PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 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. quinaprilat 204-215 angiotensin I converting enzyme Homo sapiens 47-50 8387427-1 1993 The pharmacokinetics and pharmacodynamics of the ACE inhibitor quinaprilat have been studied in six chronic haemodialysis (HD) patients and in six patients undergoing continuous ambulatory peritoneal dialysis (CAPD) after a single oral dose of 2.5 mg quinapril. quinaprilat 63-74 angiotensin I converting enzyme Homo sapiens 49-52 1546639-4 1992 Quinapril is a new ACE inhibitor that is converted to biologically active quinaprilat in the liver. quinaprilat 74-85 angiotensin I converting enzyme Homo sapiens 19-22 1711445-2 1991 Quinapril is a monoethyl ester which is hydrolysed after absorption to form an active metabolite, quinaprilat, which is a more potent angiotensin converting enzyme (ACE) inhibitor than the parent drug. quinaprilat 98-109 angiotensin I converting enzyme Homo sapiens 134-163 1711445-2 1991 Quinapril is a monoethyl ester which is hydrolysed after absorption to form an active metabolite, quinaprilat, which is a more potent angiotensin converting enzyme (ACE) inhibitor than the parent drug. quinaprilat 98-109 angiotensin I converting enzyme Homo sapiens 165-168 1711445-3 1991 Quinaprilat has a short elimination half-life but a potent binding affinity for ACE which enables once daily administration. quinaprilat 0-11 angiotensin I converting enzyme Homo sapiens 80-83 2068835-3 1991 On a weight basis quinaprilat is three times as potent an ACE inhibitor as quinapril. quinaprilat 18-29 angiotensin I converting enzyme Homo sapiens 58-61 2068835-12 1991 Quinaprilat has a strong binding capacity to tissue ACE allowing for once-daily dosing. quinaprilat 0-11 angiotensin I converting enzyme Homo sapiens 52-55 2144994-13 1990 ACE inhibition was marked and prolonged in all subjects, with 50% inhibition at 2.7 +/- 1.9% ng ml-1 of quinaprilat. quinaprilat 104-115 angiotensin I converting enzyme Homo sapiens 0-3 1691408-6 1990 However, because many older patients have impaired renal function, which can prolong the half-life of renally excreted ACE inhibitors such as quinaprilat (the active metabolite of quinapril), they should be started on lower doses of quinapril (5 mg) than are used in younger patients. quinaprilat 142-153 angiotensin I converting enzyme Homo sapiens 119-122 2193809-6 1990 Quinapril is a new non-sulphydryl ACE inhibitor whose active metabolite, quinaprilat, has a relatively short accumulation half-life compared with enalapril and lisinopril but has an enhanced affinity for the converting enzyme, allowing rapid excretion of the drug while retaining a 24-hour antihypertensive effect with once-daily dosing. quinaprilat 73-84 angiotensin I converting enzyme Homo sapiens 34-37 2539762-1 1989 Quinapril is converted to quinaprilat, a long-acting angiotensin converting enzyme (ACE) inhibitor, and is currently being studied for the treatment of hypertension and congestive heart failure. quinaprilat 26-37 angiotensin I converting enzyme Homo sapiens 84-87 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. quinaprilat 119-130 angiotensin I converting enzyme Homo sapiens 90-93 19761414-1 2009 BACKGROUND: Quinaprilat is an ACE inhibitor for intravenous use especially in patients with arterial hypertension or chronic heart failure. quinaprilat 12-23 angiotensin I converting enzyme Homo sapiens 30-33 19761414-5 2009 RESULTS: Quinaprilat is a potent nonsulfhydryl selective ACE inhibitor with a short elimination half-life of 2 - 3 h, but due to slow dissociation from tissue ACE, once daily dosing is sufficient for effective ACE inhibition. quinaprilat 9-20 angiotensin I converting enzyme Homo sapiens 57-60 19761414-5 2009 RESULTS: Quinaprilat is a potent nonsulfhydryl selective ACE inhibitor with a short elimination half-life of 2 - 3 h, but due to slow dissociation from tissue ACE, once daily dosing is sufficient for effective ACE inhibition. quinaprilat 9-20 angiotensin I converting enzyme Homo sapiens 159-162 19761414-5 2009 RESULTS: Quinaprilat is a potent nonsulfhydryl selective ACE inhibitor with a short elimination half-life of 2 - 3 h, but due to slow dissociation from tissue ACE, once daily dosing is sufficient for effective ACE inhibition. quinaprilat 9-20 angiotensin I converting enzyme Homo sapiens 159-162 19761414-10 2009 CONCLUSION: Quinaprilat is an attractive ACE inhibitor, which potently inhibits tissue ACE. quinaprilat 12-23 angiotensin I converting enzyme Homo sapiens 41-44 19761414-10 2009 CONCLUSION: Quinaprilat is an attractive ACE inhibitor, which potently inhibits tissue ACE. quinaprilat 12-23 angiotensin I converting enzyme Homo sapiens 87-90 19203070-1 2008 INTRODUCTION: Our study was designed to explore the hemodynamic effects of intravenous administration of ACE-inhibitor quinaprilat in comparison with standard inotropic-vasodilator therapy. quinaprilat 119-130 