PMID-sentid Pub_year Sent_text compound_name comp_offset prot_official_name organism prot_offset 24551095-2 2014 Recently, we showed therapeutic effects of the combination of lisinopril (L), an angiotensin converting enzyme (ACE) inhibitor, and spironolactone (S), an aldosterone antagonist, in mice lacking dystrophin and haploinsufficient for utrophin (utrn(+/-);mdx, het mice); both cardiac and skeletal muscle function and histology were improved when these mice were treated early with LS. Lisinopril 62-72 angiotensin I converting enzyme (peptidyl-dipeptidase A) 1 Mus musculus 81-110 24551095-2 2014 Recently, we showed therapeutic effects of the combination of lisinopril (L), an angiotensin converting enzyme (ACE) inhibitor, and spironolactone (S), an aldosterone antagonist, in mice lacking dystrophin and haploinsufficient for utrophin (utrn(+/-);mdx, het mice); both cardiac and skeletal muscle function and histology were improved when these mice were treated early with LS. Lisinopril 62-72 angiotensin I converting enzyme (peptidyl-dipeptidase A) 1 Mus musculus 112-115 24551095-2 2014 Recently, we showed therapeutic effects of the combination of lisinopril (L), an angiotensin converting enzyme (ACE) inhibitor, and spironolactone (S), an aldosterone antagonist, in mice lacking dystrophin and haploinsufficient for utrophin (utrn(+/-);mdx, het mice); both cardiac and skeletal muscle function and histology were improved when these mice were treated early with LS. Lisinopril 62-72 utrophin Mus musculus 232-240 24228790-0 2013 N- versus C-domain selectivity of catalytic inactivation of human angiotensin converting enzyme by lisinopril-coupled transition metal chelates. Lisinopril 99-109 angiotensin I converting enzyme Homo sapiens 66-95 25902654-1 2014 AIM: To assess effect of combined antihypertensive therapy with lisinopril and amlodipine on circadian blood pressure (BP), insulin resistance (IR), carbohydrate and lipid metabolism in patients with arterial hypertension (AH) and type 2 diabetes mellitus (DM). Lisinopril 64-74 insulin Homo sapiens 124-131 25102744-14 2014 Replacing the previous therapy different ACE inhibitors, sartans and calcium antagonists to the fixed combination amlodipine and lisinopril) (drug EKVATOR), leads to a rapid, pronounced, and safe reduction of BP and improve health in the majority of patients with previously uncorrected BP. Lisinopril 129-139 angiotensin I converting enzyme Homo sapiens 41-44 24168709-2 2013 We present a comprehensive surface plasmon resonance (SPR) study of the interaction of human somatic ACE with the pharmacological inhibitors captopril and lisinopril, the bradykinin potentiating peptide BPP-11b, and the food peptidic inhibitors from bovine alphas2-casein, F(174)ALPQYLK(181) and F(174)ALPQY(179). Lisinopril 155-165 angiotensin I converting enzyme Homo sapiens 101-104 24168709-4 2013 The results indicated that captopril and lisinopril bound ACE with two K(D)"s differing by a factor 10-20 and >30, respectively (lowest K(D) = 0.1-0.3 nM for both inhibitors). Lisinopril 41-51 angiotensin I converting enzyme Homo sapiens 58-61 24285767-8 2013 ACE inhibitors evaluated in the studies were captopril, lisinopril, perindopril, quinapril, and ramipril. Lisinopril 56-66 angiotensin I converting enzyme Homo sapiens 0-3 23178416-0 2013 Life-threatening ACE inhibitor-induced angioedema after eleven years on lisinopril. Lisinopril 72-82 angiotensin I converting enzyme Homo sapiens 17-20 23873413-4 2013 In the course of this study, the single-crystal X-ray structure of lisinopril dihydrate, [a = 14.550(2), b = 5.8917(8), c = 14.238(2) A, beta = 112.832(3) at T = 173(2) K, space group P21 , Z = 2], was determined for the first time, revealing its double zwitterionic character in the solid state. Lisinopril 67-87 H3 histone pseudogene 16 Homo sapiens 185-188 23812388-8 2013 Pretreatment with lisinopril caused increase in ANG-(1-12) and ANG I and large decreases in ANG II compared with the other two groups in both strains. Lisinopril 18-28 angiotensinogen Rattus norvegicus 92-98 23794071-2 2013 A female patient under treatment for hypertension with an angiotensin-converting enzyme inhibitor (ACE inhibitor), lisinopril, developed blisters and ulcerations on oral mucosa 3 weeks after lisinopril intake. Lisinopril 115-125 angiotensin I converting enzyme Homo sapiens 99-102 23794071-2 2013 A female patient under treatment for hypertension with an angiotensin-converting enzyme inhibitor (ACE inhibitor), lisinopril, developed blisters and ulcerations on oral mucosa 3 weeks after lisinopril intake. Lisinopril 191-201 angiotensin I converting enzyme Homo sapiens 99-102 23060470-13 2013 Pre-treatment with bisphenol-A-diglycidyl ether (BADGE), a selective PPAR-gamma antagonist, significantly abolished the beneficial effect of lisinopril/telmisartan in i.c.v. Lisinopril 141-151 peroxisome proliferator activated receptor gamma Mus musculus 69-79 23528611-9 2013 Moreover, PKI-166 and lisinopril restored the impaired contraction of isolated thoracic aortic rings to phenylephrine and angiotensin II and impaired myogenic constriction of small mesenteric arteries in 5/6Nx rats. Lisinopril 22-32 angiotensinogen Rattus norvegicus 122-136 23060470-15 2013 The results of this investigation document a potential role of PPAR-gamma in the beneficial effects of lisinopril and telmisartan in i.c.v. Lisinopril 103-113 peroxisome proliferator activated receptor gamma Mus musculus 63-73 23060470-3 2013 This study also aimed to explore the role of PPAR-gamma in lisinopril and telmisartan mediated effects in i.c.v. Lisinopril 59-69 peroxisome proliferator activated receptor gamma Mus musculus 45-55 23660814-0 2013 Molecular dynamics simulation and molecular docking studies of Angiotensin converting enzyme with inhibitor lisinopril and amyloid Beta Peptide. Lisinopril 108-118 angiotensin I converting enzyme Homo sapiens 63-92 23660814-3 2013 Keeping this view in mind, we performed molecular dynamics simulation of crystal structure complex of testis truncated version of ACE (tACE) and its inhibitor lisinopril along with Zn(2+) to understand the dynamic behavior of active site residues of tACE. Lisinopril 159-169 angiotensin I converting enzyme Homo sapiens 130-133 23660814-3 2013 Keeping this view in mind, we performed molecular dynamics simulation of crystal structure complex of testis truncated version of ACE (tACE) and its inhibitor lisinopril along with Zn(2+) to understand the dynamic behavior of active site residues of tACE. Lisinopril 159-169 ADAM metallopeptidase domain 17 Homo sapiens 135-139 23660814-3 2013 Keeping this view in mind, we performed molecular dynamics simulation of crystal structure complex of testis truncated version of ACE (tACE) and its inhibitor lisinopril along with Zn(2+) to understand the dynamic behavior of active site residues of tACE. Lisinopril 159-169 ADAM metallopeptidase domain 17 Homo sapiens 250-254 23660814-5 2013 The residues Ala 354, Glu 376, Asp 377, Glu 384, His 513, Tyr 520 and Tyr 523 of tACE stabilized lisinopril by hydrogen bonding interactions. Lisinopril 97-107 ADAM metallopeptidase domain 17 Homo sapiens 81-85 24082511-8 2013 Serum levels of aspartate aminotransferase (AST), alkaline phosphatase (ALP), and total bilirubin were significantly increased in rosuvastatin alone and its combination with lisinopril at both the doses. Lisinopril 174-184 glutamic-oxaloacetic transaminase 2 Rattus norvegicus 16-42 24450223-5 2013 The ACE inhibitors, particularly hydrophilic lysinopril, to the lesser degree than beta-adrenoblockers, prevented death of animals at the period of the CHF decompensation. Lisinopril 45-55 angiotensin I converting enzyme Rattus norvegicus 4-7 24082511-8 2013 Serum levels of aspartate aminotransferase (AST), alkaline phosphatase (ALP), and total bilirubin were significantly increased in rosuvastatin alone and its combination with lisinopril at both the doses. Lisinopril 174-184 glutamic-oxaloacetic transaminase 2 Rattus norvegicus 44-47 23455217-0 2013 Study of alteration of adrenergic receptor response by chronic use of lisinopril: an ACE inhibitor. Lisinopril 70-80 angiotensin I converting enzyme Homo sapiens 85-88 23328120-1 2013 The present study was undertaken to scientifically evaluate, validate and compare the cardioprotective effects of lisinopril (Lsp), an angiotensin converting enzyme (ACE) inhibitor and vitamin E (Vit E), an antioxidant in the setting of ischemia and reperfusion (I-R) injury. Lisinopril 114-124 angiotensin I converting enzyme Homo sapiens 135-164 23455217-3 2013 This study shows the down regulation of adrenergic receptors due to chronic use of lisinopril, an ACE inhibitor as a cause of poor response of adrenaline. Lisinopril 83-93 angiotensin I converting enzyme Homo sapiens 98-101 23705487-4 2013 Under the influence of lisinopril and lovastatin there were observed lowering in the stellate pancreatic cells activity and in expression of SMA, desmin, GFAP, vimentin and TIMP-2, the MMP-1 and TIMP-2 ratio have had increased significantly and severity of fibrotic pancreatic affection had reduced trustworthy in comparison w such, occurring in a control group. Lisinopril 23-33 desmin Rattus norvegicus 146-152 23705487-4 2013 Under the influence of lisinopril and lovastatin there were observed lowering in the stellate pancreatic cells activity and in expression of SMA, desmin, GFAP, vimentin and TIMP-2, the MMP-1 and TIMP-2 ratio have had increased significantly and severity of fibrotic pancreatic affection had reduced trustworthy in comparison w such, occurring in a control group. Lisinopril 23-33 glial fibrillary acidic protein Rattus norvegicus 154-158 23705487-4 2013 Under the influence of lisinopril and lovastatin there were observed lowering in the stellate pancreatic cells activity and in expression of SMA, desmin, GFAP, vimentin and TIMP-2, the MMP-1 and TIMP-2 ratio have had increased significantly and severity of fibrotic pancreatic affection had reduced trustworthy in comparison w such, occurring in a control group. Lisinopril 23-33 vimentin Rattus norvegicus 160-168 23705487-4 2013 Under the influence of lisinopril and lovastatin there were observed lowering in the stellate pancreatic cells activity and in expression of SMA, desmin, GFAP, vimentin and TIMP-2, the MMP-1 and TIMP-2 ratio have had increased significantly and severity of fibrotic pancreatic affection had reduced trustworthy in comparison w such, occurring in a control group. Lisinopril 23-33 TIMP metallopeptidase inhibitor 2 Rattus norvegicus 173-179 23705487-4 2013 Under the influence of lisinopril and lovastatin there were observed lowering in the stellate pancreatic cells activity and in expression of SMA, desmin, GFAP, vimentin and TIMP-2, the MMP-1 and TIMP-2 ratio have had increased significantly and severity of fibrotic pancreatic affection had reduced trustworthy in comparison w such, occurring in a control group. Lisinopril 23-33 matrix metallopeptidase 1 Rattus norvegicus 185-190 23705487-4 2013 Under the influence of lisinopril and lovastatin there were observed lowering in the stellate pancreatic cells activity and in expression of SMA, desmin, GFAP, vimentin and TIMP-2, the MMP-1 and TIMP-2 ratio have had increased significantly and severity of fibrotic pancreatic affection had reduced trustworthy in comparison w such, occurring in a control group. Lisinopril 23-33 TIMP metallopeptidase inhibitor 2 Rattus norvegicus 195-201 22728903-8 2012 Lisinopril decreased their SBP (-23 vs. -13 mmHg in controls), kidney Ang-II/I (~3-fold vs. ~2-fold) and Ile(5)-Ang-II (-70 vs. -40%), and increased kidney renin and Ile(5)-Ang-I (>2.5-fold vs. <2.5-fold). Lisinopril 0-10 spermine binding protein Rattus norvegicus 27-30 23083673-9 2012 The risk of developing eczema during the first 24 months of life was significantly reduced in infants of mothers receiving LPR+BL999 (odds ratio [OR], 0.17; 95% CI, 0.08-0.35; P < .001) and ST11+BL999 (OR, 0.16; 95% CI, 0.08-0.35; P < .001). Lisinopril 123-126 Pancreatic endocrine tumor suppressor Homo sapiens 193-203 22943192-3 2012 In this study, we examined the effects of lisinopril, an ACE inhibitor, on the levels of hippocampal NMDAR subunits; NR2A and NR2B in L-NAME (N(epsilon)-nitro-L-arginine Methyl Ester)-induced hypertensive rats. Lisinopril 42-52 angiotensin I converting enzyme Rattus norvegicus 57-60 22943192-3 2012 In this study, we examined the effects of lisinopril, an ACE inhibitor, on the levels of hippocampal NMDAR subunits; NR2A and NR2B in L-NAME (N(epsilon)-nitro-L-arginine Methyl Ester)-induced hypertensive rats. Lisinopril 42-52 glutamate ionotropic receptor NMDA type subunit 2A Rattus norvegicus 117-121 22943192-3 2012 In this study, we examined the effects of lisinopril, an ACE inhibitor, on the levels of hippocampal NMDAR subunits; NR2A and NR2B in L-NAME (N(epsilon)-nitro-L-arginine Methyl Ester)-induced hypertensive rats. Lisinopril 42-52 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 126-130 23030285-3 2012 The SMILE project involved more than 3500 patients with coronary artery disease and demonstrated that zofenopril treatment may reduce mortality and morbidity in patients with myocardial infarction, also when combined with acetyl salicylic acid and to a greater extent than lisinopril and ramipril. Lisinopril 273-283 transmembrane O-mannosyltransferase targeting cadherins 3 Homo sapiens 4-9 24022426-0 2013 Lisinopril protects against the adriamycin nephropathy and reverses the renalase reduction: potential role of renalase in adriamycin nephropathy. Lisinopril 0-10 renalase, FAD-dependent amine oxidase Rattus norvegicus 72-80 24022426-0 2013 Lisinopril protects against the adriamycin nephropathy and reverses the renalase reduction: potential role of renalase in adriamycin nephropathy. Lisinopril 0-10 renalase, FAD-dependent amine oxidase Rattus norvegicus 110-118 24022426-1 2013 AIMS: To investigate the potential role of renalase in adriamycin nephropathy and the effect of lisinopril on the regulation of renalase. Lisinopril 96-106 renalase, FAD-dependent amine oxidase Rattus norvegicus 128-136 24022426-13 2013 Lisinopril may attenuate adriamycin-induced kidney injury by controlling blood pressure, which may be partially attributed to the renalase expression and secretion. Lisinopril 0-10 renalase, FAD-dependent amine oxidase Rattus norvegicus 130-138 23285665-4 2012 It was found that ACE inhibitors (apo-perindox, prinvil, gopten) caused a significant decrease in the activity of pepsin, while indapen (a diuretic) and glucophage (an antidiabetic drug) increased the activity of this enzyme. Lisinopril 48-55 angiotensin I converting enzyme Homo sapiens 18-21 22947356-2 2012 The authors tested the additivity of the beta-blocker nebivolol, which has vasodilating activity, with the angiotensin-converting enzyme inhibitor lisinopril in patients with stage 2 diastolic hypertension. Lisinopril 147-157 angiotensin I converting enzyme Homo sapiens 107-136 22728903-8 2012 Lisinopril decreased their SBP (-23 vs. -13 mmHg in controls), kidney Ang-II/I (~3-fold vs. ~2-fold) and Ile(5)-Ang-II (-70 vs. -40%), and increased kidney renin and Ile(5)-Ang-I (>2.5-fold vs. <2.5-fold). Lisinopril 0-10 angiotensinogen Rattus norvegicus 70-76 22728903-8 2012 Lisinopril decreased their SBP (-23 vs. -13 mmHg in controls), kidney Ang-II/I (~3-fold vs. ~2-fold) and Ile(5)-Ang-II (-70 vs. -40%), and increased kidney renin and Ile(5)-Ang-I (>2.5-fold vs. <2.5-fold). Lisinopril 0-10 angiotensinogen Rattus norvegicus 112-118 22728903-8 2012 Lisinopril decreased their SBP (-23 vs. -13 mmHg in controls), kidney Ang-II/I (~3-fold vs. ~2-fold) and Ile(5)-Ang-II (-70 vs. -40%), and increased kidney renin and Ile(5)-Ang-I (>2.5-fold vs. <2.5-fold). Lisinopril 0-10 renin Rattus norvegicus 156-161 23033781-5 2012 The treatment of rats after operation with lisinopril inhibite activity of pancreatic stellate cells and characterized by significant decrease of the alpha-SMA, desmin, GFAP, vimentin and TIMP-2 expression. Lisinopril 43-53 actin gamma 2, smooth muscle Rattus norvegicus 150-159 24250503-7 2012 Very good correlation (r = 0.91; water-ethanol solvent system) between the chromatographically obtained hydrophobicity parameters and calculated log p values confirmed the selection of ACE inhibitors since lisinopril and quinapril were on the opposite sites of linear relationship. Lisinopril 206-216 angiotensin I converting enzyme Homo sapiens 185-188 23033781-5 2012 The treatment of rats after operation with lisinopril inhibite activity of pancreatic stellate cells and characterized by significant decrease of the alpha-SMA, desmin, GFAP, vimentin and TIMP-2 expression. Lisinopril 43-53 desmin Rattus norvegicus 161-167 23033781-5 2012 The treatment of rats after operation with lisinopril inhibite activity of pancreatic stellate cells and characterized by significant decrease of the alpha-SMA, desmin, GFAP, vimentin and TIMP-2 expression. Lisinopril 43-53 glial fibrillary acidic protein Rattus norvegicus 169-173 23033781-5 2012 The treatment of rats after operation with lisinopril inhibite activity of pancreatic stellate cells and characterized by significant decrease of the alpha-SMA, desmin, GFAP, vimentin and TIMP-2 expression. Lisinopril 43-53 vimentin Rattus norvegicus 175-183 23033781-5 2012 The treatment of rats after operation with lisinopril inhibite activity of pancreatic stellate cells and characterized by significant decrease of the alpha-SMA, desmin, GFAP, vimentin and TIMP-2 expression. Lisinopril 43-53 TIMP metallopeptidase inhibitor 2 Rattus norvegicus 188-194 22980373-3 2012 This study examines the effects of angiotensin converting enzyme inhibitor (Lisinopril) on blood pressure (BP) 131 +- 2.4 and proteinuria 0.198 +- 0.005 in Kurd hypertensive patients, mean arterial blood pressure and proteinuria excretion were measured weekly along the period of 12 weeks. Lisinopril 76-86 angiotensin I converting enzyme Homo sapiens 35-64 22490446-5 2012 Ang I and Ang II forming activities for serum ACE were 102+-4 and 104+-3 fmol/ml/min serum (n=3), respectively, and both products were abolished by the potent ACE inhibitor lisinopril. Lisinopril 173-183 angiotensinogen Rattus norvegicus 10-16 22490446-5 2012 Ang I and Ang II forming activities for serum ACE were 102+-4 and 104+-3 fmol/ml/min serum (n=3), respectively, and both products were abolished by the potent ACE inhibitor lisinopril. Lisinopril 173-183 angiotensin I converting enzyme Rattus norvegicus 46-49 22490446-5 2012 Ang I and Ang II forming activities for serum ACE were 102+-4 and 104+-3 fmol/ml/min serum (n=3), respectively, and both products were abolished by the potent ACE inhibitor lisinopril. Lisinopril 173-183 angiotensin I converting enzyme Rattus norvegicus 159-162 22498331-2 2012 BACKGROUND: High-affinity technetium-99m-labeled lisinopril (Tc-Lis) has been shown to specifically localize in tissues that express ACE in vivo, such as the lungs. Lisinopril 49-59 angiotensin I converting enzyme Rattus norvegicus 133-136 22540049-6 2012 Glomerulosclerosis and renal expression of type I and type IV collagen, plasminogen activator inhibitor-1, transforming growth factor-beta1, connective tissue growth factor, and fibronectin mRNA were markedly decreased in the lisinopril, eplerenone, and combination groups. Lisinopril 226-236 fibronectin 1 Rattus norvegicus 178-189 21911117-0 2011 Lisinopril inhibits endothelin-1 in the early period of hepatic reperfusion injury in a partial hepatectomy model. Lisinopril 0-10 endothelin 1 Rattus norvegicus 20-32 22369721-10 2012 The transfected cells with transporters were used to investigate drug-drug interactions (DDIs) between JBP485 and other substrates (cephalexin or lisinopril) of PEPT1 and PEPT2. Lisinopril 146-156 solute carrier family 15 member 1 Homo sapiens 161-166 22369721-10 2012 The transfected cells with transporters were used to investigate drug-drug interactions (DDIs) between JBP485 and other substrates (cephalexin or lisinopril) of PEPT1 and PEPT2. Lisinopril 146-156 solute carrier family 15 member 2 Homo sapiens 171-176 22232014-6 2012 The involvement of ACE was indicated by the ability of the ACE inhibitor, lisinopril, to inhibit the substrate V degradation. Lisinopril 74-84 angiotensin I converting enzyme Homo sapiens 19-22 22232014-6 2012 The involvement of ACE was indicated by the ability of the ACE inhibitor, lisinopril, to inhibit the substrate V degradation. Lisinopril 74-84 angiotensin I converting enzyme Homo sapiens 59-62 21878554-3 2011 Urinary clusterin levels significantly increased in high-dose treated animals of lisinopril and rosuvastatin. Lisinopril 81-91 clusterin Rattus norvegicus 8-17 21878554-4 2011 The use of lisinopril plus rosuvastatin at low dose also led to worsened renal function by raising urinary clusterin levels (217 +- 4.6 ng/ml) when compared with the control (143 +- 3.3 ng/ml). Lisinopril 11-21 clusterin Rattus norvegicus 107-116 25031933-8 2012 She was treated with an ACE inhibitor (lisinopril) and a beta-blocker (carvedilol) with improvement of her LVEF to 30%-35%. Lisinopril 39-49 angiotensin I converting enzyme Homo sapiens 24-27 22200082-4 2012 The resulting amide-linked chelate-lisinopril (EDTA-lisinopril, NTA-lisinopril, DOTA-lisinopril, and GGH-lisinopril) conjugates were used to form coordination complexes with iron, cobalt, nickel, and copper, such that lisinopril could mediate localization of the reactive metal chelates to sACE-1. Lisinopril 35-45 gamma-glutamyl hydrolase Homo sapiens 101-104 22200082-5 2012 ACE activity was assayed by monitoring cleavage of the fluorogenic substrate Mca-RPPGFSAFK(Dnp)-OH, a derivative of bradykinin, following preincubation with metal chelate-lisinopril compounds. Lisinopril 171-181 angiotensin I converting enzyme Homo sapiens 0-3 22200082-5 2012 ACE activity was assayed by monitoring cleavage of the fluorogenic substrate Mca-RPPGFSAFK(Dnp)-OH, a derivative of bradykinin, following preincubation with metal chelate-lisinopril compounds. Lisinopril 171-181 kininogen 1 Homo sapiens 116-126 22200082-8 2012 Time-dependent inactivation of sACE-1 by metal chelate-lisinopril complexes revealed a remarkable range of catalytic activities, with second-order rate constants as high as 150,000 M(-1) min(-1) (Cu-GGH-lisinopril), while catalyst-mediated cleavage of sACE-1 typically occurred at much lower rates, indicating that inactivation arose primarily from side chain modification. Lisinopril 55-65 gamma-glutamyl hydrolase Homo sapiens 199-202 22200082-10 2012 This class of metal chelate-lisinopril complexes possesses a range of high-affinity binding to ACE, introduces the advantage of irreversible catalytic turnover, and marks an important step toward the development of multiple-turnover drugs for selective inactivation of sACE-1. Lisinopril 28-38 angiotensin I converting enzyme Homo sapiens 95-98 22123131-0 2012 Peptide cotransporter 1 in intestine and organic anion transporters in kidney are targets of interaction between JBP485 and lisinopril in rats. Lisinopril 124-134 solute carrier family 15 member 1 Homo sapiens 0-23 22123131-6 2012 These findings confirmed that the pharmacokinetic mechanism of interaction between JBP485 and lisinopril could be explained by their inhibition of the same transporters in the intestinal mucosa (PEPT1) and kidneys (OATs). Lisinopril 94-104 solute carrier family 15 member 1 Homo sapiens 195-200 23082133-9 2012 Participants randomized to lisinopril vs. L-placebo had