renal ACE activity in ANG II-treated rats, compared to ANG II alone (11.4 +/- 1.0 versus 59.2 +/- 11.9 units/mg protein; P < 0.001).	Enalaprilat	0-11	angiotensinogen	Rattus norvegicus	58-64
15992826-13	2005	Intrarenal ANG II was increased in ANG II-infused rats, compared to control animals (52.9 +/- 7.1 versus 23.0 +/- 3.2 fmol/mg tissue; P < 0.001), and Enalaprilat prevented ANG II-induced increases in intrarenal ANG II (29.9 +/- 2.6 versus 52.9 +/- 7.1 fmol/mg tissue; P < 0.05).	Enalaprilat	153-164	angiotensinogen	Rattus norvegicus	11-17
15992826-13	2005	Intrarenal ANG II was increased in ANG II-infused rats, compared to control animals (52.9 +/- 7.1 versus 23.0 +/- 3.2 fmol/mg tissue; P < 0.001), and Enalaprilat prevented ANG II-induced increases in intrarenal ANG II (29.9 +/- 2.6 versus 52.9 +/- 7.1 fmol/mg tissue; P < 0.05).	Enalaprilat	153-164	angiotensinogen	Rattus norvegicus	35-41
15992826-13	2005	Intrarenal ANG II was increased in ANG II-infused rats, compared to control animals (52.9 +/- 7.1 versus 23.0 +/- 3.2 fmol/mg tissue; P < 0.001), and Enalaprilat prevented ANG II-induced increases in intrarenal ANG II (29.9 +/- 2.6 versus 52.9 +/- 7.1 fmol/mg tissue; P < 0.05).	Enalaprilat	153-164	angiotensinogen	Rattus norvegicus	35-41
15992826-13	2005	Intrarenal ANG II was increased in ANG II-infused rats, compared to control animals (52.9 +/- 7.1 versus 23.0 +/- 3.2 fmol/mg tissue; P < 0.001), and Enalaprilat prevented ANG II-induced increases in intrarenal ANG II (29.9 +/- 2.6 versus 52.9 +/- 7.1 fmol/mg tissue; P < 0.05).	Enalaprilat	153-164	angiotensinogen	Rattus norvegicus	35-41
16166566-5	2005	Enalaprilat increased basal t-PA release in premenopausal (from 0.9+/-1.0 to 5.1+/-1.7 ng/min per 100 mL, P=0.023) and postmenopausal women (from -3.9+/-2.2 to 3.9+/-1.1 ng/min per 100 mL, P=0.010) but not in young or older men (P=0.028 men versus women).	Enalaprilat	0-11	chromosome 20 open reading frame 181	Homo sapiens	28-32
16166566-6	2005	Enalaprilat potentiated the effect of exogenous BK on FBF similarly in all groups.	Enalaprilat	0-11	kininogen 1	Homo sapiens	48-50
16253075-2	2005	The aim of this study was to evaluate the effects of enalaprilat (Vasotec) administration on renal function during CO2 pneumoperitoneum, given that this drug, which is an angiotensin-converting enzyme inhibitor, by inhibiting the renin-angiotensin-aldosterone system, alters hormone-induced changes during pneumoperitoneum.	Enalaprilat	53-64	renin	Canis lupus familiaris	230-235
16148375-10	2005	Our study suggests that intrinsic differences exist between quinaprilat and enalaprilat that determine the ability to improve endotelium vasodilation, their different affinity to tissue ACE.	Enalaprilat	76-87	angiotensin I converting enzyme	Homo sapiens	186-189