angiotensin I converting enzyme Homo sapiens 105-108 19203070-6 2008 The ACE-inhibitor quinaprilat 0.5 mg/h was administered intravenously via infusion pump. quinaprilat 18-29 angiotensin I converting enzyme Homo sapiens 4-7 17098309-1 2007 We compared the haemodynamic effects of intravenous boluses of the ACE inhibitor quinaprilat with an intravenous infusion of sodium nitroprusside in 23 patients with chronic heart failure (NYHA Class III or IV). quinaprilat 81-92 angiotensin I converting enzyme Homo sapiens 67-70 14973800-12 2004 CONCLUSIONS: The present investigation shows that acute administration of an intravenous ACE inhibitor, quinaprilat, has no influence on proinflammatory cytokines during cardiac surgery with cardiopulmonary bypass. quinaprilat 104-115 angiotensin I converting enzyme Homo sapiens 89-92 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. quinaprilat 60-71 angiotensin I converting enzyme Homo sapiens 186-189 15583077-5 2005 This was comparable to the maximal shift observed with the ACE inhibitors (ACEi) quinaprilat and captopril. quinaprilat 81-92 angiotensin I converting enzyme Homo sapiens 59-62 15583077-10 2005 Quinaprilat increased the t(1/2) approximately 4-fold, indicating that 71+/-6% of Ang I metabolism was attributable to ACE. quinaprilat 0-11 angiotensin I converting enzyme Homo sapiens 119-122 12208785-7 2002 In arteries that, following repeated exposure to 0.1 microM bradykinin, no longer responded to bradykinin ("desensitized" arteries), the ACE inhibitors quinaprilat and angiotensin-(1-7) both induced complete relaxation, without affecting the organ bath fluid levels of bradykinin. quinaprilat 152-163 angiotensin I converting enzyme Homo sapiens 137-140 12808303-1 2003 Objective of the present study was to investigate the elimination kinetics of quinaprilat and perindoprilat, the active metabolites of angiotensin-converting enzyme (ACE) inhibitors quinapril and perindopril, in hypertensive patients with renal failure under haemodialysis to evaluate the appropriate duration of off-dose of these drugs before starting of low-density lipoprotein (LDL) apheresis. quinaprilat 78-89 angiotensin I converting enzyme Homo sapiens 135-164 12808303-1 2003 Objective of the present study was to investigate the elimination kinetics of quinaprilat and perindoprilat, the active metabolites of angiotensin-converting enzyme (ACE) inhibitors quinapril and perindopril, in hypertensive patients with renal failure under haemodialysis to evaluate the appropriate duration of off-dose of these drugs before starting of low-density lipoprotein (LDL) apheresis. quinaprilat 78-89 angiotensin I converting enzyme Homo sapiens 166-169 12736518-10 2003 We therefore believe that the protective effects of quinaprilat and trandolaprilat on the LPC-induced hemolysis may be related physicochemically to their highly lipophilic and ACE inhibitory structures, which probably maintain erythrocyte membrane integrity by a mechanism other than ACE inhibition, prevention of LPC micelle formation or protection against osmotic imbalance. quinaprilat 52-63 angiotensin I converting enzyme Homo sapiens 176-179 12736518-10 2003 We therefore believe that the protective effects of quinaprilat and trandolaprilat on the LPC-induced hemolysis may be related physicochemically to their highly lipophilic and ACE inhibitory structures, which probably maintain erythrocyte membrane integrity by a mechanism other than ACE inhibition, prevention of LPC micelle formation or protection against osmotic imbalance. quinaprilat 52-63 angiotensin I converting enzyme Homo sapiens 284-287 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. quinaprilat 67-78 angiotensin I converting enzyme Homo sapiens 207-210 11300367-9 2000 These effects of quinaprilat are possibly related to its higher affinity for vascular ACE. quinaprilat 17-28 angiotensin I converting enzyme Homo sapiens 86-89 11817979-1 2002 UNLABELLED: Quinapril is rapidly de-esterified after absorption to quinaprilat (the active diacid metabolite), a potent angiotensin converting enzyme (ACE) inhibitor. quinaprilat 67-78 angiotensin I converting enzyme Homo sapiens 120-149 11817979-1 2002 UNLABELLED: Quinapril is rapidly de-esterified after absorption to quinaprilat (the active diacid metabolite), a potent angiotensin converting enzyme (ACE) inhibitor. quinaprilat 67-78 angiotensin I converting enzyme Homo sapiens 151-154 11817979-2 2002 Quinapril produces favourable haemodynamic changes, and improves ventricular and endothelial function in patients with various cardiovascular disorders; these effects are mediated through the binding of quinaprilat to both tissue and plasma ACE. quinaprilat 203-214 angiotensin I converting enzyme Homo sapiens 241-244 11270506-6 2000 ACE inhibitor quinaprilat and bradykinin significantly lessened apoptosis and lactate dehydrogenase release with these effects being diminished by a kinin B2 receptor antagonist and a nitric oxide synthase