significant declines in diastolic BP (-3.3 mmHg, p=0.05), hsCRP (-0.61 microg/mL, p=0.02) and TNF-alpha (-0.17 pg/mL, p=0.04). Lisinopril 27-37 tumor necrosis factor Homo sapiens 150-159 22144768-7 2011 RESULTS: Pre-ischemic treatment with lisinopril (10 mg/kg) exerted protection against I/R-induced hepatocellular injury as evident by significant decrease in serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and total bilirubin levels, along with hepatic lipid peroxidation, expressed as malondialdehyde content, with a concurrent increase in hepatic nitric oxide content as compared to I/R group. Lisinopril 37-47 glutamic-oxaloacetic transaminase 2 Rattus norvegicus 196-222 22144768-7 2011 RESULTS: Pre-ischemic treatment with lisinopril (10 mg/kg) exerted protection against I/R-induced hepatocellular injury as evident by significant decrease in serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and total bilirubin levels, along with hepatic lipid peroxidation, expressed as malondialdehyde content, with a concurrent increase in hepatic nitric oxide content as compared to I/R group. Lisinopril 37-47 glutamic-oxaloacetic transaminase 2 Rattus norvegicus 224-227 21911117-6 2011 The levels of ALT and ET-1 decreased with lisinopril precontioning in group 4 compared with group 2 (P > .05 and P < .01) or group 3 (P < .05 and P < .001). Lisinopril 42-52 endothelin 1 Rattus norvegicus 22-26 21911117-12 2011 Lisinopril preconditioning alleviated I/R injury by decreasing the O(2)(-), NO, ONOO(-), ET-1, and ALT levels, thereby exerting a protective role on the remaining liver. Lisinopril 0-10 endothelin 1 Rattus norvegicus 89-93 21479940-11 2011 In the L-NAME plus lisinopril treated group, serum creatinine, microalbumin and urine NAG, renal MDA level and CAT activity decreased, whereas SOD, GSH-Px activities in renal tissue and serum NO levels were increased. Lisinopril 19-29 O-GlcNAcase Rattus norvegicus 86-89 21479940-11 2011 In the L-NAME plus lisinopril treated group, serum creatinine, microalbumin and urine NAG, renal MDA level and CAT activity decreased, whereas SOD, GSH-Px activities in renal tissue and serum NO levels were increased. Lisinopril 19-29 catalase Rattus norvegicus 111-114 21496825-1 2011 The separation of structurally related angiotensin-converting enzyme (ACE) inhibitors lisinopril, cilazapril, ramipril and quinapril and their corresponding active diacid forms (prilates) by conventional TLC silica gel 60 plates was contrasted with that afforded by monolithic ultra-thin-layer chromatographic (UTLC) plates. Lisinopril 86-96 angiotensin I converting enzyme Homo sapiens 70-73 21255995-0 2011 35 MHz quartz crystal microbalance and surface plasmon resonance studies on the binding of angiotensin converting enzyme with lisinopril. Lisinopril 126-136 angiotensin I converting enzyme Homo sapiens 91-120 21422380-5 2011 These effects could be blocked by the ACE inhibitor, lisinopril. Lisinopril 53-63 angiotensin I converting enzyme (peptidyl-dipeptidase A) 1 Mus musculus 38-41 21255995-2 2011 Herein, a low reagent consumption, multiparameter and highly sensitive quartz crystal microbalance (QCM) at 35-MHz fundamental frequency was utilized to monitor in situ the binding process of solution lisinopril (LIS, a carboxylic third-generation ACEI) to ACE adsorbed at a 1-dodecanethiol (C12SH)-modified Au electrode. Lisinopril 201-211 angiotensin I converting enzyme Homo sapiens 248-251 21887284-10 2011 For MMP12 N122S (rs652438), lower HRs were observed for CHD in subjects carrying at least one G allele and being treated with chlorthalidone versus lisinopril (CHD: AA = 1.07, AG = 0.80, GG = 0.49; P = 0.005). Lisinopril 148-158 matrix metallopeptidase 12 Homo sapiens 4-9 21183746-8 2011 CONCLUSIONS: The MMP3 6A/6A genotype is associated with an increased risk of stroke in hypertensive subjects taking lisinopril compared with patients treated with chlorthalidone, whereas a protective effect was found for 5A/5A individuals treated with lisinopril. Lisinopril 116-126 matrix metallopeptidase 3 Homo sapiens 17-21 21183746-8 2011 CONCLUSIONS: The MMP3 6A/6A genotype is associated with an increased risk of stroke in hypertensive subjects taking lisinopril compared with patients treated with chlorthalidone, whereas a protective effect was found for 5A/5A individuals treated with lisinopril. Lisinopril 252-262 matrix metallopeptidase 3 Homo sapiens 17-21 21980964-3 2011 RESULTS: The blood pressure (BP) control with lisinopril was reduced by concomitantly administered diclofenac sodium in non-diabetic (SBP: p=0.00002; DBP: p=0.000008) and diabetic (SBP: p=0.002; DBP: p=0.001) patients when compared with the patients receiving lisinopril alone. Lisinopril 46-56 selenium binding protein 1 Homo sapiens 134-137 21980964-3 2011 RESULTS: The blood pressure (BP) control with lisinopril was reduced by concomitantly administered diclofenac sodium in non-diabetic (SBP: p=0.00002; DBP: p=0.000008) and diabetic (SBP: p=0.002; DBP: p=0.001) patients when compared with the patients receiving lisinopril alone. Lisinopril 46-56 D-box binding PAR bZIP transcription factor Homo sapiens 150-153 21980964-3 2011 RESULTS: The blood pressure (BP) control with lisinopril was reduced by concomitantly administered diclofenac sodium in non-diabetic (SBP: p=0.00002; DBP: p=0.000008) and diabetic (SBP: p=0.002; DBP: p=0.001) patients when compared with the patients receiving lisinopril alone. Lisinopril 46-56 selenium binding protein 1 Homo sapiens 181-184 21980964-3 2011 RESULTS: The blood pressure (BP) control with lisinopril was reduced by concomitantly administered diclofenac sodium in non-diabetic (SBP: p=0.00002; DBP: p=0.000008) and diabetic (SBP: p=0.002; DBP: p=0.001) patients when compared with the patients receiving lisinopril alone. Lisinopril 46-56 D-box binding PAR bZIP transcription factor Homo sapiens 195-198 21857085-7 2011 The most commonly prescribed ACE-Is were perindopril, lisinopril and chinalapril for inhibition of left ventricular hypertrophy and perindopril, ramipril and chinalapril for inhibition of arterial wall remodeling. Lisinopril 54-64 angiotensin I converting enzyme Homo sapiens 29-32 21857085-8 2011 The ACE-Is that were used to reduce peripheral vessel resistance included perindopril, lisinopril and trandolapril. Lisinopril 87-97 angiotensin I converting enzyme Homo sapiens 4-7 21155616-12 2011 CONCLUSION: In patients with hypertension and metabolic syndrome, manidipine, both alone and in combination with the ACE inhibitor lisinopril, is significantly superior to amlodipine for improving insulin sensitivity as well as several metabolic, inflammatory and prothrombotic markers. Lisinopril 131-141 angiotensin I converting enzyme Homo sapiens 117-120 19729213-10 2010 Sex, left cardiac work index, stroke index, hemoglobin, renal failure and discharge furosemide and lisinopril doses were associated to BNP only in univariate analysis. Lisinopril 99-109 natriuretic peptide B Homo sapiens 135-138 20634797-2 2010 We evaluated the hypothesis that in patients with chronic heart failure (CHF) and activated cardiac renin-angiotensin-aldosterone system (RAAS), lipophilic ACE inhibitors with high affinity for ACE (perindopril and quinapril) will cause marked blockade of cardiac angiotensin (Ang) II and aldosterone generation, but not a hydrophilic ACE inhibitor with low affinity for ACE (lisinopril). Lisinopril 376-386 angiotensin I converting enzyme Homo sapiens 194-197 20634797-2 2010 We evaluated the hypothesis that in patients with chronic heart failure (CHF) and activated cardiac renin-angiotensin-aldosterone system (RAAS), lipophilic ACE inhibitors with high affinity for ACE (perindopril and quinapril) will cause marked blockade of cardiac angiotensin (Ang) II and aldosterone generation, but not a hydrophilic ACE inhibitor with low affinity for ACE (lisinopril). Lisinopril 376-386 angiotensin I converting enzyme Homo sapiens 194-197 20634797-2 2010 We evaluated the hypothesis that in patients with chronic heart failure (CHF) and activated cardiac renin-angiotensin-aldosterone system (RAAS), lipophilic ACE inhibitors with high affinity for ACE (perindopril and quinapril) will cause marked blockade of cardiac angiotensin (Ang) II and aldosterone generation, but not a hydrophilic ACE inhibitor with low affinity for ACE (lisinopril). Lisinopril 376-386 angiotensin I converting enzyme Homo sapiens 156-159 20634797-2 2010 We evaluated the hypothesis that in patients with chronic heart failure (CHF) and activated cardiac renin-angiotensin-aldosterone system (RAAS), lipophilic ACE inhibitors with high affinity for ACE (perindopril and quinapril) will cause marked blockade of cardiac angiotensin (Ang) II and aldosterone generation, but not a hydrophilic ACE inhibitor with low affinity for ACE (lisinopril). Lisinopril 376-386 angiotensin I converting enzyme Homo sapiens 194-197 20854382-10 2010 During lisinopril treatment, urine-NGAL was reduced (95% CI) 17% (11-50) (not significant). Lisinopril 7-17 lipocalin 2 Homo sapiens 35-39 20854382-13 2010 The ACE inhibitor lisinopril reduced urine-NGAL, but this was not statistically significant. Lisinopril 18-28 angiotensin I converting enzyme Homo sapiens 4-7 20854382-13 2010 The ACE inhibitor lisinopril reduced urine-NGAL, but this was not statistically significant. Lisinopril 18-28 lipocalin 2 Homo sapiens 43-47 21235127-1 2010 AIM: Lisinopril is a drug of the angiotensin converting enzyme (ACE) inhibitor class that is primarily used in treatment of hypertension, congestive heart failure, heart attacks and also in preventing renal and retinal complications of diabetes. Lisinopril 5-15 angiotensin I converting enzyme Homo sapiens 33-62 21235127-1 2010 AIM: Lisinopril is a drug of the angiotensin converting enzyme (ACE) inhibitor class that is primarily used in treatment of hypertension, congestive heart failure, heart attacks and also in preventing renal and retinal complications of diabetes. Lisinopril 5-15 angiotensin I converting enzyme Homo sapiens 64-67 21219847-9 2010 12 months dual blockade of the renin-angiotensin system with candesartan and lisinopril reduced ambulatory PP levels compared with high-dose lisinopril monotherapy in hypertensive T2DM subjects. Lisinopril 77-87 renin Homo sapiens 31-36 20144153-0 2010 [Evaluation of long-term therapy influence with angiotensin converting enzyme inhibitor lisinopril on morphofunctional parameters of the left ventricle, peripheral artery endothelium disfunction and painless myocardial ischemia in premenopausal women with hypertension]. Lisinopril 88-98 angiotensin I converting enzyme Homo sapiens 48-77 20233165-0 2010 Characterization of domain-selective inhibitor binding in angiotensin-converting enzyme using a novel derivative of lisinopril. Lisinopril 116-126 angiotensin I converting enzyme Homo sapiens 58-87 20180641-5 2010 Lisinopril, an ACE inhibitor, is less hypotensive for transgenic mice than for control animals. Lisinopril 0-10 angiotensin I converting enzyme (peptidyl-dipeptidase A) 1 Mus musculus 15-18 20051877-6 2010 Lisinopril significantly decreases plasma MMP-2 level and cardiac iNOS mRNA expression by 13% and 15%, respectively, in group 3 compared with 36% and 47%, respectively, in group 4 as compared with group 2. Lisinopril 0-10 matrix metallopeptidase 2 Rattus norvegicus 42-47 20051877-6 2010 Lisinopril significantly decreases plasma MMP-2 level and cardiac iNOS mRNA expression by 13% and 15%, respectively, in group 3 compared with 36% and 47%, respectively, in group 4 as compared with group 2. Lisinopril 0-10 nitric oxide synthase 2 Rattus norvegicus 66-70 20051877-7 2010 In addition, compared with Dox group, lisinopril significantly increases plasma TIMP-1 level by 23% compared with 49% in group 4. Lisinopril 38-48 TIMP metallopeptidase inhibitor 1 Rattus norvegicus 80-86 20229187-5 2010 Activation of extracellular signal-regulated kinase 1 (ERK1) and 2 (ERK2), proliferative signaling markers, and proliferating cell nuclear antigen (PCNA), an end-point marker for proliferation, was reduced following chronic treatment with lisinopril compared to that in vehicle-treated PCK rats. Lisinopril 239-249 mitogen activated protein kinase 3 Rattus norvegicus 14-53 20229187-5 2010 Activation of extracellular signal-regulated kinase 1 (ERK1) and 2 (ERK2), proliferative signaling markers, and proliferating cell nuclear antigen (PCNA), an end-point marker for proliferation, was reduced following chronic treatment with lisinopril compared to that in vehicle-treated PCK rats. Lisinopril 239-249 mitogen activated protein kinase 3 Rattus norvegicus 55-59 20229187-5 2010 Activation of extracellular signal-regulated kinase 1 (ERK1) and 2 (ERK2), proliferative signaling markers, and proliferating cell nuclear antigen (PCNA), an end-point marker for proliferation, was reduced following chronic treatment with lisinopril compared to that in vehicle-treated PCK rats. Lisinopril 239-249 mitogen activated protein kinase 1 Rattus norvegicus 68-72 20229187-5 2010 Activation of extracellular signal-regulated kinase 1 (ERK1) and 2 (ERK2), proliferative signaling markers, and proliferating cell nuclear antigen (PCNA), an end-point marker for proliferation, was reduced following chronic treatment with lisinopril compared to that in vehicle-treated PCK rats. Lisinopril 239-249 proliferating cell nuclear antigen Rattus norvegicus 112-146 20229187-5 2010 Activation of extracellular signal-regulated kinase 1 (ERK1) and 2 (ERK2), proliferative signaling markers, and proliferating cell nuclear antigen (PCNA), an end-point marker for proliferation, was reduced following chronic treatment with lisinopril compared to that in vehicle-treated PCK rats. Lisinopril 239-249 proliferating cell nuclear antigen Rattus norvegicus 148-152 20229187-8 2010 Lisinopril treatment resulted in a significant reduction (P < 0.01) in cleaved caspase-7 levels, but not caspase-3 activity, in PCK rat kidneys compared to the vehicle-treated PCK rat kidneys. Lisinopril 0-10 caspase 7 Rattus norvegicus 82-91 20229187-9 2010 Proteinuria was completely ameliorated in the presence of chronic ACE inhibition in the lisinopril-treated rats compared with the vehicle-treated PCK rats. Lisinopril 88-98 angiotensin I converting enzyme Rattus norvegicus 66-69 20112435-8 2010 Predictors included: age, eGFR, diabetes, heart failure, potassium supplements, potassium-sparing diuretics, and a high dose for the ACE-inhibitor (lisinopril). Lisinopril 148-158 angiotensin I converting enzyme Homo sapiens 133-136 20086184-14 2010 Low-dose lisinopril or candesartan may be reasonable second- or third-line agents, particularly in patients with other indications for ACE inhibitor or ARB therapy. Lisinopril 9-19 angiotensin I converting enzyme Homo sapiens 135-138 20144153-1 2010 Aim of the study was to assess influence of long-term therapy with angiotensin converting enzyme inhibitor lisinopril on morphofunctional parameters of the left ventricle (LV) and painless myocardial ischemia in 109 premenopausal women with stage II hypertension depending on functional state of peripheral artery endothelium. Lisinopril 107-117 angiotensin I converting enzyme Homo sapiens 67-96 19502542-9 2009 In the intervention study, all doses of lisinopril significantly reduced urinary albumin excretion rate and U-LFABP from baseline. Lisinopril 40-50 fatty acid binding protein 1 Homo sapiens 110-115 19431100-8 2009 Lisinopril elevated LV function and appearance of the myocardium, decreased malondialdehyde levels without an influence on infarct size, and regulated the MMP-9 enzyme level but not the MMP-9 mRNA and TIMP-1 protein levels. Lisinopril 0-10 matrix metallopeptidase 9 Rattus norvegicus 155-160 19431100-8 2009 Lisinopril elevated LV function and appearance of the myocardium, decreased malondialdehyde levels without an influence on infarct size, and regulated the MMP-9 enzyme level but not the MMP-9 mRNA and TIMP-1 protein levels. Lisinopril 0-10 matrix metallopeptidase 9 Rattus norvegicus 186-191 19502542-10 2009 The reductions in U-LFABP were 43, 46, and 40% with increasing doses of lisinopril (NS). Lisinopril 72-82 fatty acid binding protein 1 Homo sapiens 20-25 19352213-12 2009 CONCLUSION: There was evidence of pharmacogenetic effects of FGB-455 on stroke, ESRD, and mortality, suggesting that relative to those homozygous for the common allele, variant allele carriers of the FGB gene at position -455 have a better outcome if randomized to lisinopril than chlorthalidone (for mortality and ESRD) or amlodipine (for mortality and stroke). Lisinopril 265-275 fibrinogen beta chain Homo sapiens 200-203 19462500-1 2009 OBJECTIVES: To investigate whether the combination of exercise training with the angiotensin-converting enzyme inhibitor lisinopril will have an additional beneficial effect on left ventricular function in spontaneously hypertensive rats. Lisinopril 121-131 angiotensin I converting enzyme Rattus norvegicus 81-110 19403313-2 2009 A new validated ACE inhibitors pharmacophore model (hypothesis) was generated for the first time in this research from the biologically active (frozen) conformation of Lisinopril-Human ACE complex that was downloaded from PDB, using stepwise technique of CATALYST modules. Lisinopril 168-178 angiotensin I converting enzyme Homo sapiens 16-19 19403313-2 2009 A new validated ACE inhibitors pharmacophore model (hypothesis) was generated for the first time in this research from the biologically active (frozen) conformation of Lisinopril-Human ACE complex that was downloaded from PDB, using stepwise technique of CATALYST modules. Lisinopril 168-178 angiotensin I converting enzyme Homo sapiens 185-188 18234362-16 2009 However, the groups were different in using ACE inhibitors with a negative correlation (r=-0.45, p=0.04) between the MCR and lisinopril-equivalent ACE inhibitor dose. Lisinopril 125-135 angiotensin I converting enzyme Homo sapiens 44-47 18825420-11 2009 We conclude that the efficacy and safety of lisinopril is seemingly acceptable for the treatment of children with mild IgA-N. Lisinopril 44-54 IGAN1 Homo sapiens 119-124 19164508-3 2009 MWF rats with advanced nephropathy were studied at both 40 weeks and after 20 weeks of observation either with or without treatment with the ACE inhibitor lisinopril. Lisinopril 155-165 angiotensin I converting enzyme Rattus norvegicus 141-144 19164508-8 2009 Surprisingly, lisinopril not only halted age-related podocyte loss but also increased the number of glomerular podocytes above baseline, which was associated with an increased number of proliferating Wilms tumor 1-positive cells, loss of cyclin-dependent kinase inhibitor p27 expression, and increased number of parietal podocytes. Lisinopril 14-24 cyclin-dependent kinase inhibitor 1B Rattus norvegicus 272-275 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). Lisinopril 272-282 angiotensin I converting enzyme Homo sapiens 98-101 18234362-16 2009 However, the groups were different in using ACE inhibitors with a negative correlation (r=-0.45, p=0.04) between the MCR and lisinopril-equivalent ACE inhibitor dose. Lisinopril 125-135 angiotensin I converting enzyme Homo sapiens 147-150 20201315-6 2009 The lisinopril intake 5 mg a day declines PPG by 18,1%. Lisinopril 4-14 serglycin Homo sapiens 42-45 19293598-12 2009 The antiproteinuric effects of lisinopril and prednisone were achieved at least partially by restoring VEGF protein and nephrin phosphorylation. Lisinopril 31-41 vascular endothelial growth factor A Rattus norvegicus 103-107 20017344-3 2009 Group 1 included 75 patients who received ACE inhibitor lisinopril (10 mg BID) after recovery of sinus rhythm by propanorm. Lisinopril 56-66 angiotensin I converting enzyme Homo sapiens 42-45 19293598-9 2009 The intervention of prednisone and lisinopril evidently reduced proteinuria, effectively attenuated the severe lesions of podocyte foot processes, and restored the reduction in VEGF and nephrin phosphorylation. Lisinopril 35-45 vascular endothelial growth factor A Rattus norvegicus 177-181 19257863-3 2009 Hydrophilic angiotensin converting enzyme inhibitors (ACEI) (lisinopril) which are not metabolized in the liver are theoretically safest in liver cirrhosis. Lisinopril 61-71 angiotensin I converting enzyme Homo sapiens 12-41 19293598-12 2009 The antiproteinuric effects of lisinopril and prednisone were achieved at least partially by restoring VEGF protein and nephrin phosphorylation. Lisinopril 31-41 NPHS1 adhesion molecule, nephrin Rattus norvegicus 120-127 19293598-9 2009 The intervention of prednisone and lisinopril evidently reduced proteinuria, effectively attenuated the severe lesions of podocyte foot processes, and restored the reduction in VEGF and nephrin phosphorylation. Lisinopril 35-45 NPHS1 adhesion molecule, nephrin Rattus norvegicus 186-193 18496146-5 2008 Central infusion of lisinopril caused 70% inhibition of brain ACE and minimal (6%) inhibition in the kidneys. Lisinopril 20-30 angiotensin I converting enzyme Rattus norvegicus 62-65 19108791-2 2008 OBJECTIVE: The aim of this randomized, double-blind, placebo-controlled, crossover study was to quantify the combined effect of a beta-blocker (atenolol) and an ACE inhibitor (lisinopril) in lowering BP. Lisinopril 176-186 angiotensin I converting enzyme Homo sapiens 161-164 19108791-9 2008 CONCLUSIONS: The combination of the beta-blocker atenolol 25 mg plus the ACE inhibitor lisinopril 5 mg was associated with a significantly greater decrease in BP compared with either alone. Lisinopril 87-97 angiotensin I converting enzyme Homo sapiens 73-76 18713951-10 2008 Statistically significant, but very low currents were only observed for lisinopril, enalapril, quinapril, and benazepril at PEPT1 and for spirapril at PEPT2. Lisinopril 72-82 solute carrier family 15 member 1 Homo sapiens 124-129 18496513-2 2008 Here we examined the effect of chronic renal dysfunction induced by uninephrectomy on fat redistribution and lipid peroxidation in rats treated with an angiotensin-converting enzyme (ACE) inhibitor (lisinopril) for up to 10 months. Lisinopril 199-209 angiotensin I converting enzyme Rattus norvegicus 152-181 18496513-2 2008 Here we examined the effect of chronic renal dysfunction induced by uninephrectomy on fat redistribution and lipid peroxidation in rats treated with an angiotensin-converting enzyme (ACE) inhibitor (lisinopril) for up to 10 months. Lisinopril 199-209 angiotensin I converting enzyme Rattus norvegicus 183-186 20641953-14 2004 In this regard, a compound with high affinity for ACE, such as lisinopril or its derivative, would be best suited to study the expression of a radiotracer. Lisinopril 63-73 angiotensin I converting enzyme Homo sapiens 50-53 20641953-15 2004 Several derivatives of lisinopril that can incorporate rhodium or palladium while maintaining high affinity for ACE were reported and could probably be used to synthesize radiolabeled analogs of the compound (18). Lisinopril 23-33 angiotensin I converting enzyme Homo sapiens 112-115 18695719-4 2008 Lisinopril did not affect the amidase activities of FS enzymes, but stimulated Glu-plasminogen and u-PA activation and inhibited activation of t-PA-fibrin-bound Glu-plasminogen ([I]50 (12.0 +/- 0.5) mM). Lisinopril 0-10 plasminogen activator, urokinase Homo sapiens 99-103 18695719-4 2008 Lisinopril did not affect the amidase activities of FS enzymes, but stimulated Glu-plasminogen and u-PA activation and inhibited activation of t-PA-fibrin-bound Glu-plasminogen ([I]50 (12.0 +/- 