PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 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 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 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 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 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 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 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 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 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 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 12566370-8 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 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 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 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 kininogen 1 Homo sapiens 129-139 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 2557432-11 1989 Enalaprilat increased vasodilatation caused by bradykinin. Enalaprilat 0-11 kininogen 1 Homo sapiens 47-57 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 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 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 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 kininogen 1 Homo sapiens 152-154 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 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 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 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 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