inhibitor. quinaprilat 14-25 angiotensin I converting enzyme Homo sapiens 0-3 10520782-0 1999 Improvement of myocardial blood flow to ischemic regions by angiotensin-converting enzyme inhibition with quinaprilat IV: a study using [15O] water dobutamine stress positron emission tomography. quinaprilat 106-117 angiotensin I converting enzyme Homo sapiens 60-89 10520782-7 1999 In contrast, MBF in ischemic regions increased significantly after acute ACE inhibition with quinaprilat during repetitive dobutamine stress (1.10 +/- 0.13 vs. 1.69 +/- 0.17 ml/min/g, p < 0.015). quinaprilat 93-104 angiotensin I converting enzyme Homo sapiens 73-76 10520782-10 1999 CONCLUSIONS: Angiotensin-converting enzyme inhibition by quinaprilat significantly improves MBF to ischemic regions in patients with coronary artery disease. quinaprilat 57-68 angiotensin I converting enzyme Homo sapiens 13-42 8681494-8 1996 Relative to placebo, quinaprilat reduced plasma angiotensin converting enzyme (ACE) activity, angiotensin II concentration, and aldosterone concentration and increased plasma renin activity; no prominent changes in plasma catecholamine and atrial natriuretic peptide concentrations were observed. quinaprilat 21-32 angiotensin I converting enzyme Homo sapiens 48-77 9336392-2 1997 In particular, recently developed ACE inhibitors with tissue-penetrating properties, such as quinaprilat, may exert vascular effects via the bradykinin B2-receptor. quinaprilat 93-104 angiotensin I converting enzyme Homo sapiens 34-37 8681494-10 1996 CONCLUSIONS: Single and multiple intravenous doses of 0.5 to 10 mg quinaprilat are well-tolerated and produce favorable dose-dependent hemodynamic effects and hormonal changes consistent with those expected of an ACE inhibitor in patients with NYHA class III and IV congestive heart failure. quinaprilat 67-78 angiotensin I converting enzyme Homo sapiens 213-216 10024837-9 1998 CONCLUSION: Quinaprilate, at half the dose of quinapril, administered BID maintains blood pressure control, is well tolerated, and allows for safe conversion from previously applied oral ACE inhibitors. quinaprilat 12-24 angiotensin I converting enzyme Homo sapiens 187-190 9064945-0 1996 [Hemodynamic and humoral effects of parenteral therapy with intravenously administered ACE inhibitor quinaprilat in patients with advanced heart failure]. quinaprilat 101-112 angiotensin I converting enzyme Homo sapiens 87-90 9064945-5 1996 Quinaprilat is the active metabolite of quinapril, an ACE inhibitor with high affinity for the angiotensin converting enzyme, which is formulated for oral application. quinaprilat 0-11 angiotensin I converting enzyme Homo sapiens 54-57 9064945-5 1996 Quinaprilat is the active metabolite of quinapril, an ACE inhibitor with high affinity for the angiotensin converting enzyme, which is formulated for oral application. quinaprilat 0-11 angiotensin I converting enzyme Homo sapiens 95-124 9064945-10 1996 The hemodynamic changes after multiple-dose quinaprilat were similar to those observed following single doses and generally persisted during the total observation period of 6 h. Compared with placebo, quinaprilat reduced ACE activity and angiotensin II and aldosterone concentrations, and increased plasma renin activity. quinaprilat 201-212 angiotensin I converting enzyme Homo sapiens 221-224 8681494-8 1996 Relative to placebo, quinaprilat reduced plasma angiotensin converting enzyme (ACE) activity, angiotensin II concentration, and aldosterone concentration and increased plasma renin activity; no prominent changes in plasma catecholamine and atrial natriuretic peptide concentrations were observed. quinaprilat 21-32 angiotensin I converting enzyme Homo sapiens 79-82 8739020-1 1996 Quinaprilat is the active metabolite of quinapril, an orally active angiotensin-converting enzyme (ACE) inhibitor. quinaprilat 0-11 angiotensin I converting enzyme Homo sapiens 68-97 8739020-1 1996 Quinaprilat is the active metabolite of quinapril, an orally active angiotensin-converting enzyme (ACE) inhibitor. quinaprilat 0-11 angiotensin I converting enzyme Homo sapiens 99-102 7527326-2 1994 Following systemic absorption, quinapril is converted by de-esterification to quinaprilat (the active diacid metabolite), an inhibitor of angiotensin converting enzyme (ACE). quinaprilat 78-89 angiotensin I converting enzyme Homo sapiens 138-167 7527326-2 1994 Following systemic absorption, quinapril is converted by de-esterification to quinaprilat (the active diacid metabolite), an inhibitor of angiotensin converting enzyme (ACE). quinaprilat 78-89 angiotensin I converting enzyme Homo sapiens 169-172 7527326-5 1994 Quinaprilat has a short elimination half-life (approximately 2 hours), but binds potently to and dissociates slowly from ACE, thus allowing once or twice daily administration of quinapril in the treatment of patients with hypertension or congestive heart failure. quinaprilat 0-11 angiotensin I converting enzyme Homo sapiens 121-124