0.5) mM). Lisinopril 0-10 plasminogen activator, tissue type Homo sapiens 143-147 19021699-4 2008 MATERIALS AND METHODS: The binding affinity of telmisartan, valsartan, lisinopril, rosiglitazone and angiotensin II to PPARgamma was assessed in a cell-free assay system. Lisinopril 71-81 peroxisome proliferator activated receptor gamma Homo sapiens 119-128 19021699-7 2008 RESULTS: The binding affinity to PPARgamma was highest for telmisartan with a half-maximal effective concentration of 463 nM, followed by lisinopril (2.9 microM) and valsartan (6.2 microM). Lisinopril 138-148 peroxisome proliferator activated receptor gamma Homo sapiens 33-42 19021699-10 2008 The release of visfatin from adipocytes was 1.6-fold increased after treatment with lisinopril and about 2.0-fold increased with telmisartan and valsartan. Lisinopril 84-94 nicotinamide phosphoribosyltransferase Homo sapiens 15-23 19021699-12 2008 CONCLUSIONS: Our data confirm agonism of telmisartan, valsartan and lisinopril on PPARgamma. Lisinopril 68-78 peroxisome proliferator activated receptor gamma Homo sapiens 82-91 19238723-1 2008 Lisinopril, an angiotensin converting enzyme (ACE) inhibitor drug, was encapsulated in poly(lactide-co-glicolide) (PLGA) nanoparticles (NP) for site-specific delivery by catheters in prevention of restenosis. Lisinopril 0-10 angiotensin I converting enzyme Homo sapiens 15-44 19238723-1 2008 Lisinopril, an angiotensin converting enzyme (ACE) inhibitor drug, was encapsulated in poly(lactide-co-glicolide) (PLGA) nanoparticles (NP) for site-specific delivery by catheters in prevention of restenosis. Lisinopril 0-10 angiotensin I converting enzyme Homo sapiens 46-49 18084312-5 2008 In the presence of lisinopril (ACE inhibitor), but not candoxatril (NEP inhibitor) or apstatin (APP inhibitor), bradykinin also elicited hypotension. Lisinopril 19-29 angiotensin I converting enzyme Rattus norvegicus 31-34 17932766-0 2008 Captopril and lisinopril decrease acetaldehyde effects upon the prothrombin time. Lisinopril 14-24 coagulation factor II, thrombin Homo sapiens 64-75 17932766-1 2008 Captopril, a thiol-containing antihypertensive drug, and lisinopril, an amino-containing antihypertensive drug, will both prolong the prothrombin time (PT) of Level I plasma. Lisinopril 57-67 coagulation factor II, thrombin Homo sapiens 134-145 18192334-6 2008 Lisinopril significantly reduced renal ACE activity without affecting renal ACE2 activity. Lisinopril 0-10 angiotensin I converting enzyme Rattus norvegicus 39-42 18192334-9 2008 Plasma Ang(1-7) and Ang II balance is positively shifted towards the beneficial vasopeptide Ang(1-7) by the ACE inhibitor lisinopril, especially during a low sodium intake. Lisinopril 122-132 angiogenin Rattus norvegicus 7-14 18192334-9 2008 Plasma Ang(1-7) and Ang II balance is positively shifted towards the beneficial vasopeptide Ang(1-7) by the ACE inhibitor lisinopril, especially during a low sodium intake. Lisinopril 122-132 angiogenin Rattus norvegicus 92-99 18192334-9 2008 Plasma Ang(1-7) and Ang II balance is positively shifted towards the beneficial vasopeptide Ang(1-7) by the ACE inhibitor lisinopril, especially during a low sodium intake. Lisinopril 122-132 angiotensin I converting enzyme Rattus norvegicus 108-111 18500778-1 2008 Two trace impurities in the bulk drug lisinopril were detected by means of high-performance liquid chromatography coupled with mass spectrometry (HPLC/MS) with a simple and sensitive method suitable for HPLC/MSn analysis. Lisinopril 38-48 moesin Homo sapiens 208-211 18483087-0 2008 Synthesis and evaluation of a series of 99mTc(CO)3+ lisinopril complexes for in vivo imaging of angiotensin-converting enzyme expression. Lisinopril 52-62 angiotensin I converting enzyme Homo sapiens 96-125 18483087-5 2008 Uptake in the lungs, a tissue that constitutively expresses ACE, was 15.2 percentage injected dose per gram at 10 min after injection and was dramatically reduced by pretreatment with lisinopril, supporting ACE-mediated binding in vivo. Lisinopril 184-194 angiotensin I converting enzyme Homo sapiens 60-63 18483087-5 2008 Uptake in the lungs, a tissue that constitutively expresses ACE, was 15.2 percentage injected dose per gram at 10 min after injection and was dramatically reduced by pretreatment with lisinopril, supporting ACE-mediated binding in vivo. Lisinopril 184-194 angiotensin I converting enzyme Homo sapiens 207-210 18483087-7 2008 Thus, high-affinity 99mTc-labeled ACE inhibitor has been designed with potency similar to that of lisinopril and has been demonstrated to specifically localize to tissues that express ACE in vivo. Lisinopril 98-108 angiotensin I converting enzyme Homo sapiens 34-37 18084312-5 2008 In the presence of lisinopril (ACE inhibitor), but not candoxatril (NEP inhibitor) or apstatin (APP inhibitor), bradykinin also elicited hypotension. Lisinopril 19-29 kininogen 1 Homo sapiens 112-122 17913836-7 2008 Moreover, 240 nM basolateral lisinopril decreased baseline (i.e., at 5% CO(2)) J(HCO(3)) by one-half and completely eliminated the response to altering [CO(2)](BL) from 0 to 20%, but left intact the stimulatory effect of 10(-11) M basolateral ANG II. Lisinopril 29-39 angiogenin, ribonuclease, RNase A family, 5 Mus musculus 243-246 18335653-2 2008 While ACE inhibitors have been shown to elicit psoriatic erythroderma in previous cases, to our knowledge this is the first case report of iatrogenic erythroderma secondary to lisinopril in a patient without dermatologic comorbidities. Lisinopril 176-186 angiotensin I converting enzyme Homo sapiens 6-9 17913836-9 2008 Our data are consistent with the hypothesis that lisinopril readily crosses the basolateral (but not apical) membrane to block ACE in a vesicular compartment. Lisinopril 49-59 angiotensin-converting enzyme Oryctolagus cuniculus 127-130 17884087-3 2007 Compared with the lisinopril-MMP-9 model in our previous study, imidapril was stabilized effectively on the active site with less of molecular distortions. Lisinopril 18-28 matrix metallopeptidase 9 Homo sapiens 29-34 18491582-1 2008 AIM: To assess efficacy of monotherapy with ACE inhibitor lisinopril (diroton) or calcium antagonist amlodipine (normodipine) and their combination in patients with metabolic syndrome (MS). Lisinopril 58-68 angiotensin I converting enzyme Homo sapiens 44-47 19105412-1 2008 AIM: To examine antihypertensive activity, heart rate variability (HRV) and carbohydrate metabolism of ACE inhibitor lisinopril in patients with metabolic syndrome (MS). Lisinopril 117-127 angiotensin I converting enzyme Homo sapiens 103-106 17884087-4 2007 We also measured ACE and MMP-9 inhibitory activities of imidapril and lisinopril after myocardial infarction. Lisinopril 70-80 matrix metallopeptidase 9 Homo sapiens 25-30 17884087-6 2007 These findings show that imidapril inhibits MMP-9 directly like lisinopril and its hydrophobic interactions with the S1 site of MMP-9 would be important for enhancing inhibitory activity. Lisinopril 64-74 matrix metallopeptidase 9 Homo sapiens 44-49 17962170-9 2007 Mrs. S"s medical history is significant for moderate obesity and hypertension for 10 years, which is controlled with the angiotensin converting enzyme inhibitor lisinopril. Lisinopril 161-171 angiotensin I converting enzyme Homo sapiens 121-150 17676311-10 2007 CONCLUSIONS/INTERPRETATION: We have shown in vivo that vascular tissue AI to AII conversion gradually increases over time in patients with type 2 diabetes being treated with lisinopril. Lisinopril 174-184 angiotensinogen Homo sapiens 71-73 17676311-10 2007 CONCLUSIONS/INTERPRETATION: We have shown in vivo that vascular tissue AI to AII conversion gradually increases over time in patients with type 2 diabetes being treated with lisinopril. Lisinopril 174-184 angiotensinogen Homo sapiens 77-80 17889307-5 2007 Selected animals were also treated with the angiotensin-converting enzyme (ACE) inhibitor lisinopril (3 mg/l in diet) for 6 weeks. Lisinopril 90-100 angiotensin I converting enzyme Rattus norvegicus 75-78 17329864-5 2007 PH induced the expression of hepatocyte growth factor (HGF) mRNA in remnant liver, and this PH-induced up-regulation of HGF mRNA was further enhanced not only by lisinopril but also by candesartan and losartan. Lisinopril 162-172 hepatocyte growth factor Rattus norvegicus 29-53 17512521-0 2007 Inhibition of matrix metalloproteinase-9 activity by lisinopril after myocardial infarction in hamsters. Lisinopril 53-63 matrix metallopeptidase 9 Homo sapiens 14-40 17512521-4 2007 Lisinopril significantly inhibited both angiotensin-converting enzyme and matrix metalloproteinase-9 activities, but candesartan cilexetil did not. Lisinopril 0-10 matrix metallopeptidase 9 Homo sapiens 74-100 17636698-10 2007 Treatment with either captopril, enalapril or lisinopril reduced albumin excretion rate in comparison with control patients.A significantly greater lowering of blood pressure was experienced by initially normotensive patients in the angiotensin converting enzyme inhibitor than in the placebo group. Lisinopril 46-56 angiotensin I converting enzyme Homo sapiens 233-262 17320031-5 2007 The specificity of the activity was demonstrated by the complete inhibition of the hydrolysis by the ACE inhibitor lisinopril. Lisinopril 115-125 angiotensin-converting enzyme Cricetulus griseus 101-104 17184180-1 2007 Lisinopril is an inhibitor of the renin-angiotensin system. Lisinopril 0-10 renin Homo sapiens 34-39 17184180-3 2007 The authors note that lisinopril contained lipid peroxidation, elevated tissue glutathione levels, and influenced the activity of antioxidant enzymes such as catalase and glutathione peroxidase. Lisinopril 22-32 catalase Homo sapiens 158-166 17639718-2 2007 The specific inhibitors lisinopril (ACE) and thiorphan (NEP) were used for identification of these enzyme activities, Lisinopril 24-34 angiotensin I converting enzyme Homo sapiens 36-39 17308006-6 2007 In vitro incubation with captopril, lisinopril, or quinapril significantly reduced MMP-2 activity, as did in vivo treatment. Lisinopril 36-46 matrix metallopeptidase 2 Rattus norvegicus 83-88 17458439-10 2007 During the 10 years between his initial episode of angioedema and the second, he had not developed any secondary medical conditions, and he had been taking the ACE inhibitor lisinopril for 7 years. Lisinopril 174-184 angiotensin I converting enzyme Homo sapiens 160-163 17275782-1 2007 To characterize the inhibitory specificity of angiotensin converting enzyme (ACE) inhibitors for matrix metalloproteinase 9 (MMP-9) activity, molecular modeling of these complex was performed referring the recent X-ray structure analyses using lisinopril as an ACE inhibitor. Lisinopril 244-254 angiotensin I converting enzyme Homo sapiens 46-75 17275782-1 2007 To characterize the inhibitory specificity of angiotensin converting enzyme (ACE) inhibitors for matrix metalloproteinase 9 (MMP-9) activity, molecular modeling of these complex was performed referring the recent X-ray structure analyses using lisinopril as an ACE inhibitor. Lisinopril 244-254 angiotensin I converting enzyme Homo sapiens 77-80 17275782-1 2007 To characterize the inhibitory specificity of angiotensin converting enzyme (ACE) inhibitors for matrix metalloproteinase 9 (MMP-9) activity, molecular modeling of these complex was performed referring the recent X-ray structure analyses using lisinopril as an ACE inhibitor. Lisinopril 244-254 matrix metallopeptidase 9 Homo sapiens 97-123 17275782-1 2007 To characterize the inhibitory specificity of angiotensin converting enzyme (ACE) inhibitors for matrix metalloproteinase 9 (MMP-9) activity, molecular modeling of these complex was performed referring the recent X-ray structure analyses using lisinopril as an ACE inhibitor. Lisinopril 244-254 matrix metallopeptidase 9 Homo sapiens 125-130 17275782-3 2007 Lisinopril was effectively stabilized by specific hydrogen bonds and hydrophobic interactions in the active site of MMP-9, and its hydrophobic group appeared to interact preferentially with the S1 site compared with the S1" site. Lisinopril 0-10 matrix metallopeptidase 9 Homo sapiens 116-121 17329864-5 2007 PH induced the expression of hepatocyte growth factor (HGF) mRNA in remnant liver, and this PH-induced up-regulation of HGF mRNA was further enhanced not only by lisinopril but also by candesartan and losartan. Lisinopril 162-172 hepatocyte growth factor Rattus norvegicus 55-58 17329864-5 2007 PH induced the expression of hepatocyte growth factor (HGF) mRNA in remnant liver, and this PH-induced up-regulation of HGF mRNA was further enhanced not only by lisinopril but also by candesartan and losartan. Lisinopril 162-172 hepatocyte growth factor Rattus norvegicus 120-123 17329864-6 2007 Administration of icatibant inhibited up to 40% of the lisinopril-induced up-regulation of HGF mRNA. Lisinopril 55-65 hepatocyte growth factor Rattus norvegicus 91-94 17926488-5 2007 The study found a decrease in the frequency of VLP detection from 40% (8 patients) to 10% (2 patients) after therapy with the ACE inhibitor lisinopril. Lisinopril 140-150 angiotensin I converting enzyme Homo sapiens 126-129 17268012-6 2007 RESULTS: There was specific binding of FBL to ACE; mean FBL binding was 6.6 +/- 5.2 PSL/mm2, compared with 3.4 +/- 2.5 PSL/mm2 in segments incubated in solution containing cold, 10(-6) M lisinopril (P < 0.0001). Lisinopril 187-197 fibrillarin Homo sapiens 39-42 17268012-6 2007 RESULTS: There was specific binding of FBL to ACE; mean FBL binding was 6.6 +/- 5.2 PSL/mm2, compared with 3.4 +/- 2.5 PSL/mm2 in segments incubated in solution containing cold, 10(-6) M lisinopril (P < 0.0001). Lisinopril 187-197 angiotensin I converting enzyme Homo sapiens 46-49 18389599-0 2007 [Correction of portal hypertension by beta-adrenoblockers (atenolol and metoprolol) and inhibitors of ACE (lisinopril and enalapril) in liver cirrhosis]. Lisinopril 107-117 angiotensin I converting enzyme Homo sapiens 102-105 17926488-7 2007 In the group receiving bi-component therapy with lisinopril, an ACE inhibitor, and nifedipine, a calcium antagonist, the number of patients with VLP fell from 4 subjects (28.6%) to 1 subject. Lisinopril 49-59 angiotensin I converting enzyme Homo sapiens 64-67 16766648-3 2006 The control of blood pressure elicited by 12-day administration of either lisinopril (mean difference change = 92 +/- 2, P < 0.05) or losartan (mean difference change = 69 +/- 2, P < 0.05) was associated with 54% and 33% increases in cardiac ACE2 mRNA and 54% and 43% increases in cardiac ACE mRNA, respectively. Lisinopril 74-84 angiotensin I converting enzyme 2 Rattus norvegicus 242-246 16766648-3 2006 The control of blood pressure elicited by 12-day administration of either lisinopril (mean difference change = 92 +/- 2, P < 0.05) or losartan (mean difference change = 69 +/- 2, P < 0.05) was associated with 54% and 33% increases in cardiac ACE2 mRNA and 54% and 43% increases in cardiac ACE mRNA, respectively. Lisinopril 74-84 angiotensin I converting enzyme Rattus norvegicus 242-245 16342299-6 2006 Inclusion of Perindopril into the essential drug list resulted in an overall increase in utilization of ACE inhibitors: use of captopril and enalapril declined while lisinopril and perindopril increased. Lisinopril 166-176 angiotensin I converting enzyme Homo sapiens 104-107 16766648-4 2006 Lisinopril induced a 3.1-fold (P < 0.05) increase in renal cortical expression of ACE2, whereas losartan increased ACE2 mRNA 3.5-fold (P < 0.05). Lisinopril 0-10 angiotensin I converting enzyme 2 Rattus norvegicus 82-86 16945058-3 2006 This report describes a case of acute compromise of renal function associated with hypotension in a 7-year-old boy treated with the ACE inhibitor lisinopril and the ARB losartan. Lisinopril 146-156 angiotensin I converting enzyme Homo sapiens 132-135 16784843-1 2006 With a view to developing a more C-domain-selective angiotensin I-converting enzyme (ACE)-inhibitor, a novel analogue of lisinopril has been synthesized which incorporates a bulky P(2)(") tryptophan functionality. Lisinopril 121-131 angiotensin I converting enzyme Homo sapiens 52-83 16784843-1 2006 With a view to developing a more C-domain-selective angiotensin I-converting enzyme (ACE)-inhibitor, a novel analogue of lisinopril has been synthesized which incorporates a bulky P(2)(") tryptophan functionality. Lisinopril 121-131 angiotensin I converting enzyme Homo sapiens 85-88 16981424-10 2006 Based on the above evidence, the fixed-dose combination of the CCB-ACE inhibitor (amlodipine-lisinopril) has not only effective blood pressure reducing properties, but also results in cardiovascular risk reduction, good tolerability and favourable compliance. Lisinopril 93-103 angiotensin I converting enzyme Homo sapiens 67-70 16574603-1 2006 The role of ACE inhibitors (Lisinopril) in reproductive function remains controversial. Lisinopril 28-38 angiotensin I converting enzyme Rattus norvegicus 12-15 16807546-4 2006 In the second, lisinopril-infused rats were infused with either Ang II or vehicle. Lisinopril 15-25 angiotensinogen Rattus norvegicus 64-70 16284359-4 2006 Therefore, the current study investigated the ability of lisinopril, an angiotensin-converting enzyme (ACE) inhibitor, to modulate oxidative stress in the lung after chronic EtOH ingestion in a well-established rat model. Lisinopril 57-67 angiotensin I converting enzyme Rattus norvegicus 72-101 16458281-5 2006 The antifibrotic effect of lisinopril has shown to be due to inhibition of synthesis of angiotensin II that causes stimulation of fibroblast proliferation and collagen synthesis. Lisinopril 27-37 angiotensinogen Rattus norvegicus 88-102 16458281-15 2006 CONCLUSION: The antifibrotic effect of lisinopril may be due to inhibition of angiotensin II or proline moiety, which is a common structural in all ACEI, drugs. Lisinopril 39-49 angiotensinogen Rattus norvegicus 78-92 16636307-9 2006 With the intervention of lisinopril, prednisone, and ATRA, changes in the expression of nephrin, podocin, and CD2AP were diverse, which was different from that detected in ADR rats. Lisinopril 25-35 NPHS1 adhesion molecule, nephrin Rattus norvegicus 88-95 16636307-9 2006 With the intervention of lisinopril, prednisone, and ATRA, changes in the expression of nephrin, podocin, and CD2AP were diverse, which was different from that detected in ADR rats. Lisinopril 25-35 NPHS2 stomatin family member, podocin Rattus norvegicus 97-104 16636307-9 2006 With the intervention of lisinopril, prednisone, and ATRA, changes in the expression of nephrin, podocin, and CD2AP were diverse, which was different from that detected in ADR rats. Lisinopril 25-35 CD2-associated protein Rattus norvegicus 110-115 16636307-10 2006 After lisinopril and prednisone intervention, podocin exhibited prominent earlier changes compared with those of nephrin and CD2AP, whereas CD2AP showed more prominent changes after ATRA intervention. Lisinopril 6-16 NPHS2 stomatin family member, podocin Rattus norvegicus 46-53 16636307-12 2006 In summary, we conclude that the antiproteinuric effects of lisinopril, prednisone, and ATRA were achieved by changes in the expression and distribution of the important podocyte molecules nephrin, podocin, CD2AP, and alpha-actinin-4. Lisinopril 60-70 NPHS1 adhesion molecule, nephrin Rattus norvegicus 189-196 16636307-12 2006 In summary, we conclude that the antiproteinuric effects of lisinopril, prednisone, and ATRA were achieved by changes in the expression and distribution of the important podocyte molecules nephrin, podocin, CD2AP, and alpha-actinin-4. Lisinopril 60-70 NPHS2 stomatin family member, podocin Rattus norvegicus 198-205 16636307-12 2006 In summary, we conclude that the antiproteinuric effects of lisinopril, prednisone, and ATRA were achieved by changes in the expression and distribution of the important podocyte molecules nephrin, podocin, CD2AP, and alpha-actinin-4. Lisinopril 60-70 CD2-associated protein Rattus norvegicus 207-212 16636307-12 2006 In summary, we conclude that the antiproteinuric effects of lisinopril, prednisone, and ATRA were achieved by changes in the expression and distribution of the important podocyte molecules nephrin, podocin, CD2AP, and alpha-actinin-4. Lisinopril 60-70 actinin alpha 4 Rattus norvegicus 218-233 16564798-1 2006 PURPOSE: To analyze the effect of angiotensin-converting enzyme (ACE) inhibitor lisinopril on inflammatory cystoid macular edema and visual acuity. Lisinopril 80-90 angiotensin I converting enzyme Homo sapiens 65-68 16395266-11 2006 Lisinopril normalized baseline glomerular transforming growth factor-beta and alpha-smooth muscle actin overexpression, and prevented worsening of interstitial changes. Lisinopril 0-10 actin gamma 2, smooth muscle Rattus norvegicus 78-103 16564798-1 2006 PURPOSE: To analyze the effect of angiotensin-converting enzyme (ACE) inhibitor lisinopril on inflammatory cystoid macular edema and visual acuity. Lisinopril 80-90 angiotensin I converting enzyme Homo sapiens 34-63 16284359-10 2006 Chronic EtOH ingestion also increased the levels of the NADPH oxidase subunit, gp91phox, an effect that was attenuated by lisinopril, but had no effect on lung p22phox or p47phox levels. Lisinopril 122-132 cytochrome b-245 beta chain Rattus norvegicus 79-87 16284359-4 2006 Therefore, the current study investigated the ability of lisinopril, an angiotensin-converting enzyme (ACE) inhibitor, to modulate oxidative stress in the lung after chronic EtOH ingestion in a well-established rat model. Lisinopril 57-67 angiotensin I converting enzyme Rattus norvegicus 103-106 16148376-3 2005 The goal of the investigation was the evaluation of the efficacy of combined treatment of AF with Cordaron and ACE inhibitor Diroton (lizinopril) (D) in patients with chronic heart failure (CHF). Lisinopril 125-132 angiotensin I converting enzyme Homo sapiens 111-114 17047617-0 2006 [Clinico-metabolic and anti-ischemic effects of angiotensin converting enzyme inhibitor lisinopril and its role in the process of left ventricular remodeling in patients with diabetic heart]. Lisinopril 88-98 angiotensin I converting enzyme Homo sapiens 48-77 16033330-4 2005 We demonstrate here that a 1:1 stoichiometry for the binding of the common ACE inhibitors, captopril and lisinopril, to human s-ACE is enough to abolish enzymatic activity towards FA {N-[3-(2-furyl)acryloyl]}-Phe-GlyGly, Cbz (benzyloxycarbonyl)-Phe-His-Leu or Hip (N-benzoylglycyl)-His-Leu. Lisinopril 105-115 angiotensin I converting enzyme Homo sapiens 75-78 16033330-4 2005 We demonstrate here that a 1:1 stoichiometry for the binding of the common ACE inhibitors, captopril and lisinopril, to human s-ACE is enough to abolish enzymatic activity towards FA {N-[3-(2-furyl)acryloyl]}-Phe-GlyGly, Cbz (benzyloxycarbonyl)-Phe-His-Leu or Hip (N-benzoylglycyl)-His-Leu. Lisinopril 105-115 angiotensin I converting enzyme Homo sapiens 128-131 16221218-1 2005 BACKGROUND: Angiotensin-converting enzyme (ACE)2, a homologue of ACE, which is insensitive to ACE inhibitors and forms angiotensin-(1-7) [Ang-(1-7)] from angiotensin II (Ang II) with high efficiency was investigated in response to chronic blockade with lisinopril, losartan, and both drugs combined. Lisinopril 253-263 angiotensin I converting enzyme Rattus norvegicus 12-41 16221218-1 2005 BACKGROUND: Angiotensin-converting enzyme (ACE)2, a homologue of ACE, which is insensitive to ACE inhibitors and forms angiotensin-(1-7) [Ang-(1-7)] from angiotensin II (Ang II) with high efficiency was investigated in response to chronic blockade with lisinopril, losartan, and both drugs combined. Lisinopril 253-263 angiotensin I converting enzyme 2 Rattus norvegicus 43-48 16221218-1 2005 BACKGROUND: Angiotensin-converting enzyme (ACE)2, a homologue of ACE, which is insensitive to ACE inhibitors and forms angiotensin-(1-7) [Ang-(1-7)] from angiotensin II (Ang II) with high efficiency was investigated in response to chronic blockade with lisinopril, losartan, and both drugs combined. Lisinopril 253-263 angiotensin I converting enzyme Rattus norvegicus 43-46 16221218-1 2005 BACKGROUND: Angiotensin-converting enzyme (ACE)2, a homologue of ACE, which is insensitive to ACE inhibitors and forms angiotensin-(1-7) [Ang-(1-7)] from angiotensin II (Ang II) with high efficiency was investigated in response to chronic blockade with lisinopril, losartan, and both drugs combined. Lisinopril 253-263 angiotensin I converting enzyme Rattus norvegicus 65-68 16221218-1 2005 BACKGROUND: Angiotensin-converting enzyme (ACE)2, a homologue of ACE, which is insensitive to ACE inhibitors and forms angiotensin-(1-7) [Ang-(1-7)] from angiotensin II (Ang II) with high efficiency was investigated in response to chronic blockade with lisinopril, losartan, and both drugs combined. Lisinopril 253-263 angiogenin Rattus norvegicus 138-146 16221218-1 2005 BACKGROUND: Angiotensin-converting enzyme (ACE)2, a homologue of ACE, which is insensitive to ACE inhibitors and forms angiotensin-(1-7) [Ang-(1-7)] from angiotensin II (Ang II) with high efficiency was investigated in response to chronic blockade with lisinopril, losartan, and both drugs combined. Lisinopril 253-263 angiotensinogen Rattus norvegicus 170-176 16221218-8 2005 Lisinopril augmented plasma levels and urinary excretion rates of Ang I and Ang-(1-7), while plasma Ang II was reduced with no effect on urinary Ang II. Lisinopril 0-10 angiogenin Rattus norvegicus 76-84 16221218-10 2005 Combination therapy mimicked the effects obtained with lisinopril on plasma and urinary Ang I and Ang-(1-7) levels. Lisinopril 55-65 angiogenin Rattus norvegicus 98-106 16221218-11 2005 Renal cortex Aogen mRNA increased in rats medicated with either lisinopril or the combination, whereas all three treatments produced a robust increase in renal renin mRNA. Lisinopril 64-74 angiotensinogen Rattus norvegicus 13-18 16221218-13 2005 Renal cortex ACE2 activity was significantly augmented in rats medicated with lisinopril or losartan but not changed in those given the combination. Lisinopril 78-88 angiotensin I converting enzyme 2 Rattus norvegicus 13-17 15908476-8 2005 In parallel, lisinopril treatment limited TGF-beta1 protein release into the alveolar space during endotoxemia. Lisinopril 13-23 transforming growth factor, beta 1 Rattus norvegicus 42-51 15908024-1 2005 The present study was aimed to investigate the effect of ACE inhibition on trinitrobenzene sulphonic acid (TNBS)-induced colonic inflammation in rats by using captopril and lisinopril. Lisinopril 173-183 angiotensin I converting enzyme Rattus norvegicus 57-60 16124935-6 2005 ACE inhibitor, Lisinopril (Zestril(r)), was prescribed in combination with Moduretic(r), Calcium channel blocker and beta-blocker in 6.5%, 8.5% and 0.7% respectively. Lisinopril 15-25 angiotensin I converting enzyme Homo sapiens 0-3 16124935-6 2005 ACE inhibitor, Lisinopril (Zestril(r)), was prescribed in combination with Moduretic(r), Calcium channel blocker and beta-blocker in 6.5%, 8.5% and 0.7% respectively. Lisinopril 27-34 angiotensin I converting enzyme Homo sapiens 0-3 16114794-1 2005 We report a case of a 46-year-old white male with renal graft artery stenosis who developed acute renal shutdown with total anuria while on the ACE inhibitor lisinopril, one week following the discontinuation of aspirin. Lisinopril 158-168 angiotensin I converting enzyme Homo sapiens 144-147 16321616-5 2005 At trough, the systolic blood pressure response to exogenous angiotensin I was 58% +/- 19% with 20 mg lisinopril (mean +/- SD), 58% +/- 11% with 20 mg olmesartan medoxomil, 62% +/- 16% with 40 mg olmesartan medoxomil, and 76% +/- 12% with the highest dose of olmesartan medoxomil (80 mg) (P = .016 versus 20 mg lisinopril and P = .0015 versus 20 mg olmesartan medoxomil). Lisinopril 102-112 angiotensinogen Homo sapiens 61-74 16321616-5 2005 At trough, the systolic blood pressure response to exogenous angiotensin I was 58% +/- 19% with 20 mg lisinopril (mean +/- SD), 58% +/- 11% with 20 mg olmesartan medoxomil, 62% +/- 16% with 40 mg olmesartan medoxomil, and 76% +/- 12% with the highest dose of olmesartan medoxomil (80 mg) (P = .016 versus 20 mg lisinopril and P = .0015 versus 20 mg olmesartan medoxomil). Lisinopril 311-321 angiotensinogen Homo sapiens 61-74 15869762-7 2005 While no treatment was given to rats in group 1, Lisinopril (an ACE inhibitor) was given to rats in group 2 and group 3 for post-operative 7 days in drinking water at 50 and 5 mg/l concentrations, respectively. Lisinopril 49-59 angiotensin I converting enzyme Rattus norvegicus 64-67 15908024-10 2005 On the other hand, although stimulation of lipid peroxidation and increase in serum TNF-alpha level were successfully prevented by lisinopril, the morphology of the lesions remained unchanged. Lisinopril 131-141 tumor necrosis factor Rattus norvegicus 84-93 16307311-1 2005 Crystal structures of angiotensin-converting enzyme (ACE) complexed with three inhibitors (lisinopril, captopril, enalapril) provided experimental data for testing the validity of a prior active site model predicting the bound conformation of the inhibitors. Lisinopril 91-101 angiotensin I converting enzyme Homo sapiens 22-51 16307311-1 2005 Crystal structures of angiotensin-converting enzyme (ACE) complexed with three inhibitors (lisinopril, captopril, enalapril) provided experimental data for testing the validity of a prior active site model predicting the bound conformation of the inhibitors. Lisinopril 91-101 angiotensin I converting enzyme Homo sapiens 53-56 16148376-3 2005 The goal of the investigation was the evaluation of the efficacy of combined treatment of AF with Cordaron and ACE inhibitor Diroton (lizinopril) (D) in patients with chronic heart failure (CHF). Lisinopril 134-144 angiotensin I converting enzyme Homo sapiens 111-114 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. Lisinopril 87-97 angiotensin I converting enzyme Homo sapiens 71-74 15933779-8 2005 ACE activity in lung, heart and kidney homogenates, but not in liver homogenates, was completely abolished by 0.5 microM lisinopril or captopril. Lisinopril 121-131 angiotensin I converting enzyme Homo sapiens 0-3 15889206-1 2005 A 76-year-old woman with acute myocardial infarction underwent percutaneous coronary angioplasty followed by treatment with an angiotensin-converting enzyme (ACE) inhibitor, lisinopril. Lisinopril 174-184 angiotensin I converting enzyme Homo sapiens 127-156 15889206-1 2005 A 76-year-old woman with acute myocardial infarction underwent percutaneous coronary angioplasty followed by treatment with an angiotensin-converting enzyme (ACE) inhibitor, lisinopril. Lisinopril 174-184 angiotensin I converting enzyme Homo sapiens 158-161 15836856-9 2005 Although no treatment was given to rats in group 1, lisinopril (an ACE inhibitor) was given to rats in group 2 for postoperative 7 days in drinking water. Lisinopril 52-62 angiotensin I converting enzyme Rattus norvegicus 67-70 16091636-7 2005 The use of lisinopril during initial hospitalization was associated with elevation of catalase activity, lowering of creatinine and elimination of proteinuria. Lisinopril 11-21 catalase Homo sapiens 86-94 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. Lisinopril 53-63 angiotensin-converting enzyme Sus scrofa 110-113 16514812-7 2005 Compared to captopril, administration of lisinopril in hospital increased catalase activity, lowered blood creatinine, eliminated protein in the urine. Lisinopril 41-51 catalase Homo sapiens 74-82 14644762-7 2004 The effect of lisinopril was prevented by pretreatment with a bradykinin antagonist (HOE-130) and dichloroisocoumarine, an inhibitor of kinine-forming enzymes. Lisinopril 14-24 kininogen 1 Homo sapiens 62-72 15499219-9 2004 CONCLUSION: MMF and the ACE inhibitor lisinopril attenuated the progression of the fibrogenic process of UUO in an equivalent manner. Lisinopril 38-48 angiotensin I converting enzyme Rattus norvegicus 24-27 14769834-4 2004 In NEP-inhibited rats, extravasation produced by the ACE inhibitors captopril and lisinopril was markedly enhanced. Lisinopril 82-92 membrane metallo-endopeptidase Rattus norvegicus 3-6 14769834-4 2004 In NEP-inhibited rats, extravasation produced by the ACE inhibitors captopril and lisinopril was markedly enhanced. Lisinopril 82-92 angiotensin I converting enzyme Rattus norvegicus 53-56 15311107-7 2004 Lisinopril, omapatrilat and irbesartan inhibited this increase of angiotensin II, but had no effect on angiotensin I levels. Lisinopril 0-10 angiotensinogen Rattus norvegicus 66-80 14614522-10 2003 However, an interaction between the ACE inhibitor and spironolactone potentiating the effects of either drug alone was observed with a lower dose of spironolactone (lisinopril and 8 mg.kg-1.day-1 spironolactone). Lisinopril 165-175 angiotensin I converting enzyme Rattus norvegicus 36-39 15850766-3 2004 The results of ALLHAT showed that the diuretic chlorthalidone, the CCB amlodipine, and the ACE inhibitor lisinopril were equally effective in preventing the primary outcome-fatal coronary heart disease or nonfatal myocardial infarction. Lisinopril 105-115 angiotensin I converting enzyme Homo sapiens 91-94 14695037-1 2003 STUDY OBJECTIVE: As the results of the Heart Outcomes Prevention Evaluation trial suggested that patients with both coronary artery disease (CAD) and diabetes mellitus would benefit from angiotensin-converting enzyme (ACE) inhibitor therapy, our objective was to increase the percentage of patients with both of these conditions receiving the goal dosage (20 mg/day) or highest tolerated dosage of the ACE inhibitor lisinopril through intervention of a clinical pharmacy service. Lisinopril 416-426 angiotensin I converting enzyme Homo sapiens 218-221 15106813-6 2004 RESULTS: Lisinopril dose-dependently reduced ACE activity in control and TGF-beta1-treated cardiac fibroblasts. Lisinopril 9-19 angiotensin I converting enzyme Rattus norvegicus 45-48 15106813-6 2004 RESULTS: Lisinopril dose-dependently reduced ACE activity in control and TGF-beta1-treated cardiac fibroblasts. Lisinopril 9-19 transforming growth factor, beta 1 Rattus norvegicus 73-82 15106813-9 2004 TGF-beta1 (600 pmol/l) increased (P < 0.05) the production of soluble and non-soluble collagen, and this effect was decreased (P < 0.05) by lisinopril. Lisinopril 146-156 transforming growth factor, beta 1 Rattus norvegicus 0-9 14609329-5 2003 The model explains why the classical ACE inhibitor lisinopril is unable to bind to ACE2. Lisinopril 51-61 angiotensin I converting enzyme Homo sapiens 37-40 14597946-8 2003 CONCLUSIONS: This study shows a comparable effect of ACE inhibition (lisinopril) and of AT1 receptor antagonism (valsartan) on cardiac vagal control of heart rate, whereas valsartan has shown a more effective modulation of sympathetic activity measured by plasma norepinephrine levels. Lisinopril 69-79 angiotensin I converting enzyme Homo sapiens 53-56 12911535-0 2003 Combining lisinopril and l-arginine slows disease progression and reduces endothelin-1 in passive Heymann nephritis. Lisinopril 10-20 endothelin 1 Rattus norvegicus 74-86 12911535-14 2003 Exaggerated urinary ET-1 of PHN was reduced by 23% and 40% after l-arginine and lisinopril, respectively, and by 62% with the combination. Lisinopril 80-90 endothelin 1 Rattus norvegicus 20-24 12901857-0 2003 Structural basis of the lisinopril-binding specificity in N- and C-domains of human somatic ACE. Lisinopril 24-34 angiotensin I converting enzyme Homo sapiens 92-95 12935891-5 2003 However, active site titration with lisinopril assayed by hydrolysis of FA-Phe-Gly-Gly revealed that 1 mol of inhibitor/mol of enzyme abolished the activity of either two-domain or single-domain ACE forms, indicating that a single active site functions in bovine somatic ACE. Lisinopril 36-46 angiotensin I converting enzyme Bos taurus 195-198 12935891-5 2003 However, active site titration with lisinopril assayed by hydrolysis of FA-Phe-Gly-Gly revealed that 1 mol of inhibitor/mol of enzyme abolished the activity of either two-domain or single-domain ACE forms, indicating that a single active site functions in bovine somatic ACE. Lisinopril 36-46 angiotensin I converting enzyme Bos taurus 271-274 12901857-2 2003 The present work describes the molecular modeling of the N-terminal human somatic ACE in complex with the inhibitor lisinopril, identifying the residues involved in the inhibitor-binding pocket. Lisinopril 116-126 angiotensin I converting enzyme Homo sapiens 82-85 12824823-7 2003 RESULTS: TNF-alpha-induced cytotoxicity, but not angiotensin II-induced cytotoxicity, was prevented by lisinopril, indicating that de novo angiotensin II synthesis is required for TNF-alpha-induced apoptosis in these cells. Lisinopril 103-113 tumor necrosis factor Rattus norvegicus 9-18 12636872-7 2003 During treatment with the ACE inhibitor lisinopril, proteinuria was lowered by 79+/-9% (mean+/-S.E.M.). Lisinopril 40-50 angiotensin I converting enzyme Rattus norvegicus 26-29 12824823-7 2003 RESULTS: TNF-alpha-induced cytotoxicity, but not angiotensin II-induced cytotoxicity, was prevented by lisinopril, indicating that de novo angiotensin II synthesis is required for TNF-alpha-induced apoptosis in these cells. Lisinopril 103-113 angiotensinogen Rattus norvegicus 139-153 12816171-10 2003 The high-dose lisinopril group also had lower heart failure hospital costs (dollars 5114 vs dollars 6361, P = .006) but higher ACE inhibitor drug costs (dollars 1368 vs dollars 855, P = .0001). Lisinopril 14-24 angiotensin I converting enzyme Homo sapiens 127-130 12586636-8 2003 The ANG-converting enyzme (ACE) inhibitor lisinopril inhibited the maximal response to ANG I in AA and muscular EA by 75 +/- 9% (n = 13) and 70 +/- 7% (n = 13), respectively, but had no effect in thin EA (n = 14). Lisinopril 42-52 angiotensin I converting enzyme Rattus norvegicus 4-25 12586636-8 2003 The ANG-converting enyzme (ACE) inhibitor lisinopril inhibited the maximal response to ANG I in AA and muscular EA by 75 +/- 9% (n = 13) and 70 +/- 7% (n = 13), respectively, but had no effect in thin EA (n = 14). Lisinopril 42-52 angiotensin I converting enzyme Rattus norvegicus 27-30 12676181-4 2003 However, AT(1) receptor binding was significantly higher in the prostate of the TG rat treated with the ACE inhibitor lisinopril compared to the untreated TG rat and comparable to the control SD rat. Lisinopril 118-128 angiotensin I converting enzyme Rattus norvegicus 104-107 24944377-3 2003 Another widely used combination of ACE inhibitor and diuretic is lisinopril plus hydrochlorothiazide (L + H). Lisinopril 65-75 angiotensin I converting enzyme Homo sapiens 35-38 12714865-7 2003 RESULTS: When all patients were considered, lisinopril provided higher values of TPR [0.63/0.66 for systolic/diastolic blood pressure (SBP/DBP)], MER (1.02/0.77) and SI (1.01/0.87) than losartan (0.35/0.51, 0.60/0.60 and 0.64/0.53, respectively). Lisinopril 44-54 selenium binding protein 1 Homo sapiens 135-138 12714865-7 2003 RESULTS: When all patients were considered, lisinopril provided higher values of TPR [0.63/0.66 for systolic/diastolic blood pressure (SBP/DBP)], MER (1.02/0.77) and SI (1.01/0.87) than losartan (0.35/0.51, 0.60/0.60 and 0.64/0.53, respectively). Lisinopril 44-54 D-box binding PAR bZIP transcription factor Homo sapiens 139-142 12507898-7 2003 In diabetic Ren-2, vascular endothelial growth factor (VEGF) and VEGFR-2 mRNA were increased in retinae and irides and reduced with LIS. Lisinopril 132-135 kinase insert domain receptor Rattus norvegicus 65-72 12671898-2 2003 We assessed the effects of lisinopril, an angiotensin-converting enzyme (ACE) inhibitor, on spontaneously occurring chronic pancreatitis. Lisinopril 27-37 angiotensin I converting enzyme Rattus norvegicus 42-71 12671898-2 2003 We assessed the effects of lisinopril, an angiotensin-converting enzyme (ACE) inhibitor, on spontaneously occurring chronic pancreatitis. Lisinopril 27-37 angiotensin I converting enzyme Rattus norvegicus 73-76 12671898-6 2003 Lisinopril significantly reduced serum ACE activity but it did not affect pancreatic activity. Lisinopril 0-10 angiotensin I converting enzyme Rattus norvegicus 39-42 12671898-7 2003 High doses of lisinopril suppressed the overexpression of TGF-beta1 mRNA measured by reverse-transcription polymerase chain reaction (RT-PCR) and decreased the number of alpha-SMA-positive cells (activated pancreatic stellate cells) in the pancreas. Lisinopril 14-24 transforming growth factor, beta 1 Rattus norvegicus 58-67 12671898-7 2003 High doses of lisinopril suppressed the overexpression of TGF-beta1 mRNA measured by reverse-transcription polymerase chain reaction (RT-PCR) and decreased the number of alpha-SMA-positive cells (activated pancreatic stellate cells) in the pancreas. Lisinopril 14-24 actin gamma 2, smooth muscle Rattus norvegicus 170-179 12540854-0 2003 Crystal structure of the human angiotensin-converting enzyme-lisinopril complex. Lisinopril 61-71 angiotensin I converting enzyme Homo sapiens 31-60 12540854-4 2003 Here we present the X-ray structure of human testicular ACE and its complex with one of the most widely used inhibitors, lisinopril (N2-[(S)-1-carboxy-3-phenylpropyl]-L-lysyl-L-proline; also known as Prinivil or Zestril), at 2.0 A resolution. Lisinopril 121-131 angiotensin I converting enzyme Homo sapiens 56-59 12540854-4 2003 Here we present the X-ray structure of human testicular ACE and its complex with one of the most widely used inhibitors, lisinopril (N2-[(S)-1-carboxy-3-phenylpropyl]-L-lysyl-L-proline; also known as Prinivil or Zestril), at 2.0 A resolution. Lisinopril 133-184 angiotensin I converting enzyme Homo sapiens 56-59 12540854-4 2003 Here we present the X-ray structure of human testicular ACE and its complex with one of the most widely used inhibitors, lisinopril (N2-[(S)-1-carboxy-3-phenylpropyl]-L-lysyl-L-proline; also known as Prinivil or Zestril), at 2.0 A resolution. Lisinopril 200-208 angiotensin I converting enzyme Homo sapiens 56-59 12540854-4 2003 Here we present the X-ray structure of human testicular ACE and its complex with one of the most widely used inhibitors, lisinopril (N2-[(S)-1-carboxy-3-phenylpropyl]-L-lysyl-L-proline; also known as Prinivil or Zestril), at 2.0 A resolution. Lisinopril 212-219 angiotensin I converting enzyme Homo sapiens 56-59 12507898-7 2003 In diabetic Ren-2, vascular endothelial growth factor (VEGF) and VEGFR-2 mRNA were increased in retinae and irides and reduced with LIS. Lisinopril 132-135 vascular endothelial growth factor A Rattus norvegicus 19-53 12507898-7 2003 In diabetic Ren-2, vascular endothelial growth factor (VEGF) and VEGFR-2 mRNA were increased in retinae and irides and reduced with LIS. Lisinopril 132-135 vascular endothelial growth factor A Rattus norvegicus 55-59 12566371-3 2003 METHODS AND RESULTS: In this longitudinal study, we evaluated the extent to which uptitration of the ACE inhibitor lisinopril to maximum tolerated doses (median [range]: 30 [10 to 40] mg/d) ameliorated proteinuria and dyslipidemia in 28 patients with nondiabetic chronic nephropathies. Lisinopril 115-125 angiotensin I converting enzyme Homo sapiens 101-104 14734829-3 2003 Because angiotensin II has been implicated in the progression of other cardiomyopathies, this investigation was undertaken to determine whether treatment with an angiotensinconverting enzyme (ACE) inhibitor, lisinopril, reduces the time-dependent effects of doxorubicin on cardiac gene expression and myocellular apoptosis. Lisinopril 208-218 angiotensin-converting enzyme Oryctolagus cuniculus 192-195 14989248-0 2003 [Pharmacoeconomical aspects of the use of angiotensin converting enzyme inhibitors in clinical practice (lisinopril use)]. Lisinopril 105-115 angiotensin I converting enzyme Homo sapiens 42-71 14520846-1 2003 AIM: To study the data of 24-h monitoring of blood pressure (MBP) and effects of an ACE inhibitor lisinopril (diroton) in hypertensive patients with polycythemia vera (PV). Lisinopril 98-108 angiotensin I converting enzyme Homo sapiens 84-87 14520846-1 2003 AIM: To study the data of 24-h monitoring of blood pressure (MBP) and effects of an ACE inhibitor lisinopril (diroton) in hypertensive patients with polycythemia vera (PV). Lisinopril 110-117 angiotensin I converting enzyme Homo sapiens 84-87 12381651-8 2002 Lisinopril inhibited MMP-9 significantly but did not inhibit MMP-2 in vitro (IC50 MMP-2: 7.4 (0.88); MMP-9: 7.86 (2.23)). Lisinopril 0-10 matrix metallopeptidase 9 Homo sapiens 21-26 12444164-4 2002 Neutralization of TGFbeta1 by anti-TGFbeta1 or lisinopril resulted in less collagen deposition and less accumulation of myofibroblasts, and levels of active TGFbeta1 and ACE were reduced in thyroids of treated mice compared with those of untreated controls. Lisinopril 47-57 transforming growth factor, beta 1 Mus musculus 18-26 12444164-5 2002 Other profibrotic molecules, such as platelet-derived growth factor, monocyte chemotactic protein-1, and IL-13, were also reduced in thyroids of anti-TGFbeta1- and lisinopril-treated mice compared with those of controls. Lisinopril 164-174 chemokine (C-C motif) ligand 2 Mus musculus 69-99 12444164-5 2002 Other profibrotic molecules, such as platelet-derived growth factor, monocyte chemotactic protein-1, and IL-13, were also reduced in thyroids of anti-TGFbeta1- and lisinopril-treated mice compared with those of controls. Lisinopril 164-174 interleukin 13 Mus musculus 105-110 12410850-5 2002 Several ACE inhibitors (such as captopril, enalapril and lisinopril) are dialyzable, whereas all of the AIIAs studied are not. Lisinopril 57-67 angiotensin I converting enzyme Homo sapiens 8-11 12372680-0 2002 Antihypertensive effects of angiotensin converting enzyme inhibition by lisinopril in post-transplant patients. Lisinopril 72-82 angiotensin I converting enzyme Homo sapiens 28-57 12421219-3 2002 CASE REPORT: A patient with mitomycin-associated hemolytic-uremic syndrome received SPA treatments after her ACE inhibitor, lisinopril, was held. Lisinopril 124-134 surfactant protein A1 Homo sapiens 84-87 12421219-3 2002 CASE REPORT: A patient with mitomycin-associated hemolytic-uremic syndrome received SPA treatments after her ACE inhibitor, lisinopril, was held. Lisinopril 124-134 angiotensin I converting enzyme Homo sapiens 109-112 12421219-4 2002 Lisinopril was restarted before her 18th SPA treatment, and immediately after return of treated plasma she developed facial redness and hypotension, which resolved after the return stopped and recurred when restarted. Lisinopril 0-10 surfactant protein A1 Homo sapiens 41-44 12652106-5 2002 High doses of the angiotensin-converting enzyme (ACE) inhibitor lisinopril in patients with heart failure have been shown to significantly reduce the risk of death or hospitalization for heart failure and for any reason. Lisinopril 64-74 angiotensin I converting enzyme Homo sapiens 18-47 12191747-13 2002 CONCLUSIONS: Contrary to expectation, the aerobic exercise capacity of patients was found to be greater with the lower dose of lisinopril, suggesting that therapy with ACE inhibitors for heart failure may require tailoring the doses to the individual to optimize functional benefits in relation to the assumed prognostic benefits. Lisinopril 127-137 angiotensin I converting enzyme Homo sapiens 168-171 12140727-3 2002 In the EUCLID Study, the angiotensin converting enzyme (ACE) inhibitor lisinopril reduced the risk of progression of retinopathy by approximately 50%, and also significantly reduced the risk of progression to proliferative retinopathy. Lisinopril 71-81 angiotensin I converting enzyme Homo sapiens 25-54 12140727-3 2002 In the EUCLID Study, the angiotensin converting enzyme (ACE) inhibitor lisinopril reduced the risk of progression of retinopathy by approximately 50%, and also significantly reduced the risk of progression to proliferative retinopathy. Lisinopril 71-81 angiotensin I converting enzyme Homo sapiens 56-59 12138278-8 2002 Also, the level of gene expression of transforming growth factor-beta (TGF-beta) and plasminogen activator inhibitor-1 (PAI-1) in the renal cortex were reduced, suggesting that lisinopril improved extracellular matrix (ECM) metabolism. Lisinopril 177-187 transforming growth factor, beta 1 Rattus norvegicus 71-79 12138278-8 2002 Also, the level of gene expression of transforming growth factor-beta (TGF-beta) and plasminogen activator inhibitor-1 (PAI-1) in the renal cortex were reduced, suggesting that lisinopril improved extracellular matrix (ECM) metabolism. Lisinopril 177-187 serpin family E member 1 Rattus norvegicus 85-118 12138278-8 2002 Also, the level of gene expression of transforming growth factor-beta (TGF-beta) and plasminogen activator inhibitor-1 (PAI-1) in the renal cortex were reduced, suggesting that lisinopril improved extracellular matrix (ECM) metabolism. Lisinopril 177-187 serpin family E member 1 Rattus norvegicus 120-125 12138278-10 2002 Suppression of TGF-beta and PAI-1 expression contributed to the preventive effect of lisinopril on ECM deposition in renal tissue. Lisinopril 85-95 transforming growth factor, beta 1 Rattus norvegicus 15-23 12138278-10 2002 Suppression of TGF-beta and PAI-1 expression contributed to the preventive effect of lisinopril on ECM deposition in renal tissue. Lisinopril 85-95 serpin family E member 1 Rattus norvegicus 28-33 12384621-8 2002 CONCLUSIONS: ACE-inhibitors (lisinopril) or alternatively the use of angiotensin II receptor antagonists, like Iosartan at low doses, is an effective and safe treatment for patients developing post-transplantation erythrocytosis (PTE). Lisinopril 29-39 angiotensin I converting enzyme Homo sapiens 13-16 12103269-0 2002 Differential effects of the angiotensin-converting enzyme inhibitor lisinopril versus the beta-adrenergic receptor blocker atenolol on hemodynamics and left ventricular contractile function in experimental mitral regurgitation. Lisinopril 68-78 angiotensin I converting enzyme Homo sapiens 28-57 12103269-5 2002 Three months after the creation, the ACE inhibitor lisinopril 20 mg was given orally daily. Lisinopril 51-61 angiotensin I converting enzyme Homo sapiens 37-40 12652106-5 2002 High doses of the angiotensin-converting enzyme (ACE) inhibitor lisinopril in patients with heart failure have been shown to significantly reduce the risk of death or hospitalization for heart failure and for any reason. Lisinopril 64-74 angiotensin I converting enzyme Homo sapiens 49-52 12652106-15 2002 Sensitivity analysis shows that the use of high doses of ACE inhibitor lisinopril does not result in higher health care expenditures for the whole system or even savings through a wide variety of practice patterns and unit costs. Lisinopril 71-81 angiotensin I converting enzyme Homo sapiens 57-60 12051731-9 2002 Immunoreactive AT1-R was detected mainly on the neovascularized vascular endothelial cells in which expression was reduced by TCV-116 and lisinopril. Lisinopril 138-148 angiotensin II, type I receptor-associated protein Mus musculus 15-20 12138046-2 2002 My physician initially prescribed lisinopril, an angiotensin-converting enzyme (ACE) inhibitor. Lisinopril 34-44 angiotensin I converting enzyme Homo sapiens 49-78 12138046-2 2002 My physician initially prescribed lisinopril, an angiotensin-converting enzyme (ACE) inhibitor. Lisinopril 34-44 angiotensin I converting enzyme Homo sapiens 80-83 11967013-17 2002 Up-regulation of monocyte chemoattractant protein-1 (MCP-1) mRNA in PHN kidneys was not affected by lisinopril, it was inhibited by 30% after simvastatin, and almost completely normalized by lisinopril plus simvastatin. Lisinopril 191-201 C-C motif chemokine ligand 2 Rattus norvegicus 17-51 12070465-8 2002 CONCLUSIONS: ACE-inhibitors (lisinopril) or alternatively the use of angiotensin II receptor antagonists, like Losartan, at low doses, is an effective and safe treatment for patients developing post-transplantation erythrocytosis (PTE). Lisinopril 29-39 angiotensin I converting enzyme Homo sapiens 13-16 11967013-17 2002 Up-regulation of monocyte chemoattractant protein-1 (MCP-1) mRNA in PHN kidneys was not affected by lisinopril, it was inhibited by 30% after simvastatin, and almost completely normalized by lisinopril plus simvastatin. Lisinopril 191-201 C-C motif chemokine ligand 2 Rattus norvegicus 53-58 11939620-7 2002 Blocking insulin"s increase in LPR by pyruvate (0.5 mmol/L) or oxaloacetate (0.5 mmol/L) completely inhibited the insulin-stimulated component of cGMP production. Lisinopril 31-34 insulin Canis lupus familiaris 9-16 11869839-0 2002 Gradual reactivation over time of vascular tissue angiotensin I to angiotensin II conversion during chronic lisinopril therapy in chronic heart failure. Lisinopril 108-118 angiotensinogen Homo sapiens 50-63 11869839-0 2002 Gradual reactivation over time of vascular tissue angiotensin I to angiotensin II conversion during chronic lisinopril therapy in chronic heart failure. Lisinopril 108-118 angiotensinogen Homo sapiens 67-81 11869839-5 2002 METHODS: Vascular AI/AII conversion was studied in patients with chronic heart failure (CHF) taking chronic lisinopril therapy by the differential infusion of AI and AII into the brachial artery. Lisinopril 108-118 NLR family pyrin domain containing 3 Homo sapiens 18-24 11869839-5 2002 METHODS: Vascular AI/AII conversion was studied in patients with chronic heart failure (CHF) taking chronic lisinopril therapy by the differential infusion of AI and AII into the brachial artery. Lisinopril 108-118 NLR family pyrin domain containing 3 Homo sapiens 21-24 11869839-8 2002 A third study examined whether increasing the dose of lisinopril affected subsequent vascular ACE inhibition. Lisinopril 54-64 angiotensin I converting enzyme Homo sapiens 94-97 11939620-7 2002 Blocking insulin"s increase in LPR by pyruvate (0.5 mmol/L) or oxaloacetate (0.5 mmol/L) completely inhibited the insulin-stimulated component of cGMP production. Lisinopril 31-34 insulin Canis lupus familiaris 114-121 11673247-3 2001 The FAPGG hydrolysis was decreased by 82.5% and 67.5% by EDTA and dithioerythritol, respectively, and was totally inhibited by specific ACE inhibitors such as captopril, P-Glu-Trp-Pro-Arg-Pro-Glu-Ile-Pro-Pro, and lisinopril. Lisinopril 213-223 angiotensin I converting enzyme Homo sapiens 136-139 11872207-0 2002 Effect of hypertension therapy with the angiotensin-converting enzyme inhibitor lisinopril on hyperandrogenism in women with polycystic ovary syndrome. Lisinopril 80-90 angiotensin I converting enzyme Homo sapiens 40-69 11872207-1 2002 OBJECTIVE: To investigate the effect of an angiotensin-converting enzyme inhibitor, lisinopril, on serum androgen and sex-hormone-binding globulin (SHBG) levels in hypertensive women with polycystic ovary syndrome (PCOS). Lisinopril 84-94 angiotensin I converting enzyme Homo sapiens 43-72 11872207-1 2002 OBJECTIVE: To investigate the effect of an angiotensin-converting enzyme inhibitor, lisinopril, on serum androgen and sex-hormone-binding globulin (SHBG) levels in hypertensive women with polycystic ovary syndrome (PCOS). Lisinopril 84-94 sex hormone binding globulin Homo sapiens 118-146 11872207-1 2002 OBJECTIVE: To investigate the effect of an angiotensin-converting enzyme inhibitor, lisinopril, on serum androgen and sex-hormone-binding globulin (SHBG) levels in hypertensive women with polycystic ovary syndrome (PCOS). Lisinopril 84-94 sex hormone binding globulin Homo sapiens 148-152 11872207-9 2002 CONCLUSION(S): Use of lisinopril, an angiotensin-converting enzyme inhibitor, results in decreased free T levels independently of SHBG. Lisinopril 22-32 angiotensin I converting enzyme Homo sapiens 37-66 11872207-9 2002 CONCLUSION(S): Use of lisinopril, an angiotensin-converting enzyme inhibitor, results in decreased free T levels independently of SHBG. Lisinopril 22-32 sex hormone binding globulin Homo sapiens 130-134 11824589-1 2002 In order to simulate the in vivo binding behavior of angiotensin-converting enzyme (ACE) inhibitors to the zinc-containing active center of ACE, the in vitro interaction between lisinopril and zinc or nickel ions was investigated in aqueous solutions of different pH by using attenuated total reflection (ATR)/Fourier transform infrared (FT-IR) spectroscopy with second-derivative IR spectral analysis. Lisinopril 178-188 angiotensin I converting enzyme Homo sapiens 53-82 11824589-1 2002 In order to simulate the in vivo binding behavior of angiotensin-converting enzyme (ACE) inhibitors to the zinc-containing active center of ACE, the in vitro interaction between lisinopril and zinc or nickel ions was investigated in aqueous solutions of different pH by using attenuated total reflection (ATR)/Fourier transform infrared (FT-IR) spectroscopy with second-derivative IR spectral analysis. Lisinopril 178-188 angiotensin I converting enzyme Homo sapiens 84-87 11824589-1 2002 In order to simulate the in vivo binding behavior of angiotensin-converting enzyme (ACE) inhibitors to the zinc-containing active center of ACE, the in vitro interaction between lisinopril and zinc or nickel ions was investigated in aqueous solutions of different pH by using attenuated total reflection (ATR)/Fourier transform infrared (FT-IR) spectroscopy with second-derivative IR spectral analysis. Lisinopril 178-188 angiotensin I converting enzyme Homo sapiens 140-143 11604391-4 2001 The inhibition of aggregation was specifically blocked by preincubation of ACE with an ACE inhibitor, lisinopril. Lisinopril 102-112 angiotensin I converting enzyme Homo sapiens 75-78 11604391-4 2001 The inhibition of aggregation was specifically blocked by preincubation of ACE with an ACE inhibitor, lisinopril. Lisinopril 102-112 angiotensin I converting enzyme Homo sapiens 87-90 11989672-1 2001 The liquid membrane phenomenon in angiotensin converting enzyme (ACE) inhibitors namely, captopril and lisinopril has been studied. Lisinopril 103-113 angiotensin I converting enzyme Homo sapiens 34-63 11989672-1 2001 The liquid membrane phenomenon in angiotensin converting enzyme (ACE) inhibitors namely, captopril and lisinopril has been studied. Lisinopril 103-113 angiotensin I converting enzyme Homo sapiens 65-68 11963285-8 2002 Following ACE inhibition by lisinopril, BNP and sodium plasma levels rose, but BNP values remained significantly lower than the initial ones. Lisinopril 28-38 angiotensin I converting enzyme Homo sapiens 10-13 11929321-16 2002 Lisinopril is the only ACE inhibitor that exhibits a linear dose-response curve. Lisinopril 0-10 angiotensin I converting enzyme Homo sapiens 23-26 12435880-0 2002 Protein kinase C beta isoenzymes in diabetic kidneys and their relation to nephroprotective actions of the ACE inhibitor lisinopril. Lisinopril 121-131 protein kinase C, beta Rattus norvegicus 0-21 12435880-0 2002 Protein kinase C beta isoenzymes in diabetic kidneys and their relation to nephroprotective actions of the ACE inhibitor lisinopril. Lisinopril 121-131 angiotensin I converting enzyme Rattus norvegicus 107-110 12435880-2 2002 We investigated the influence of streptozotocin (STZ)-induced diabetes mellitus and of treatment with the ACE inhibitor lisinopril (4 mg/kg p.o. Lisinopril 120-130 angiotensin I converting enzyme Rattus norvegicus 106-109 12435880-6 2002 Lisinopril lowered renocortical albumin content and proteinuria in STZ diabetes and attenuated the enhanced accumulation of macrophages expressing PKC beta 2 as well as the increase of membrane-associated expression of PKC beta 1 and PKC beta 2 in the renal cortex. Lisinopril 0-10 protein kinase C, beta Rattus norvegicus 147-155 12435880-6 2002 Lisinopril lowered renocortical albumin content and proteinuria in STZ diabetes and attenuated the enhanced accumulation of macrophages expressing PKC beta 2 as well as the increase of membrane-associated expression of PKC beta 1 and PKC beta 2 in the renal cortex. Lisinopril 0-10 protein kinase C, beta Rattus norvegicus 219-227 12435880-6 2002 Lisinopril lowered renocortical albumin content and proteinuria in STZ diabetes and attenuated the enhanced accumulation of macrophages expressing PKC beta 2 as well as the increase of membrane-associated expression of PKC beta 1 and PKC beta 2 in the renal cortex. Lisinopril 0-10 protein kinase C, beta Rattus norvegicus 219-227 12435880-7 2002 The data suggest that the nephroprotective actions of the ACE inhibitor lisinopril in experimental diabetes mellitus were associated with and thus could be mediated in part by inhibition of diabetes-induced activation of PKC beta isoenzymes in the renal cortex. Lisinopril 72-82 angiotensin I converting enzyme Rattus norvegicus 58-61 12435880-7 2002 The data suggest that the nephroprotective actions of the ACE inhibitor lisinopril in experimental diabetes mellitus were associated with and thus could be mediated in part by inhibition of diabetes-induced activation of PKC beta isoenzymes in the renal cortex. Lisinopril 72-82 protein kinase C, beta Rattus norvegicus 221-229 11468543-4 2001 The aim of the present study was to compare the effect of an angiotensin converting enzyme (ACE) inhibitor (lisinopril) with a calcium channel blocker (CCB) (controlled release nifedipine) in treatment of posttransplant hypertension focusing on changes in LVH. Lisinopril 108-118 angiotensin I converting enzyme Homo sapiens 61-90 11845579-0 2001 [Reversible impairment of renal function during treatment with lisinopril, an ACE-inhibitor (case report)]. Lisinopril 63-73 angiotensin I converting enzyme Homo sapiens 78-81 11845579-2 2001 New members of this group of drugs are developed and registered and today in Croatia exist a dozen ACE inhibitors from different pharmaceutical companies like lisinopril, cilazapril, ramipril, trandolapril, enalapril etc. Lisinopril 159-169 angiotensin I converting enzyme Homo sapiens 99-102 11845579-4 2001 The aim of the article was to present a 72 year old patient with reversible impairment of renal function during treatment with ACE inhibitor lisinopril. Lisinopril 141-151 angiotensin I converting enzyme Homo sapiens 127-130 11811369-5 2001 A significant improvement in endothelial dysfunction may be observed in hypertensive patients after prolonged treatment with ACE inhibitors (cilazapril, lisinopril), calcium entry blockers (nifedipine), and angiotensin II receptor blockers (losartan), while atenolol and hydrochlorotiazide proved to be ineffective in this regard despite similar blood pressure reductions. Lisinopril 153-163 angiotensin I converting enzyme Homo sapiens 125-128 11468543-4 2001 The aim of the present study was to compare the effect of an angiotensin converting enzyme (ACE) inhibitor (lisinopril) with a calcium channel blocker (CCB) (controlled release nifedipine) in treatment of posttransplant hypertension focusing on changes in LVH. Lisinopril 108-118 angiotensin I converting enzyme Homo sapiens 92-95 11563960-1 2001 The interaction of three forms of bovine angiotensin-converting enzyme (ACE) with the competitive peptide inhibitor lisinopril with a fluorescent label was studied using fluorescence polarization. Lisinopril 116-126 angiotensin I converting enzyme Bos taurus 72-75 11410114-12 2001 The mechanism could be either that lisinopril limits the angiotensin II-induced production of superoxide radicals which would normally inactivate NO, or that lisinopril may increase bradykinin-mediated NO release. Lisinopril 35-45 angiotensinogen Homo sapiens 57-71 11410114-12 2001 The mechanism could be either that lisinopril limits the angiotensin II-induced production of superoxide radicals which would normally inactivate NO, or that lisinopril may increase bradykinin-mediated NO release. Lisinopril 158-168 kininogen 1 Homo sapiens 182-192 11508274-1 2001 AIMS/HYPOTHESIS: The results of the EUCLID trial (EURODIAB Controlled Trial of Lisinopril in Insulin-dependent Diabetes Mellitus) highlighted the importance of the renin-angiotensin system in the pathogenesis of diabetic retinopathy. Lisinopril 79-89 renin Rattus norvegicus 164-169 11408523-3 2001 Functional recording of isometric tension showed that Ang I (3 x 10(-7) M) induced a tension of 0.17 +/- 0.05 g (n = 5), which was reduced to about 60% by pretreatment with an ACE inhibitor, lisinopril (10(-6) M), and almost completely blocked by lisinopril in combination with a chymase inhibitor, chymostatin (10(-4) M). Lisinopril 191-201 angiotensin I converting enzyme Canis lupus familiaris 176-179 11408523-3 2001 Functional recording of isometric tension showed that Ang I (3 x 10(-7) M) induced a tension of 0.17 +/- 0.05 g (n = 5), which was reduced to about 60% by pretreatment with an ACE inhibitor, lisinopril (10(-6) M), and almost completely blocked by lisinopril in combination with a chymase inhibitor, chymostatin (10(-4) M). Lisinopril 247-257 angiotensin I converting enzyme Canis lupus familiaris 176-179 11358940-1 2001 We have previously demonstrated that antihypertensive treatment with doxazosin (DZN), an alpha-adrenergic blocker, and lisinopril (LIS), an ACE inhibitor, reverse glomerular sclerosis in corpulent spontaneously hypertensive rats with type 2 diabetes. Lisinopril 119-129 angiotensin I converting enzyme Rattus norvegicus 140-143 11425338-2 2001 Detergent-extracted canine testes were sonicated in the presence of protease inhibitors and purified on an affinity column with the ACE inhibitor, lisinopril, as an affinity ligand for ACE. Lisinopril 147-157 angiotensin I converting enzyme Canis lupus familiaris 132-135 11425338-2 2001 Detergent-extracted canine testes were sonicated in the presence of protease inhibitors and purified on an affinity column with the ACE inhibitor, lisinopril, as an affinity ligand for ACE. Lisinopril 147-157 angiotensin I converting enzyme Canis lupus familiaris 185-188 11425338-4 2001 The specific activity of ACE in the starting testicular extracts was 3.53 +/- 0.99 mU mg(-1) protein with a 1588 times enrichment in ACE activity after lisinopril affinity chromatography (4239 +/- 2600 mU mg(-1) protein). Lisinopril 152-162 angiotensin I converting enzyme Canis lupus familiaris 25-28 11425338-5 2001 The recovery efficiency of ACE after lisinopril affinity chromatography was 71.2%. Lisinopril 37-47 angiotensin I converting enzyme Canis lupus familiaris 27-30 11425338-12 2001 The results of this study demonstrate that ACE is present in canine testis and retains its enzyme activity after purification with lisinopril affinity chromatography. Lisinopril 131-141 angiotensin I converting enzyme Canis lupus familiaris 43-46 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. Lisinopril 52-62 angiotensin I converting enzyme Homo sapiens 37-40 11358940-1 2001 We have previously demonstrated that antihypertensive treatment with doxazosin (DZN), an alpha-adrenergic blocker, and lisinopril (LIS), an ACE inhibitor, reverse glomerular sclerosis in corpulent spontaneously hypertensive rats with type 2 diabetes. Lisinopril 131-134 angiotensin I converting enzyme Rattus norvegicus 140-143 11316852-8 2001 Lisinopril and L-158,809 fully prevented the decrease in nephrin transcripts to levels comparable to those of control rats. Lisinopril 0-10 NPHS1 adhesion molecule, nephrin Rattus norvegicus 57-64 11316852-9 2001 Consistent with nephrin mRNA expression, immunostaining of the protein showed a progressive decrease in kidneys from PHN rats that was completely abolished by lisinopril and L-158,809. Lisinopril 159-169 NPHS1 adhesion molecule, nephrin Rattus norvegicus 16-23 11350567-15 2001 CONCLUSIONS: In type 1 diabetic patients with low-grade microalbuminuria, 2 years of ACE-i treatment with lisinopril significantly reduced E-UAE. Lisinopril 106-116 angiotensin I converting enzyme Homo sapiens 85-88 11348042-7 2001 Lisinopril did not significantly reduce the plasma norepinephrine concentration, but there was a significant reduction in the plasma ANP and BNP concentrations. Lisinopril 0-10 natriuretic peptide B Homo sapiens 141-144 11303049-7 2001 In contrast, lisinopril infusion (5 and 10 mg/kg/30 min) affected the metabolism of both AcSDKP and angiotensin I. Lisinopril 13-23 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 100-113 11247797-7 2001 Simultaneous with kallikrein formation, bradykinin (5.0 or 10.3 pmol/10(6) HUVEC in the absence or presence of lisinopril, respectively) is liberated from cell-bound HK. Lisinopril 111-121 kininogen 1 Homo sapiens 40-50 11331849-8 2001 All three ACE inhibitors prevented AAA development (mean DeltaAD: CP, 67% +/- 4%; LP, 18% +/- 12%; and EP, 14% +/- 3%; each P <.05 vs controls). Lisinopril 82-84 angiotensin I converting enzyme Rattus norvegicus 10-13 11433128-9 2001 CONCLUSIONS: Variation in circadian systolic blood pressure is useful in reflecting the influence of the magnitude of dose of the ACE inhibitor lisinopril on the pharmacodynamics of patients with heart failure. Lisinopril 144-154 angiotensin I converting enzyme Homo sapiens 130-133 11334854-3 2001 The aim was to assess whether promotion of vasodilation by treatment with the aldose reductase inhibitor, ZD5522 (3",5"-dimethyl-4"-nitromethylsulphonyl-2-(2-tolyl)acetanilide), coupled with reduced vasoconstriction using the angiotensin-converting enzyme inhibitor, lisinopril, interacted positively to improve neurovascular function. Lisinopril 267-277 aldo-keto reductase family 1 member B1 Rattus norvegicus 78-94 11343399-2 2001 I"m diabetic, and for years I have been on a different ACE inhibitor (lisinopril). Lisinopril 70-80 angiotensin I converting enzyme Homo sapiens 55-58 11403651-3 2001 The bovine atrial ACE exhibited similar sensitivities to inhibition by lisinopril and captopril as lung ACE (the Ki values for the atrial and lung enzymes differed insignificantly). Lisinopril 71-81 angiotensin I converting enzyme Bos taurus 18-21 11437859-2 2001 METHODS: Samples (299/354 of those with retinal photographs) from the EUCLID placebo-controlled clinical trial of the ACE inhibitor lisinopril in mainly normoalbuminuric non-hypertensive Type 1 diabetic patients were used. Lisinopril 132-142 angiotensin I converting enzyme Homo sapiens 118-121 11249939-4 2001 In the extract from human vascular tissues, the angiotensin II formation was inhibited by 8% with lisinopril and by 95% with chymostatin. Lisinopril 98-108 angiotensinogen Homo sapiens 48-62 11249939-6 2001 In the extract from rat vascular tissues, the angiotensin II formation was suppressed to 4% by lisinopril, but not by chymostatin. Lisinopril 95-105 angiotensinogen Rattus norvegicus 46-60 11102838-4 2001 Whereas PMSF, a potent inhibitor of serine proteases has no effect, captopril and lisinopril, both known to be specific inhibitors of mammalian angiotensin I converting enzyme (ACE), effectively inhibit TMOF breakdown in fly hemolymph. Lisinopril 82-92 angiotensin I converting enzyme Homo sapiens 144-175 11230305-10 2001 Blockade of the renin-angiotensin system by lisinopril or high salt restored the responses observed in the SS group fed a low salt diet. Lisinopril 44-54 renin Rattus norvegicus 16-21 11053977-6 2001 In rats treated with lisinopril (5 mg/kg/24 h) GBM staining was significantly better preserved for HS as well as for HSPG core protein. Lisinopril 21-31 syndecan 2 Rattus norvegicus 117-121 11296854-11 2001 Both lisinopril and losartan blocked elevation in VEGF expression and inhibited the angiogenesis induced by stimulation. Lisinopril 5-15 vascular endothelial growth factor A Rattus norvegicus 50-54 11151038-0 2001 Angiotensin-converting enzyme inhibition by lisinopril enhances liver regeneration in rats. Lisinopril 44-54 angiotensin I converting enzyme Rattus norvegicus 0-29 11151038-4 2001 We have investigated the effect of ACE inhibition by lisinopril on liver regeneration after partial hepatectomy. Lisinopril 53-63 angiotensin I converting enzyme Rattus norvegicus 35-38 11151038-10 2001 Plasma ACE activity measured by radioenzymatic assay was significantly higher in the saline group than in the lisinopril-treated group (P<0.001), with 81% ACE inhibition. Lisinopril 110-120 angiotensin I converting enzyme Rattus norvegicus 7-10 11151038-10 2001 Plasma ACE activity measured by radioenzymatic assay was significantly higher in the saline group than in the lisinopril-treated group (P<0.001), with 81% ACE inhibition. Lisinopril 110-120 angiotensin I converting enzyme Rattus norvegicus 158-161 12426159-6 2001 Losartan and lisinopril both decreased ACE mRNA expression levels that were positively correlated with the difference of the diastolic blood pressure whereas nisodipine elevated ACE mRNA expression, showing inverse correlation to the difference of thediastolic blood pressure. Lisinopril 13-23 angiotensin I converting enzyme Homo sapiens 39-42 11102838-4 2001 Whereas PMSF, a potent inhibitor of serine proteases has no effect, captopril and lisinopril, both known to be specific inhibitors of mammalian angiotensin I converting enzyme (ACE), effectively inhibit TMOF breakdown in fly hemolymph. Lisinopril 82-92 angiotensin I converting enzyme Homo sapiens 177-180 11831455-1 2001 Captopril, enalapril, and lisinopril are angiotensin-converting enzyme (ACE) inhibitors widely prescribed for hypertension and heart failure. Lisinopril 26-36 angiotensin I converting enzyme Homo sapiens 41-70 11831455-1 2001 Captopril, enalapril, and lisinopril are angiotensin-converting enzyme (ACE) inhibitors widely prescribed for hypertension and heart failure. Lisinopril 26-36 angiotensin I converting enzyme Homo sapiens 72-75 11113723-0 2000 Low doses vs. high doses of the angiotensin converting-enzyme inhibitor lisinopril in chronic heart failure: a cost-effectiveness analysis based on the Assessment of Treatment with Lisinopril and Survival (ATLAS) study. Lisinopril 72-82 angiotensin I converting enzyme Homo sapiens 32-61 11096048-5 2000 In both models, increased urinary protein excretion over time was associated with a remarkable increase in NF-kB activity, which was almost completely suppressed by reducing proteinuria with lisinopril. Lisinopril 191-201 nuclear factor kappa B subunit 1 Rattus norvegicus 107-112 11096048-7 2000 Lisinopril inhibited MCP-1 upregulation and limited interstitial inflammation. Lisinopril 0-10 C-C motif chemokine ligand 2 Rattus norvegicus 21-26 11096048-8 2000 In a group of PHN rats with advanced disease and severe proteinuria, a dose of lisinopril high enough to inhibit renal ACE activity failed to reduce proteinuria and also did not limit NF-kB activation, which was sustained over time, along with MCP-1 gene overexpression and interstitial inflammation. Lisinopril 79-89 angiotensin I converting enzyme Rattus norvegicus 119-122 11113723-2 2000 OBJECTIVE: A cost-effectiveness analysis of high and low doses of the angiotensin-converting enzyme (ACE) inhibitor lisinopril in the treatment of chronic heart failure. Lisinopril 116-126 angiotensin I converting enzyme Homo sapiens 70-99 11113723-2 2000 OBJECTIVE: A cost-effectiveness analysis of high and low doses of the angiotensin-converting enzyme (ACE) inhibitor lisinopril in the treatment of chronic heart failure. Lisinopril 116-126 angiotensin I converting enzyme Homo sapiens 101-104 11004022-5 2000 Under dehydrated conditions, the enhanced endotoxin-induced fever was significantly inhibited by the angiotensin-converting enzyme inhibitor lisinopril, but the IL-1beta fever was not. Lisinopril 141-151 angiotensin I converting enzyme Rattus norvegicus 101-130 11116132-4 2000 The ACE inhibitor lisinopril and the angiotensin type 1 receptor antagonist losartan both increased retinal renin levels and prevented inner retinal blood vessel growth. Lisinopril 18-28 angiotensin I converting enzyme Rattus norvegicus 4-7 11116132-4 2000 The ACE inhibitor lisinopril and the angiotensin type 1 receptor antagonist losartan both increased retinal renin levels and prevented inner retinal blood vessel growth. Lisinopril 18-28 renin Rattus norvegicus 108-113 11053044-4 2000 The ANG-converting enzyme (ACE) inhibitor lisinopril abolished the generation of ANG-(1---5), as well as that of smaller metabolites. Lisinopril 42-52 angiotensin I converting enzyme Rattus norvegicus 4-25 11053044-4 2000 The ANG-converting enzyme (ACE) inhibitor lisinopril abolished the generation of ANG-(1---5), as well as that of smaller metabolites. Lisinopril 42-52 angiotensin I converting enzyme Rattus norvegicus 27-30 11025447-5 2000 Apoptosis in response to TNF-alpha was inhibited in a dose-dependent manner by the nonselective ANGII receptor antagonist saralasin or by the nonthiol ACE inhibitor lisinopril; the inhibition of TNF-induced apoptosis was maximal at 50 microgram/ml saralasin (101% inhibition) and at 0.5 microgram/ml lisinopril (86% inhibition). Lisinopril 165-175 tumor necrosis factor Homo sapiens 25-34 11025447-5 2000 Apoptosis in response to TNF-alpha was inhibited in a dose-dependent manner by the nonselective ANGII receptor antagonist saralasin or by the nonthiol ACE inhibitor lisinopril; the inhibition of TNF-induced apoptosis was maximal at 50 microgram/ml saralasin (101% inhibition) and at 0.5 microgram/ml lisinopril (86% inhibition). Lisinopril 165-175 angiotensin I converting enzyme Homo sapiens 151-154 11025447-5 2000 Apoptosis in response to TNF-alpha was inhibited in a dose-dependent manner by the nonselective ANGII receptor antagonist saralasin or by the nonthiol ACE inhibitor lisinopril; the inhibition of TNF-induced apoptosis was maximal at 50 microgram/ml saralasin (101% inhibition) and at 0.5 microgram/ml lisinopril (86% inhibition). Lisinopril 165-175 tumor necrosis factor Homo sapiens 25-28 11967821-11 2000 RESULTS: Fibroblasts contained two types of activity of hip-his-leu degradation, namely a lisinopril-dependent activity (ACE activity) and a lisinopril-independent activity ("ACE-like" activity) which is performed by peptidase(s) other than ACE. Lisinopril 90-100 angiotensin I converting enzyme Rattus norvegicus 121-124 11025447-5 2000 Apoptosis in response to TNF-alpha was inhibited in a dose-dependent manner by the nonselective ANGII receptor antagonist saralasin or by the nonthiol ACE inhibitor lisinopril; the inhibition of TNF-induced apoptosis was maximal at 50 microgram/ml saralasin (101% inhibition) and at 0.5 microgram/ml lisinopril (86% inhibition). Lisinopril 300-310 tumor necrosis factor Homo sapiens 25-34 11025447-5 2000 Apoptosis in response to TNF-alpha was inhibited in a dose-dependent manner by the nonselective ANGII receptor antagonist saralasin or by the nonthiol ACE inhibitor lisinopril; the inhibition of TNF-induced apoptosis was maximal at 50 microgram/ml saralasin (101% inhibition) and at 0.5 microgram/ml lisinopril (86% inhibition). Lisinopril 300-310 tumor necrosis factor Homo sapiens 25-28 11025447-8 2000 Exposure to TNF-alpha increased the concentration of ANGII in the serum-free extracellular medium by fivefold in A549 cell cultures and by 40-fold in primary AEC preparations; further, exposure to TNF-alpha for 40 h caused a net cell loss of 70%, which was completely abrogated by either the caspase inhibitor ZVAD-fmk, lisinopril, or saralasin. Lisinopril 320-330 tumor necrosis factor Homo sapiens 12-21 11025447-8 2000 Exposure to TNF-alpha increased the concentration of ANGII in the serum-free extracellular medium by fivefold in A549 cell cultures and by 40-fold in primary AEC preparations; further, exposure to TNF-alpha for 40 h caused a net cell loss of 70%, which was completely abrogated by either the caspase inhibitor ZVAD-fmk, lisinopril, or saralasin. Lisinopril 320-330 angiotensinogen Homo sapiens 53-58 11025447-8 2000 Exposure to TNF-alpha increased the concentration of ANGII in the serum-free extracellular medium by fivefold in A549 cell cultures and by 40-fold in primary AEC preparations; further, exposure to TNF-alpha for 40 h caused a net cell loss of 70%, which was completely abrogated by either the caspase inhibitor ZVAD-fmk, lisinopril, or saralasin. Lisinopril 320-330 tumor necrosis factor Homo sapiens 197-206 10968433-1 2000 BACKGROUND: We aimed to assess in patients with congestive heart failure whether dual inhibition of neutral endopeptidase and angiotensin-converting enzyme (ACE) with the vasopeptidase inhibitor omapatrilat is better than ACE inhibition alone with lisinopril on functional capacity and clinical outcome. Lisinopril 248-258 angiotensin I converting enzyme Homo sapiens 157-160 11030016-5 2000 Captopril and lisinopril are the only ACE inhibitors that are not prodrugs requiring activation through hepatic biotransformation. Lisinopril 14-24 angiotensin I converting enzyme Homo sapiens 38-41 11030016-6 2000 Differences among the ACE inhibitors in lipophilicity are described; fosinopril has the greatest lipophilicity and lisinopril the least. Lisinopril 115-125 angiotensin I converting enzyme Homo sapiens 22-25 11030016-9 2000 Lisinopril is the only ACE inhibitor that does not require hepatic metabolism. Lisinopril 0-10 angiotensin I converting enzyme Homo sapiens 23-26 11079227-0 2000 [Effect of angiotensin converting enzyme inhibitor lisinopril on sympathetic heart rate response during exercise in the early phase of acute myocardial infarction]. Lisinopril 51-61 angiotensin I converting enzyme Homo sapiens 11-40 11079227-6 2000 The subjects consisted of 25 patients (mean age 60.2 +/- 10.7 years) treated with ACE inhibitor lisinopril from the initial stage and 40 control subjects (mean age 57.7 +/- 7.6 years). Lisinopril 96-106 angiotensin I converting enzyme Homo sapiens 82-85 10993857-12 2000 CONCLUSIONS: In patients with hypertensive heart disease, angiotensin-converting enzyme inhibition with lisinopril can regress myocardial fibrosis, irrespective of LVH regression, and it is accompanied by improved LV diastolic function. Lisinopril 104-114 angiotensin I converting enzyme Homo sapiens 58-87 10993857-2 2000 In spontaneously hypertensive rats, myocardial fibrosis was regressed and LV diastolic function was improved by treatment with the angiotensin-converting enzyme inhibitor lisinopril. Lisinopril 171-181 angiotensin I converting enzyme Rattus norvegicus 131-160 10892668-8 2000 Acute treatment with the cyclooxygenase (COX) inhibitor indomethacin increased blood pressure to a similar extent to that of CGS 24592, as well as blocked the increase in pressure with the neprilysin inhibitor in the lisinopril/losartan group. Lisinopril 217-227 membrane metallo-endopeptidase Rattus norvegicus 189-199 10983838-2 2000 SHR were fed alcohol for six weeks while taking the angiotensin converting enzyme (ACE) inhibitor lisinopril. Lisinopril 98-108 angiotensin I converting enzyme Rattus norvegicus 83-86 10983838-6 2000 The enzyme activities of the proteases cathepsin D and dipeptidyl aminopepetidase I increased in control+lisinopril rats, however, this effect was not evident in alcohol+lisinopril rats. Lisinopril 105-115 cathepsin D Rattus norvegicus 39-50 10983838-6 2000 The enzyme activities of the proteases cathepsin D and dipeptidyl aminopepetidase I increased in control+lisinopril rats, however, this effect was not evident in alcohol+lisinopril rats. Lisinopril 170-180 cathepsin D Rattus norvegicus 39-50 10826406-4 2000 Lisinopril and captopril reduced the ACE activity in homogenates of T-lymphocytes in a concentration-dependent manner. Lisinopril 0-10 angiotensin I converting enzyme Homo sapiens 37-40 10908091-1 2000 The Assessment of Treatment with Lisinopril and Survival (ATLAS) results have been widely quoted by proponents advocating the use of "high" doses of angiotensin-converting enzyme (ACE) inhibitors for the treatment of heart failure. Lisinopril 33-43 angiotensin I converting enzyme Homo sapiens 149-178 10908091-1 2000 The Assessment of Treatment with Lisinopril and Survival (ATLAS) results have been widely quoted by proponents advocating the use of "high" doses of angiotensin-converting enzyme (ACE) inhibitors for the treatment of heart failure. Lisinopril 33-43 angiotensin I converting enzyme Homo sapiens 180-183 10878699-0 2000 Effect of lisinopril on tissue levels of neuropeptide Y in normotensive and spontaneously hypertensive rats. Lisinopril 10-20 neuropeptide Y Rattus norvegicus 41-55 10878699-5 2000 Lisinopril treatment increased NPY levels in atria and skeletal muscle extracts of SHR by 15% and 70% respectively (P < 0.05). Lisinopril 0-10 neuropeptide Y Rattus norvegicus 31-34 10824049-4 2000 It was decided to perform a randomised double blind, crossover study with the long acting calcium channel blocker amlodipine and the long acting ACE inhibitor lisinopril, given either alone or in combination in essential hypertension. Lisinopril 159-169 angiotensin I converting enzyme Homo sapiens 145-148 10826406-5 2000 Lisinopril exhibited a more pronounced inhibition of ACE in T-lymphocytes than did captopril. Lisinopril 0-10 angiotensin I converting enzyme Homo sapiens 53-56 10852646-1 2000 UNLABELLED: The ACE inhibitor lisinopril is a lysine derivative of enalaprilat, the active metabolite of enalapril. Lisinopril 30-40 angiotensin I converting enzyme Homo sapiens 16-19 10825662-10 2000 The Ki values for specific mammalian ACE inhibitors, such as captopril and lisinopril, were 1.38 and 2.07 nM, respectively. Lisinopril 75-85 angiotensin I converting enzyme Homo sapiens 37-40 10797820-4 2000 Two hours after the initiation of a treatment with ACE inhibitor administered orally (lisinopril, Zestril), a circulatory failure in conjunction with an acute renal insufficiency occurred. Lisinopril 86-96 angiotensin I converting enzyme Homo sapiens 51-54 10797820-4 2000 Two hours after the initiation of a treatment with ACE inhibitor administered orally (lisinopril, Zestril), a circulatory failure in conjunction with an acute renal insufficiency occurred. Lisinopril 98-105 angiotensin I converting enzyme Homo sapiens 51-54 10805052-0 2000 Comparison of the AT1-receptor blocker, candesartan cilexetil, and the ACE inhibitor, lisinopril, in fixed combination with low dose hydrochlorothiazide in hypertensive patients. Lisinopril 86-96 angiotensin I converting enzyme Homo sapiens 71-74 10893698-0 2000 Role of angiotensin-converting enzyme inhibitor, lisinopril, on spermatozoal functions in rats. Lisinopril 49-59 angiotensin I converting enzyme Rattus norvegicus 8-37 10949912-8 2000 ACE kinetic and inhibition studies were performed using specific substrates (Hip-His-Leu and Acetyl-Seryl-Aspartyl-Acetyl-Lysyl-Proline) and inhibitors (lisinopril, captopril and quinaprilat) for each C- and N-terminal active site. Lisinopril 153-163 angiotensin I converting enzyme Rattus norvegicus 0-3 10949912-14 2000 Furthermore, the chronic inhibition of serum and exudate ACE levels by lisinopril treatment did not affect the exudate volume in F344/N rats, indicating that several factors besides ACE were involved in the control of carrageenan-induced exudation. Lisinopril 71-81 angiotensin I converting enzyme Rattus norvegicus 57-60 10703672-7 2000 In the third series, lisinopril reduced BP from 121 +/- 5 to 68 +/- 2 mmHg and proteinuria from 355 +/- 90 to 101 +/- 10 mg/24 h. Subsequent intraperitoneal infusion of bradykinin antagonist (HOE 140; 1 mg/kg per 24 h) for 2 wk did not affect BP (72 +/- 2 mmHg) or proteinuria (92 +/- 15 mg/24 h). Lisinopril 21-31 kininogen 1 Homo sapiens 169-179 10686803-2 1999 The Atlas Study was set up to compare the efficacy and safety of low doses and high doses of ACE inhibition by lisinopril on the risk of death and hospitalization in chronic heart failure. Lisinopril 111-121 angiotensin I converting enzyme Homo sapiens 93-96 11450501-0 2000 The influence of the ACE inhibitor lisinopril on the glomerular metabolism of proteolytic enzymes in diabetic rats. Lisinopril 35-45 angiotensin I converting enzyme Rattus norvegicus 21-24 10642323-5 2000 The addition of the ACE inhibitor lisinopril to the perfusion buffer augmented levels of Ang-(1-7) in periods 3 (144+/-39 fmol) and 4 (163+/-35 fmol; P<0.05 versus 1 or 2, n=8). Lisinopril 34-44 angiotensin I converting enzyme Rattus norvegicus 20-23 10642323-7 2000 The addition of the neprilysin inhibitor SCH 39370 reduced Ang-(1-7) release in the lisinopril buffer from 177+/-32 (period 1) and 173+/-39 (period 2) fmol to 112+/-24 (period 3) and 87+/-23 fmol (period 4; P<0.05 versus 1 or 2, n=6). Lisinopril 84-94 membrane metallo-endopeptidase Rattus norvegicus 20-30 10609621-5 1999 Approximately 0.3 mM of alacepril inhibited 50% of oxygen radical production of lung alveolar macrophages in both rats and guinea pigs, whereas a higher concentration (1-5 mM) of lisinopril, an ACE inhibitor without SH-group, was necessary to inhibit 50% of oxygen radical production of lung alveolar macrophages in the animals. Lisinopril 179-189 LOW QUALITY PROTEIN: angiotensin-converting enzyme Cavia porcellus 194-197 10805421-5 2000 In all concentrations, lisinopril significantly increased PRA and decreased ACE activities. Lisinopril 23-33 angiotensin I converting enzyme Gallus gallus 76-79 10587334-0 1999 Comparative effects of low and high doses of the angiotensin-converting enzyme inhibitor, lisinopril, on morbidity and mortality in chronic heart failure. Lisinopril 90-100 angiotensin I converting enzyme Homo sapiens 49-78 10600897-16 1999 Apoptosis in response to either Fas activator was inhibited in a dose-dependent manner by the nonthiol ACE inhibitor lisinopril or the nonselective ANG II receptor antagonist saralasin, with maximal inhibitions of 82 and 93% at doses of 0.5 and 5 microg/ml, respectively. Lisinopril 117-127 angiotensin I converting enzyme Homo sapiens 103-106 10535387-2 1999 In the present study, we measured plasma levels of nitric oxide (NO) and the related vasoactive factors bradykinin, 6-keto prostaglandin F1alpha (6-keto PGF1alpha) a stable metabolite of prostacyclin, and cyclic guanosine-3",5"-monophosphate (cGMP) before and after a 4-week treatment with the ACE inhibitor lisinopril in 17 patients with essential hypertension. Lisinopril 308-318 kininogen 1 Homo sapiens 104-114 10516341-4 1999 Animals treated with the ACE inhibitor lisinopril from 20 weeks of age (time when proteinuria is already important) and age-matched untreated rats were followed for 10 weeks. Lisinopril 39-49 angiotensin I converting enzyme Rattus norvegicus 25-28 10615405-11 1999 Furthermore, the basal O2- release from HVECs was inhibited in cells treated with angiotensin-converting enzyme (ACE) inhibitor, Lisinopril (10(-6) M), and this event could be reversed by ANG II. Lisinopril 129-139 angiotensin I converting enzyme Homo sapiens 82-111 10615405-11 1999 Furthermore, the basal O2- release from HVECs was inhibited in cells treated with angiotensin-converting enzyme (ACE) inhibitor, Lisinopril (10(-6) M), and this event could be reversed by ANG II. Lisinopril 129-139 angiotensin I converting enzyme Homo sapiens 113-116 10615405-11 1999 Furthermore, the basal O2- release from HVECs was inhibited in cells treated with angiotensin-converting enzyme (ACE) inhibitor, Lisinopril (10(-6) M), and this event could be reversed by ANG II. Lisinopril 129-139 angiotensinogen Homo sapiens 188-194 10334975-8 1999 The angiotensin-converting enzyme inhibitors captopril, enalapril, lisinopril, perindopril, quinapril and trandolapril at 10(-7) mol/l, but not fosinopril, significantly increased 11beta-HSD2 activity after pretreatment for 16 or 24 h (P<0.05-P<0.01 compared with control). Lisinopril 67-77 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 180-191 10371365-4 1999 Both sampatrilat and lisinopril decreased plasma ACE concentrations after 28 and 56 days. Lisinopril 21-31 angiotensin I converting enzyme Homo sapiens 49-52 10371365-5 1999 The decrease in plasma ACE concentrations (U/L) was greater after lisinopril (-9.33 +/- 0.52) as compared with sampatrilat (-6.31 +/- 0.70) (P = .0001) therapy. Lisinopril 66-76 angiotensin I converting enzyme Homo sapiens 23-26 10371365-6 1999 Lisinopril, but not sampatrilat, increased plasma renin activity. Lisinopril 0-10 renin Homo sapiens 50-55 10371365-7 1999 Lisinopril produced a transient decrease in mean 24-h ABP (mm Hg) at 28 days (SBP = -9.0 +/- 2.3, DBP = -5.7 +/- 1.3; P < .01), which returned to pretreatment values by 56 days of therapy. Lisinopril 0-10 selenium binding protein 1 Homo sapiens 78-81 10371365-7 1999 Lisinopril produced a transient decrease in mean 24-h ABP (mm Hg) at 28 days (SBP = -9.0 +/- 2.3, DBP = -5.7 +/- 1.3; P < .01), which returned to pretreatment values by 56 days of therapy. Lisinopril 0-10 D-box binding PAR bZIP transcription factor Homo sapiens 98-101 10391670-0 1999 Effects of lisinopril administration on blood bcl-2 concentrations in patients with immunoglobulin A nephropathy. Lisinopril 11-21 BCL2 apoptosis regulator Homo sapiens 46-51 10391670-3 1999 A 6-month course of 5 mg/day lisinopril given to subjects with proteinuria significantly reduced blood bcl-2 concentrations and caused a reduction in proteinuria. Lisinopril 29-39 BCL2 apoptosis regulator Homo sapiens 103-108 10196019-7 1999 Endothelin-1 (ET-1) levels, formed in excessive amounts by the kidneys of these animals, were reduced by molsidomine and lisinopril, but not by triple therapy. Lisinopril 121-131 endothelin 1 Homo sapiens 0-12 10330045-13 1999 The nonthiol ACE inhibitor lisinopril blocked apoptosis induced by angiotensinogen, but not apoptosis induced by purified ANG II. Lisinopril 27-37 angiotensin I converting enzyme Homo sapiens 13-16 10459879-11 1999 After long-term treatment with lisinopril, levels of cardiotrophin-1 mRNA were not changed, although it morphologically prevented the development of left ventricular hypertrophy. Lisinopril 31-41 cardiotrophin 1 Rattus norvegicus 53-68 10338459-6 1999 A single dose of lisinopril was administered during study days to ensure sustained ACE inhibition. Lisinopril 17-27 angiotensin I converting enzyme Homo sapiens 83-86 10344043-3 1999 The incidence of dry cough associated with two of these therapies, the novel All receptor antagonist telmisartan and the ACE inhibitor lisinopril, was assessed in a multicentre, randomised, parallel-group, double-blind, placebo-controlled, 8-week study of 88 patients with mild to moderate hypertension who previously demonstrated ACE inhibitor-related cough. Lisinopril 135-145 angiotensin I converting enzyme Homo sapiens 121-124 10193670-0 1999 Effects on plasma angiotensin-converting enzyme activity and circulating renin of lisinopril and enalapril alone and in combination with propranolol in healthy volunteers. Lisinopril 82-92 renin Homo sapiens 73-78 10193670-6 1999 Plasma renin activity increased almost ten times after ingestion of both angiotensin-converting enzyme inhibitors, but the effect lasted significantly longer after lisinopril than after enalapril. Lisinopril 164-174 renin Homo sapiens 7-12 10091486-0 1999 Eruptions induced by the ACE inhibitor, lisinopril. Lisinopril 40-50 angiotensin I converting enzyme Homo sapiens 25-28 11501132-9 1999 After treatment with ACE inhibitor-Lisinopril, the ACE activities, AII levels and calcium contents were significantly decreased compared to the burn group. Lisinopril 35-45 angiotensin I converting enzyme Rattus norvegicus 21-24 11501132-9 1999 After treatment with ACE inhibitor-Lisinopril, the ACE activities, AII levels and calcium contents were significantly decreased compared to the burn group. Lisinopril 35-45 angiotensin I converting enzyme Rattus norvegicus 51-54 11501132-9 1999 After treatment with ACE inhibitor-Lisinopril, the ACE activities, AII levels and calcium contents were significantly decreased compared to the burn group. Lisinopril 35-45 angiotensinogen Rattus norvegicus 67-70 10188971-3 1999 With daily oral administration of lisinopril (5 mg kg(-1), twice a day), which is an inhibitor of angiotensin converting enzyme, a major kininase in plasma, the development of hypertension was not suppressed. Lisinopril 34-44 angiotensin I converting enzyme Rattus norvegicus 98-127 10822412-8 1999 The ESPRIT Study was the first to enroll hyper-tensive sibling pairs into a therapeutic trial, designed to assess responses to ACE inhibitor treatment with lisinopril. Lisinopril 156-166 angiotensin I converting enzyme Homo sapiens 127-130 10075388-0 1999 Reduced bcl-2 concentrations in hypertensive patients after lisinopril or nifedipine administration. Lisinopril 60-70 BCL2 apoptosis regulator Homo sapiens 8-13 10075388-4 1999 Treatment of hypertensive patients with hypotensive drugs caused a reduction in bcl-2 concentrations, which was more marked after administration of lisinopril than of nifedipine. Lisinopril 148-158 BCL2 apoptosis regulator Homo sapiens 80-85 10075388-6 1999 Moreover, lisinopril and nifedipine appear to be capable of reducing bcl-2 concentrations, with potentially beneficial effects on vascular modifications in patients with hypertension. Lisinopril 10-20 BCL2 apoptosis regulator Homo sapiens 69-74 9869013-7 1998 RESULTS: Lisinopril induced a marked increase in plasma renin activity (from 1.1+/-0.2 to 6.4+/-1.3 ng/ml per h, P< 0.01) and a reduction in mean arterial pressure (from 109.6+/-3.1 to 98.7+/-2.9 mmHg, P < 0.01) without affecting the heart rate. Lisinopril 9-19 renin Homo sapiens 56-61 9877521-0 1998 Lisinopril decreases plasma free testosterone in male hypertensive patients and increases sex hormone binding globulin in female hypertensive patients. Lisinopril 0-10 sex hormone binding globulin Homo sapiens 90-118 9877521-4 1998 Lisinopril had no effect on plasma T, f-T, or E2 concentrations in female patients, but significantly increased the plasma SHBG concentration (before, 48.0 6.1 nmol/l; after, 62.7+/-6.7 nmol/l: p < 0.01). Lisinopril 0-10 sex hormone binding globulin Homo sapiens 123-127 9877521-5 1998 The results of this preliminary study suggest that lisinopril affects plasma f-T and SHBG concentrations. Lisinopril 51-61 sex hormone binding globulin Homo sapiens 85-89 9877521-6 1998 The clinical implications of lisinopril-induced changes in plasma f-T and SHBG concentrations remain to be clarified. Lisinopril 29-39 sex hormone binding globulin Homo sapiens 74-78 9886768-9 1998 The angiotensin converting enzyme (ACE) inhibitor lisinopril blunted the reflex responses to PBG in anaesthetized as well as conscious animals. Lisinopril 50-60 angiotensin I converting enzyme Rattus norvegicus 4-33 9886768-9 1998 The angiotensin converting enzyme (ACE) inhibitor lisinopril blunted the reflex responses to PBG in anaesthetized as well as conscious animals. Lisinopril 50-60 angiotensin I converting enzyme Rattus norvegicus 35-38 9853182-7 1998 Angiotensin-converting enzyme inhibitors and nitrates were uptitrated over 6 months to a final dose of lisinopril 53 +/- 31 mg/day, and isosorbide dinitrate 217 +/- 213 mg/day. Lisinopril 103-113 angiotensin I converting enzyme Homo sapiens 0-29 9725973-4 1998 Approximately 100 cases of pancreatitis induced by angiotensin-converting enzyme inhibitor have been reported to the US Food and Drug Administration, of which about 20 involved lisinopril. Lisinopril 177-187 angiotensin I converting enzyme Homo sapiens 51-80 9833600-0 1998 Comparative effects of lisinopril and losartan on insulin sensitivity in the treatment of non diabetic hypertensive patients. Lisinopril 23-33 insulin Homo sapiens 50-57 9833600-1 1998 AIMS: The aim of this study was to compare the effects of the ACE-inhibitor lisinopril and the angiotensin II receptor antagonist losartan on insulin sensitivity in the treatment of non diabetic hypertensives. Lisinopril 76-86 insulin Homo sapiens 142-149 9833600-6 1998 RESULTS: Both lisinopril and losartan significantly reduced SBP (by a mean of 20.2 and 17.2 mmHg, respectively) and DBP (by a mean of 15.2 and 12.3 mmHg, respectively), with no difference between the two treatments. Lisinopril 14-24 selenium binding protein 1 Homo sapiens 60-63 9833600-6 1998 RESULTS: Both lisinopril and losartan significantly reduced SBP (by a mean of 20.2 and 17.2 mmHg, respectively) and DBP (by a mean of 15.2 and 12.3 mmHg, respectively), with no difference between the two treatments. Lisinopril 14-24 D-box binding PAR bZIP transcription factor Homo sapiens 116-119 9833600-7 1998 GIR, used as an indicator of insulin sensitivity, was significantly increased by lisinopril (+1.5 mg min(-1) kg(-1), P<0.05 vs baseline) but not by losartan (+0.42 mg min(-1) kig(-1), NS), the difference between the two drugs being statistically significant (P<0.05). Lisinopril 81-91 insulin Homo sapiens 29-36 9833600-9 1998 CONCLUSIONS: In conclusion, with all cautions due to an absence in this study of a randomized placebo phase, our findings suggest that lisinopril improved insulin sensitivity whereas losartan did not affect it. Lisinopril 135-145 insulin Homo sapiens 155-162 9797801-9 1998 Lisinopril but not sampatrilat significantly increased plasma renin activity, whereas sampatrilat but not lisinopril significantly increased urinary cGMP excretion. Lisinopril 0-10 renin Homo sapiens 62-67 9766448-0 1998 Lisinopril, an angiotensin I-converting enzyme inhibitor, prevents entry of murine hematopoietic stem cells into the cell cycle after irradiation in vivo. Lisinopril 0-10 angiotensin I converting enzyme (peptidyl-dipeptidase A) 1 Mus musculus 15-46 9766448-5 1998 In the present paper, we report on the in vivo effect of lisinopril, an ACE inhibitor, on the proliferative status of murine hematopoietic stem cells triggered into S-phase by irradiation. Lisinopril 57-67 angiotensin I converting enzyme (peptidyl-dipeptidase A) 1 Mus musculus 72-75 9766448-6 1998 Administration of lisinopril (10 mg/kg) 1 hour after irradiation led to a 90 to 100% inhibition of murine plasma ACE activity as observed during the first 4 hours postirradiation. Lisinopril 18-28 angiotensin I converting enzyme (peptidyl-dipeptidase A) 1 Mus musculus 113-116 9831227-8 1998 The power of the high-frequency spectral component increased in all animal preparations under treatment with prazosin, dl-propranolol, endothelin-1 and the angiotensin converting enzyme (ACE) inhibitors captopril, lisinopril, quinapril and ramipril. Lisinopril 214-224 angiotensin I converting enzyme Rattus norvegicus 187-190 9752892-10 1998 In conclusion, we could not demonstrate an antiproteinuric effect of the long-acting dihydropyridine calcium channel blocker amlodipine, whereas therapy with the ACE-inhibitor lisinopril resulted in a decrease in proteinuria. Lisinopril 176-186 angiotensin I converting enzyme Homo sapiens 162-165 9612349-10 1998 With lisinopril, renal renin concentration increased at both pH values. Lisinopril 5-15 renin Rattus norvegicus 23-28 9714110-5 1998 Measurements were repeated in 26 hypertensive patients after 1 year of treatment with the ACE inhibitor lisinopril. Lisinopril 104-114 angiotensin I converting enzyme Homo sapiens 90-93 9715782-5 1998 The primary analysis of ABP data revealed that both lisinopril and HCTZ effectively lowered mean 24-h systolic (SBP) and diastolic (DBP) blood pressure compared with placebo, (mean change from baseline SBP/DBP: -12.0/-8.2, -10.6/-5.5, and -0.3/-0.5 mm Hg, respectively); however, lisinopril lowered DBP better than HCTZ (P < .05). Lisinopril 52-62 selenium binding protein 1 Homo sapiens 112-115 9715782-5 1998 The primary analysis of ABP data revealed that both lisinopril and HCTZ effectively lowered mean 24-h systolic (SBP) and diastolic (DBP) blood pressure compared with placebo, (mean change from baseline SBP/DBP: -12.0/-8.2, -10.6/-5.5, and -0.3/-0.5 mm Hg, respectively); however, lisinopril lowered DBP better than HCTZ (P < .05). Lisinopril 52-62 D-box binding PAR bZIP transcription factor Homo sapiens 132-135 9715782-5 1998 The primary analysis of ABP data revealed that both lisinopril and HCTZ effectively lowered mean 24-h systolic (SBP) and diastolic (DBP) blood pressure compared with placebo, (mean change from baseline SBP/DBP: -12.0/-8.2, -10.6/-5.5, and -0.3/-0.5 mm Hg, respectively); however, lisinopril lowered DBP better than HCTZ (P < .05). Lisinopril 52-62 selenium binding protein 1 Homo sapiens 202-205 9715782-5 1998 The primary analysis of ABP data revealed that both lisinopril and HCTZ effectively lowered mean 24-h systolic (SBP) and diastolic (DBP) blood pressure compared with placebo, (mean change from baseline SBP/DBP: -12.0/-8.2, -10.6/-5.5, and -0.3/-0.5 mm Hg, respectively); however, lisinopril lowered DBP better than HCTZ (P < .05). Lisinopril 52-62 D-box binding PAR bZIP transcription factor Homo sapiens 206-209 9715782-5 1998 The primary analysis of ABP data revealed that both lisinopril and HCTZ effectively lowered mean 24-h systolic (SBP) and diastolic (DBP) blood pressure compared with placebo, (mean change from baseline SBP/DBP: -12.0/-8.2, -10.6/-5.5, and -0.3/-0.5 mm Hg, respectively); however, lisinopril lowered DBP better than HCTZ (P < .05). Lisinopril 52-62 D-box binding PAR bZIP transcription factor Homo sapiens 206-209 9648069-16 1998 Partial suppression of HSP47 mRNA expression by lisinopril at day 4 and day 7 after ureteral obstruction suggests that there are other immediate trigger(s) that induce the HSP47 mRNA expression. Lisinopril 48-58 serine (or cysteine) peptidase inhibitor, clade H, member 1 Mus musculus 23-28 9663927-13 1998 After treatment with lisinopril hypertensive patients with higher than normal insulin resistance indexes at baseline exhibited normalization of this parameter and significant increases of binding protein 1 levels and binding protein 1 : binding protein 3 ratio, with no significant changes in insulin-like growth factor I levels. Lisinopril 21-31 insulin Homo sapiens 78-85 9663927-13 1998 After treatment with lisinopril hypertensive patients with higher than normal insulin resistance indexes at baseline exhibited normalization of this parameter and significant increases of binding protein 1 levels and binding protein 1 : binding protein 3 ratio, with no significant changes in insulin-like growth factor I levels. Lisinopril 21-31 insulin like growth factor 1 Homo sapiens 293-321 9655179-3 1998 Lisinopril, an ACE inhibitor without a -SH group in its structure, did not produce endothelium-dependent relaxation. Lisinopril 0-10 angiotensin-converting enzyme Oryctolagus cuniculus 15-18 9710808-7 1998 Pharmacologic intervention studies with lisinopril or losartan indicate Ang II plays a role in the reciprocal regulation of ACE mRNA expression, which modulates Ang II levels at sites of repair. Lisinopril 40-50 angiotensinogen Rattus norvegicus 72-78 9710808-7 1998 Pharmacologic intervention studies with lisinopril or losartan indicate Ang II plays a role in the reciprocal regulation of ACE mRNA expression, which modulates Ang II levels at sites of repair. Lisinopril 40-50 angiotensin I converting enzyme Rattus norvegicus 124-127 9710808-7 1998 Pharmacologic intervention studies with lisinopril or losartan indicate Ang II plays a role in the reciprocal regulation of ACE mRNA expression, which modulates Ang II levels at sites of repair. Lisinopril 40-50 angiotensinogen Rattus norvegicus 161-167 9612349-12 1998 Ribonuclease protection assay showed both rat and mouse renin gene expression in the kidney, which increased with lisinopril. Lisinopril 114-124 renin Rattus norvegicus 56-61 9797190-8 1998 However, when the responses to infusions of acetylcholine and bradykinin were normalized with respect to that to infusion of sodium nitroprusside, only the vasodilatation in response to infusion of bradykinin was shown to have been increased by lisinopril treatment. Lisinopril 245-255 kininogen 1 Homo sapiens 198-208 9657538-1 1998 The aim of the study was to compare the effects of two long-acting antihypertensive agents, the calcium-antagonist amlodipine and the ACE inhibitor lisinopril, on left ventricular mass and diastolic filling in patients with mild to moderate diastolic hypertension from primary care centres. Lisinopril 148-158 angiotensin I converting enzyme Homo sapiens 134-137 9797190-2 1998 OBJECTIVE: To test whether antihypertensive treatment with the angiotensin converting enzyme inhibitor lisinopril can improve vasodilatation in response to endothelium-dependent agonists in essential hypertensive patients. Lisinopril 103-113 angiotensin I converting enzyme Homo sapiens 63-92 9797190-6 1998 Acute and prolonged lisinopril treatments significantly (P < 0.05 or less) improved vasodilatation in response to infusion of bradykinin (from 3.7 +/- 0.4 to 24.5 +/- 4.9 and from 3.7 +/- 0.3 to 22.1 +/- 4.9 ml/100 ml per min, respectively), but not in response to infusions of acetylcholine and of sodium nitroprusside. Lisinopril 20-30 kininogen 1 Homo sapiens 129-139 9797190-9 1998 CONCLUSIONS: Administration of lisinopril to patients with essential hypertension can selectively increase vasodilatation in response to infusion of bradykinin. Lisinopril 31-41 kininogen 1 Homo sapiens 149-159 9797190-7 1998 Chronic lisinopril treatment increased (P < 0.05) the response to infusions of not only bradykinin (from 3.5 +/- 0.5 to 27.6 +/- 5.3 ml/100 ml per min), but also of acetylcholine (from 3.5 +/- 0.5 to 27.8 +/- 8.0 ml/100 ml per min) and sodium nitroprusside (from 3.4 +/- 0.6 to 25.9 +/- 8.5 ml/100 ml per min). Lisinopril 8-18 kininogen 1 Homo sapiens 91-101 9568846-8 1998 Maximum TGF responses were 8.9 +/- 1.0 and 17.5 +/- 1.5 mmHg in 11- and 26-week-old rats that had been treated with the ACE-i lisinopril in the drinking water started when the animals were 7 weeks of age. Lisinopril 126-136 angiotensin I converting enzyme Rattus norvegicus 120-123 9416888-0 1997 Effect of the ACE inhibitor lisinopril on mortality in diabetic patients with acute myocardial infarction: data from the GISSI-3 study. Lisinopril 28-38 angiotensin I converting enzyme Homo sapiens 14-17 9461243-1 1998 Blockade of angiotensin II (Ang II) function during 8 days of oral therapy with lisinopril (20 mg/kg) and losartan (10 mg/kg) normalized the arterial pressure (112+/-3/70+/-3 mm Hg) and raised the plasma concentrations of the vasodilator peptide angiotensin-(1-7) [Ang-(1-7)] of 21 male spontaneously hypertensive rats (SHR). Lisinopril 80-90 angiotensinogen Rattus norvegicus 12-26 9461243-1 1998 Blockade of angiotensin II (Ang II) function during 8 days of oral therapy with lisinopril (20 mg/kg) and losartan (10 mg/kg) normalized the arterial pressure (112+/-3/70+/-3 mm Hg) and raised the plasma concentrations of the vasodilator peptide angiotensin-(1-7) [Ang-(1-7)] of 21 male spontaneously hypertensive rats (SHR). Lisinopril 80-90 angiotensinogen Rattus norvegicus 28-34 9433426-12 1998 Patients on lisinopril had significantly lower HbA1c at baseline than those on placebo (6.9% vs 7.3 p = 0.05). Lisinopril 12-22 hemoglobin subunit alpha 1 Homo sapiens 47-51 9453328-6 1998 Pretreatment with the nonselective antagonist [Sar1,Thr8]-Ang II abolished any additional pressor effects of either neprilysin inhibitor in spontaneously hypertensive rats treated with lisinopril or losartan. Lisinopril 185-195 angiotensinogen Rattus norvegicus 58-64 9453329-5 1998 In a pulmonary membrane preparation, the ACE inhibitor lisinopril attenuated the metabolism of low concentrations of 125I-Ang-(1-7). Lisinopril 55-65 angiotensin I converting enzyme Homo sapiens 41-44 9453329-5 1998 In a pulmonary membrane preparation, the ACE inhibitor lisinopril attenuated the metabolism of low concentrations of 125I-Ang-(1-7). Lisinopril 55-65 angiopoietin 1 Homo sapiens 122-130 9506682-12 1998 Blocking of AngII activity prevented almost completely the formation of microaneurysms in ATS rats (percent of glomeruli with microaneurysms: ATS, 11.5%+/-3.5%; ATS + lisinopril, 0.4%+/-0.2%; ATS + L-158,809, 0.8%+/-0.8%; controls, 0%). Lisinopril 167-177 angiotensinogen Rattus norvegicus 12-17 9506682-14 1998 TGF-beta1 mRNA levels in kidneys of ATS rats were 3.6-fold higher than those of controls and were reduced by 46% and 32% after treatment with lisinopril and L-158,809, respectively. Lisinopril 142-152 transforming growth factor, beta 1 Rattus norvegicus 0-9 9506682-15 1998 Urinary TGF-beta1 excretion increased in ATS (37.3+/-6.0 ng/d v controls, 13.8+/-3.4 ng/d; P< 0.01) but was normalized by lisinopril and L-158,809 (7.6+/-1.9 ng/d and 6.4+/-0.4 ng/d, respectively; P < 0.01). Lisinopril 125-135 transforming growth factor, beta 1 Rattus norvegicus 8-17 9506845-0 1998 Calorimetric analysis of lisinopril binding to angiotensin I-converting enzyme. Lisinopril 25-35 angiotensin I converting enzyme Homo sapiens 47-78 9506845-1 1998 Isothermal titration microcalorimetry has been used to measure changes in enthalpy and heat capacity for binding of lisinopril to the angiotensin I-converting enzyme (ACE; EC 3.4.15.1) and to its apoenzyme at pH 7.5 over a temperature range of 15-30 degrees C. Calorimetric measurements indicate that lisinopril binds to two sites in the monomer of both holo- and apo-ACE. Lisinopril 116-126 angiotensin I converting enzyme Homo sapiens 134-165 9506845-1 1998 Isothermal titration microcalorimetry has been used to measure changes in enthalpy and heat capacity for binding of lisinopril to the angiotensin I-converting enzyme (ACE; EC 3.4.15.1) and to its apoenzyme at pH 7.5 over a temperature range of 15-30 degrees C. Calorimetric measurements indicate that lisinopril binds to two sites in the monomer of both holo- and apo-ACE. Lisinopril 116-126 angiotensin I converting enzyme Homo sapiens 167-170 9506845-1 1998 Isothermal titration microcalorimetry has been used to measure changes in enthalpy and heat capacity for binding of lisinopril to the angiotensin I-converting enzyme (ACE; EC 3.4.15.1) and to its apoenzyme at pH 7.5 over a temperature range of 15-30 degrees C. Calorimetric measurements indicate that lisinopril binds to two sites in the monomer of both holo- and apo-ACE. Lisinopril 116-126 angiotensin I converting enzyme Homo sapiens 368-371 9506845-1 1998 Isothermal titration microcalorimetry has been used to measure changes in enthalpy and heat capacity for binding of lisinopril to the angiotensin I-converting enzyme (ACE; EC 3.4.15.1) and to its apoenzyme at pH 7.5 over a temperature range of 15-30 degrees C. Calorimetric measurements indicate that lisinopril binds to two sites in the monomer of both holo- and apo-ACE. Lisinopril 301-311 angiotensin I converting enzyme Homo sapiens 167-170 9506845-5 1998 Although the binding of lisinopril to holo- and apo-ACE is favored by entropy changes, this is more positive for the holoenzyme. Lisinopril 24-34 angiotensin I converting enzyme Homo sapiens 52-55 9416888-11 1997 CONCLUSIONS: Early treatment with the ACE inhibitor lisinopril in diabetic patients with acute MI is associated with a decreased 6-week mortality. Lisinopril 52-62 angiotensin I converting enzyme Homo sapiens 38-41 9549290-6 1997 RESULTS: A significative decrease of Hct values and a decrease of serum erythropoietin values was observed in patients treated with lisinopril. Lisinopril 132-142 erythropoietin Homo sapiens 72-86 9594434-3 1997 The inhibitory constants (IC50) ranged between 5.6 nM for serum ACE with lisinopril and 70000 nM for renal ACE with enalapril while Ki ranged from 1.0 nM for serum ACE with lisinopril to 12000 nM for kidney ACE with enalapril. Lisinopril 73-83 angiotensin-converting enzyme Ovis aries 64-67 9407415-6 1997 Therefore, we performed a cross sectional analysis of short-term responses to ACEi (enalapril or lisinopril) in 88 patients with stable non-diabetic proteinuria (> 1.0 g/day) and variable sodium intake. Lisinopril 97-107 angiotensin I converting enzyme Homo sapiens 78-82 9415815-4 1997 In addition, the relative potencies of captopril, lisinopril and enalapril were different for testicular ACE(C > L > E) and epididymal ACE(L > C > E). Lisinopril 50-60 angiotensin-converting enzyme Ovis aries 105-108 9415815-4 1997 In addition, the relative potencies of captopril, lisinopril and enalapril were different for testicular ACE(C > L > E) and epididymal ACE(L > C > E). Lisinopril 50-60 angiotensin-converting enzyme Ovis aries 141-144 9360002-2 1997 The specific goal of this study was to evaluate whether short-term administration of the ACE inhibitor lisinopril in hypertensive patients with an altered diastolic pattern induced an improvement of left ventricular dynamics, assessed by the echocardio-Doppler technique, independently of effects on left ventricular mass. Lisinopril 103-113 angiotensin I converting enzyme Homo sapiens 89-92 9350589-8 1997 Long-term treatment with lisinopril reduced the neuronal responsiveness to angiotensin II in SDR significantly in comparison with that of untreated SDR controls. Lisinopril 25-35 angiotensinogen Rattus norvegicus 75-89 9350589-9 1997 Lisinopril-treated SDR had a significantly lower responsiveness to angiotensin II than did hypertensive transgenic rats that had been treated with lisinopril. Lisinopril 0-10 angiotensinogen Rattus norvegicus 67-81 9350589-10 1997 CONCLUSION: The results show for the first time that administration of angiotensin II induced changes in discharge rates of somatosensory neurons, and that long-term administration of lisinopril caused a significant difference between the neuronal responsiveness to angiotensin of normotensive SDR and that of hypertensive transgenic rats. Lisinopril 184-194 angiotensinogen Rattus norvegicus 71-85 9262354-23 1997 PGE2 (100 ng), of the angiotensin-converting enzyme (ACE) inhibitor lisinopril (5 and 10 microg) attenuated the PGE2-induced fever. Lisinopril 68-78 angiotensin I converting enzyme Rattus norvegicus 22-51 9293971-5 1997 Additional groups of MI rats were treated with the ACE inhibitor lisinopril, alone or in combination with icatibant. Lisinopril 65-75 angiotensin I converting enzyme Rattus norvegicus 51-54 9262354-23 1997 PGE2 (100 ng), of the angiotensin-converting enzyme (ACE) inhibitor lisinopril (5 and 10 microg) attenuated the PGE2-induced fever. Lisinopril 68-78 angiotensin I converting enzyme Rattus norvegicus 53-56 9186076-14 1997 We conclude that chronic ACE inhibition with fosinopril and lisinopril alone or in combination with furosemide lowers BP in older blacks and nonblacks with hypertension and chronic renal insufficiency. Lisinopril 60-70 angiotensin I converting enzyme Homo sapiens 25-28 9200654-1 1997 The aim of our study was to evaluate whether inhibition of ACE (lisinopril 10-20 mg/day) can reduce the rate of decline in kidney function more than reducing blood pressure with conventional antihypertensive treatment (atenolol 50-100 mg/day), usually in combination with a diuretic. Lisinopril 64-74 angiotensin I converting enzyme Homo sapiens 59-62 9200654-11 1997 In conclusion, the relentless decline in kidney function characteristically found in hypertensive NIDDM patients with diabetic nephropathy can be reduced equally effectively by two antihypertensive treatments, the beta-blocker atenolol and the ACE inhibitor lisinopril. Lisinopril 258-268 angiotensin I converting enzyme Homo sapiens 244-247 9269212-4 1997 METHODS: We carried out a randomised, double-blind, placebo-controlled trial of the ACE inhibitor lisinopril in 530 men and women with IDDM aged 20-59 years with normoalbuminuria or microalbuminuria. Lisinopril 98-108 angiotensin I converting enzyme Homo sapiens 84-87 9194514-8 1997 The maximal blood pressure lowering achieved with SC-52458 was similar to the maximal effect observed with the angiotensin converting enzyme inhibitor lisinopril. Lisinopril 151-161 angiotensin I converting enzyme Canis lupus familiaris 111-140 9179532-2 1997 Lisinopril, like other ACE inhibitors, lowers blood pressure and preserves renal function in hypertensive patients with non-insulin-dependent or insulin-dependent diabetes mellitus (NIDDM or IDDM) and early or overt nephropathy, without adversely affecting glycaemic control or lipid profiles. Lisinopril 0-10 angiotensin I converting enzyme Homo sapiens 23-26 9179532-2 1997 Lisinopril, like other ACE inhibitors, lowers blood pressure and preserves renal function in hypertensive patients with non-insulin-dependent or insulin-dependent diabetes mellitus (NIDDM or IDDM) and early or overt nephropathy, without adversely affecting glycaemic control or lipid profiles. Lisinopril 0-10 insulin Homo sapiens 124-131 9179532-11 1997 The tolerability profile of lisinopril is typical of ACE inhibitors and appears to be similar in diabetic and nondiabetic individuals. Lisinopril 28-38 angiotensin I converting enzyme Homo sapiens 53-56 9179532-15 1997 Like other ACE inhibitors, lisinopril should thus be viewed as a first-line agent for reducing blood pressure and preventing or attenuating nephropathy in hypertensive diabetic patients with IDDM or NIDDM and microalbuminuria or overt renal disease. Lisinopril 27-37 angiotensin I converting enzyme Homo sapiens 11-14 9218184-6 1997 ACE inhibitor treatment with 10 mg/kg body weight lisinopril daily for 14 days by gavage reduced neointima proliferation in hypertensive and normotensive rats (neointima: media ratio: 0.35 +/- 0.02 for SHR, P < 0.01, versus untreated SHR with balloon injury; 0.28 +/- 0.01 for SD, P < 0.01, versus untreated SD rats with balloon injury). Lisinopril 50-60 angiotensin I converting enzyme Rattus norvegicus 0-3 9187274-4 1997 We demonstrate that captopril, lisinopril, and fosinoprilat are potent inhibitors of AcSDKP hydrolysis by wild-type ACE, with K(i) values in the subnanomolar range. Lisinopril 31-41 angiotensin I converting enzyme Homo sapiens 116-119 9250369-2 1997 Therefore, the aim of our study was to determine whether the ACE inhibitor lisinopril would modulate intercellular resistance of guinea pig ventricular myocytes. Lisinopril 75-85 LOW QUALITY PROTEIN: angiotensin-converting enzyme Cavia porcellus 61-64 9179087-3 1997 It measured the effectiveness of lisinopril, an angiotensin-converting enzyme inhibitor, in reducing the echocardiographic signs of MR severity over a one-year period. Lisinopril 33-43 angiotensin I converting enzyme Homo sapiens 48-77 8938667-12 1996 The oedema induced by collagenase was also increased by lisinopril, another ACE inhibitor, administered locally in combination with apstatin, an inhibitor of aminopeptidase P (AmP). Lisinopril 56-66 angiotensin I converting enzyme Rattus norvegicus 76-79 9140680-1 1997 The present study was performed in order to compare the efficacy, safety, and tolerability of lisinopril, a long-acting angiotensin-converting enzyme (ACE) inhibitor, with captopril, the shorter acting ACE inhibitor available, in the treatment of elderly patients (mean age 70 +/- 0.5 years) with congestive heart failure (mean left ventricular ejection fraction 33.5 +/- 1%). Lisinopril 94-104 angiotensin I converting enzyme Homo sapiens 120-149 9140680-1 1997 The present study was performed in order to compare the efficacy, safety, and tolerability of lisinopril, a long-acting angiotensin-converting enzyme (ACE) inhibitor, with captopril, the shorter acting ACE inhibitor available, in the treatment of elderly patients (mean age 70 +/- 0.5 years) with congestive heart failure (mean left ventricular ejection fraction 33.5 +/- 1%). Lisinopril 94-104 angiotensin I converting enzyme Homo sapiens 151-154 9469796-1 1997 OBJECTIVE: To evaluate the effects of long-term antihypertensive therapy with the angiotensin converting enzyme inhibitor lisinopril on structural alterations and the endothelial function of small resistance arteries in hypertensive patients with left ventricular hypertrophy. Lisinopril 122-132 angiotensin I converting enzyme Homo sapiens 82-111 8890833-5 1996 To address this question, a large multinational, double-blind clinical trial (Assessment of Treatment With Lisinopril and Survival [ATLAS]) was launched to compare the effects of low and high doses of the ACE inhibitor lisinopril on the survival of patients with heart failure. Lisinopril 219-229 angiotensin I converting enzyme Homo sapiens 205-208 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. Lisinopril 206-216 angiotensin I converting enzyme Homo sapiens 0-3 9125659-0 1997 Lisinopril-induced isolated visceral angioedema: review of ACE-inhibitor-induced small bowel angioedema. Lisinopril 0-10 angiotensin I converting enzyme Homo sapiens 59-62 9124549-3 1997 The objective of this study was to test the hypothesis that a modest physiological increase in plasma AVP would potentiate the responses of heart rate (HR), forearm vascular resistance (FVR), plasma norepinephrine (NE), or systemic NE spillover to baroreflex unloading and loading after pretreatment with lisinopril in healthy human volunteers. Lisinopril 305-315 arginine vasopressin Homo sapiens 102-105 9124549-10 1997 During AVP infusion after lisinopril, HR decreased from 67 +/- 6.5 to 62 +/- 4.5 beats/min (P < 0.05). Lisinopril 26-36 arginine vasopressin Homo sapiens 7-10 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. Lisinopril 0-10 angiotensin I converting enzyme Homo sapiens 96-99 9061270-12 1997 Economic studies suggest that lisinopril is cost saving compared with other ACE inhibitors in some markets. Lisinopril 30-40 angiotensin I converting enzyme Homo sapiens 76-79 9061270-13 1997 When given according to the GISSI-3 protocol, lisinopril appears to be one of the less expensive of the successful ACE inhibitor regimens for acute myocardial infarction. Lisinopril 46-56 angiotensin I converting enzyme Homo sapiens 115-118 9061270-18 1997 Lisinopril is well tolerated and the profile of adverse events seen is typical of ACE inhibitors as a class. Lisinopril 0-10 angiotensin I converting enzyme Homo sapiens 82-85 8915971-9 1996 Lisinopril increased rat renin and angiotensinogen gene expression both in SDH and TGR, but it did not influence mouse renin gene expression in TGR. Lisinopril 0-10 renin Rattus norvegicus 25-50 8891468-2 1996 Following establishment of its efficacy in hypertension and congestive heart failure, the ACE inhibitor lisinopril has now been shown to reduce mortality and cardiovascular morbidity in patients with myocardial infarction when administered as early treatment. Lisinopril 104-114 angiotensin I converting enzyme Homo sapiens 90-93 8891468-16 1996 Lisinopril has a tolerability profile resembling that of other ACE inhibitors, can be given once daily and may be less costly than other members of its class. Lisinopril 0-10 angiotensin I converting enzyme Homo sapiens 63-66 8915971-9 1996 Lisinopril increased rat renin and angiotensinogen gene expression both in SDH and TGR, but it did not influence mouse renin gene expression in TGR. Lisinopril 0-10 renin Rattus norvegicus 25-30 8670080-1 1996 A soluble 67 kDa angiotensin-converting enzyme (ACE) has been purified by lisinopril-Sepharose affinity column chromatography from adult houseflies, Musca domestica. Lisinopril 74-84 angiotensin-converting enzyme Musca domestica 17-46 8707393-4 1996 It has been shown in 14-week-old SHR with early hypertensive heart disease that myocardial fibrosis could be reversed and myocardial diastolic stiffness normalized by 12-week treatment with the angiotensin-converting enzyme inhibitor lisinopril. Lisinopril 234-244 angiotensin I converting enzyme Rattus norvegicus 194-223 8707393-8 1996 Thus, long-term angiotensin-converting enzyme inhibition with lisinopril normalized arterial pressure and LVH, reversed myocardial fibrosis, and improved abnormal myocardial diastolic stiffness in advanced hypertensive heart disease in SHR. Lisinopril 62-72 angiotensin I converting enzyme Rattus norvegicus 16-45 8707393-10 1996 The fibrolytic response to lisinopril was at least partly due to enhanced collagen degradation by activation of tissue matrix metalloproteinase 1. Lisinopril 27-37 matrix metallopeptidase 1 Rattus norvegicus 119-145 8837313-0 1996 The ACE-inhibitor lisinopril affects plasma insulin levels but not fibrinolytic parameters. Lisinopril 18-28 angiotensin I converting enzyme Homo sapiens 4-7 8837313-0 1996 The ACE-inhibitor lisinopril affects plasma insulin levels but not fibrinolytic parameters. Lisinopril 18-28 insulin Homo sapiens 44-51 8837313-4 1996 Therefore the present study examines the relationship between insulin and PAI-1 plasma levels during intravenous glucose tolerance tests before and after administration with the ACE-inhibitor lisinopril in 12 male obese patients with angiographically proven coronary artery disease and borderline hypertension. Lisinopril 192-202 angiotensin I converting enzyme Homo sapiens 178-181 8837313-7 1996 Stimulated levels of insulin during glucose tolerance test also significantly decreased by lisinopril (peak insulin from 57 +/- 10 to 41.2 +/- 7.3 uU/ml, p < or = 0.02). Lisinopril 91-101 insulin Homo sapiens 21-28 8837313-7 1996 Stimulated levels of insulin during glucose tolerance test also significantly decreased by lisinopril (peak insulin from 57 +/- 10 to 41.2 +/- 7.3 uU/ml, p < or = 0.02). Lisinopril 91-101 insulin Homo sapiens 108-115 8837313-9 1996 Our data confirm a beneficial effect of lisinopril on plasma levels of insulin but failed to demonstrate any profibrinolytic effect in this study population, thus questioning the postulated mechanism of influencing endogenous fibrinolysis by changes of plasma insulin. Lisinopril 40-50 insulin Homo sapiens 71-78 8807457-6 1996 It can be concluded that under routine medical care ACE inhibitor lisinopril is a well tolerated, effective drug for treatment of hypertensive type II diabetic patients. Lisinopril 66-76 angiotensin I converting enzyme Homo sapiens 52-55 8670080-1 1996 A soluble 67 kDa angiotensin-converting enzyme (ACE) has been purified by lisinopril-Sepharose affinity column chromatography from adult houseflies, Musca domestica. Lisinopril 74-84 angiotensin-converting enzyme Musca domestica 48-51 8698434-4 1996 Lisinopril treatment increased plasma renin activity and reduced 24-hour systolic and diastolic pressures (from 159 +/- 14 to 121 +/- 8 and from 103 +/- 7 to 80 +/- 3 mm Hg, respectively) and left ventricular mass index (from 159 +/- 33 to 134 +/- 26 g/m2); moreover, in 12 of 30 patients, left ventricular mass normalization was achieved. Lisinopril 0-10 renin Homo sapiens 38-43 8699329-1 1996 Peptidic drugs such as beta-lactam aminocephalosporin antibiotics (e.g., cephalexin) and the ACE inhibitors lisinopril, quinapril, and benzazepril are apparently absorbed, at least in part, by the intestinal dipeptide transporter system (DTS). Lisinopril 108-118 angiotensin I converting enzyme Rattus norvegicus 93-96 7557704-1 1995 The efficacy, tolerability and impact on quality of life of the ACE inhibitor lisinopril were evaluated in a 12-week open, multicenter post-marketing surveillance study. Lisinopril 78-88 angiotensin I converting enzyme Homo sapiens 64-67 8849595-3 1996 METHODS: Endothelin-1 release into the media was evaluated by radioimmunoassay under basal conditions and after 24 h treatment of endothelial cells with cocaine hydrochloride (HCl), or cocaine HCl and ACE inhibitors, captopril and lisinopril. Lisinopril 231-241 endothelin 1 Homo sapiens 9-21 8849595-6 1996 Furthermore, cocaine-stimulated ET-1 release was inhibited by administration of angiotensin-converting enzyme inhibitors captopril and lisinopril. Lisinopril 135-145 endothelin 1 Homo sapiens 32-36 7586374-6 1995 Administration of lisinopril attenuated the development of left and right ventricular hypertrophy in this model and was accompanied by an attenuation of the upregulation of the ACE, collagen type I-alpha, and vimentin mRNAs. Lisinopril 18-28 angiotensin I converting enzyme Rattus norvegicus 177-180 7586374-6 1995 Administration of lisinopril attenuated the development of left and right ventricular hypertrophy in this model and was accompanied by an attenuation of the upregulation of the ACE, collagen type I-alpha, and vimentin mRNAs. Lisinopril 18-28 vimentin Rattus norvegicus 209-217 7586374-7 1995 Because the activity of the circulating RAS in the aortocaval shunt rats was not higher than that in the sham-operated rats, the effects of lisinopril in attenuating the ventricular hypertrophy may be due to inhibition of the increased ACE in the ventricle. Lisinopril 140-150 angiotensin I converting enzyme Rattus norvegicus 236-239 7585774-1 1995 Results from SOLVD, SAVE, AIRE, GISSI-III, ISIS-IV, and the Chinese Captopril Trial suggest that therapy with ACE inhibitors, at least with enalapril, captopril, ramipril, and lisinopril, induce significant reduction in morbidity and mortality rates in patients with ischemic heart disease, myocardial infarction, and a wide range of ventricular function and myocardial infarction. Lisinopril 176-186 angiotensin I converting enzyme Homo sapiens 110-113 8594963-1 1995 Angio-oedema is a recognised complication of angiotensin converting enzyme (ACE) inhibitor therapy, occurring in 0.1% to 0.5% of patients taking captopril, enalapril, or lisinopril. Lisinopril 170-180 angiotensin I converting enzyme Homo sapiens 45-74 8594963-1 1995 Angio-oedema is a recognised complication of angiotensin converting enzyme (ACE) inhibitor therapy, occurring in 0.1% to 0.5% of patients taking captopril, enalapril, or lisinopril. Lisinopril 170-180 angiotensin I converting enzyme Homo sapiens 76-79 8570098-7 1995 Hydrolysis of this substrate by ACE-like enzyme is inhibited at 80% by 10 microM captopril or 10 microM lisinopril (IC50 of 200 nM and 50 nM, respectively). Lisinopril 104-114 LOW QUALITY PROTEIN: angiotensin-converting enzyme Cavia porcellus 32-35 7664216-7 1995 In a recent multicentre study in which patients with a prior history of ACE inhibitor-related cough were randomized into three treatment groups, the percentage of patients with a dry cough was significantly higher in the lisinopril group (72%) than in the losartan (29%) or the hydrychlorothiazide (34%) groups. Lisinopril 221-231 angiotensin I converting enzyme Homo sapiens 72-75 7637261-6 1995 Nephrectomized animals were left untreated or treated with the ACE inhibitor lisinopril in drinking water. Lisinopril 77-87 angiotensin I converting enzyme Rattus norvegicus 63-66 7602241-0 1995 Inhibition of angiotensin-converting enzyme and attenuation of myocardial fibrosis by lisinopril in rats receiving angiotensin II. Lisinopril 86-96 angiotensinogen Rattus norvegicus 115-129 7602241-4 1995 We sought to determine whether the ACE inhibitor lisinopril would attenuate fibrous tissue ACE binding and fibrous tissue formation in the myocardium of rats receiving AngII. Lisinopril 49-59 angiotensin I converting enzyme Rattus norvegicus 35-38 7602241-4 1995 We sought to determine whether the ACE inhibitor lisinopril would attenuate fibrous tissue ACE binding and fibrous tissue formation in the myocardium of rats receiving AngII. Lisinopril 49-59 angiotensin I converting enzyme Rattus norvegicus 91-94 7602241-4 1995 We sought to determine whether the ACE inhibitor lisinopril would attenuate fibrous tissue ACE binding and fibrous tissue formation in the myocardium of rats receiving AngII. Lisinopril 49-59 angiotensinogen Rattus norvegicus 168-173 7602241-6 1995 Cardiac ACE binding density was localized and quantified by in vitro autoradiography with [125I]-labeled 351A, a tyrosyl derivative of lisinopril, while fibrosis was identified by light microscopy in serial sections stained with picrosirius red. Lisinopril 135-145 angiotensin I converting enzyme Rattus norvegicus 8-11 7674133-0 1995 Toxicodynamic analysis of inflammatory reactions by an angiotensin converting enzyme inhibitor (lisinopril) in guinea-pig skin. Lisinopril 96-106 LOW QUALITY PROTEIN: angiotensin-converting enzyme Cavia porcellus 55-84 7794953-3 1995 The kinetic transport parameters of three ACE-inhibitors, enalapril, enalaprilat, and lisinopril, have been determined in an in vivo system using rat intestine. Lisinopril 86-96 angiotensin I converting enzyme Rattus norvegicus 42-45 7669481-15 1995 The results of this study indicate that lisinopril reduces levels of plasma fibrinogen and confirm that different antihypertensive drugs may elicit different metabolic effects, which may variously influence the overall risk profile of the hypertensive patients. Lisinopril 40-50 fibrinogen beta chain Homo sapiens 76-86 7789045-5 1995 The influence of the angiotensin-converting enzyme inhibitor, lisinopril, on the response of the renin-angiotensin system and serum potassium to nebulized salbutamol was investigated in a randomized, double-blind, crossover study in eight healthy volunteers using a factorial block design. Lisinopril 62-72 renin Homo sapiens 97-102 7796449-0 1995 Prevention of angiotensin II induced myocyte necrosis and coronary vascular damage by lisinopril and losartan in the rat. Lisinopril 86-96 angiotensinogen Rattus norvegicus 14-28 7613528-10 1995 Both lisinopril and cilazapril suppressed hypothalamic angiotensinogen mRNA. Lisinopril 5-15 angiotensinogen Rattus norvegicus 55-70 7600744-0 1995 Is ACE inhibition with lisinopril helpful in diabetic neuropathy? Lisinopril 23-33 angiotensin I converting enzyme Homo sapiens 3-6 7789045-9 1995 Baseline plasma renin concentrations were increased [160.1 (20.6) mu-units/ml] and baseline plasma angiotensin II concentrations were reduced [1.4 (0.1) pg/ml] by lisinopril, P < 0.05 versus placebo in each case. Lisinopril 163-173 angiotensinogen Homo sapiens 99-113 7721400-6 1995 In the kidney, expression of the transgene and the endogenous renin gene increased, suggesting that both are modulated by lisinopril in a similar manner. Lisinopril 122-132 renin Rattus norvegicus 62-67 7721400-3 1995 This study analyzes the effects of the converting enzyme inhibitor lisinopril, which specifically interferes with the renin-angiotensin system, and the direct vasodilator dihydralazine on the renal and extrarenal expression of renin and angiotensinogen. Lisinopril 67-77 renin Rattus norvegicus 118-123 7721400-3 1995 This study analyzes the effects of the converting enzyme inhibitor lisinopril, which specifically interferes with the renin-angiotensin system, and the direct vasodilator dihydralazine on the renal and extrarenal expression of renin and angiotensinogen. Lisinopril 67-77 renin Rattus norvegicus 227-232 7721400-9 1995 Cardiac hypertrophy was reduced by lisinopril but not dihydralazine and was positively correlated with cardiac angiotensinogen expression. Lisinopril 35-45 angiotensinogen Rattus norvegicus 111-126 7755273-5 1995 This concept arose from quantitative in vitro autoradiography using an iodinated derivative of lisinopril (125I-351A) as ligand to localize angiotensin converting enzyme (ACE) binding density within the heart. Lisinopril 95-105 angiotensin I converting enzyme Homo sapiens 171-174 7619667-0 1995 Bronchospasm and cough as adverse reactions to the ACE inhibitors captopril, enalapril and lisinopril. Lisinopril 91-101 angiotensin I converting enzyme Homo sapiens 51-54 7596197-4 1995 Lisinopril inhibition curves of tissue ACE activity were similar in aging hamsters with and without cardiomyopathy. Lisinopril 0-10 angiotensin I converting enzyme Homo sapiens 39-42 7780654-5 1995 In contrast, transport and intracellular accumulation of the angiotensin-converting enzyme (ACE) inhibitor, lisinopril, were low (lower than the paracellular marker mannitol) and were not stimulated by apical acidification. Lisinopril 108-118 angiotensin I converting enzyme Homo sapiens 61-90 7780654-5 1995 In contrast, transport and intracellular accumulation of the angiotensin-converting enzyme (ACE) inhibitor, lisinopril, were low (lower than the paracellular marker mannitol) and were not stimulated by apical acidification. Lisinopril 108-118 angiotensin I converting enzyme Homo sapiens 92-95 7867186-15 1995 In addition, serum PIIIP and PIP concentrations decreased significantly (P < .001) to normal values in patients treated with lisinopril. Lisinopril 128-138 prolactin induced protein Homo sapiens 29-32 7769811-4 1995 The influences of acute (single dose) beta 1-selective blockade by bisoprolol or angiotensin-converting enzyme (ACE) inhibition by lisinopril were analyzed by a double-blind placebo-controlled trial. Lisinopril 131-141 angiotensin I converting enzyme Homo sapiens 81-110 7769811-4 1995 The influences of acute (single dose) beta 1-selective blockade by bisoprolol or angiotensin-converting enzyme (ACE) inhibition by lisinopril were analyzed by a double-blind placebo-controlled trial. Lisinopril 131-141 angiotensin I converting enzyme Homo sapiens 112-115 7620708-15 1995 CFP displaced the binding of [125I]-351A (the p-hydroxybenzamidine derivative of lisinopril) from preparations of rat plasma ACE and solubilized lung membrane ACE (KD = 1.2 and 0.14 microM respectively), and inhibited rat plasma ACE activity (KI = 2.4 microM). Lisinopril 81-91 complement factor properdin Rattus norvegicus 0-3 7860891-0 1995 Multiple episodes of angioedema associated with lisinopril, an ACE inhibitor. Lisinopril 48-58 angiotensin I converting enzyme Homo sapiens 63-66 8021010-8 1994 In SHR, vasoconstriction in response to angiotensinogen-rich, renin-free plasma was dose dependent, was inhibited by lisinopril, and was not found 24 hours after bilateral nephrectomy. Lisinopril 117-127 renin Rattus norvegicus 62-67 8751015-2 1995 Compared to placebo, lisinopril significantly decreased blood pressure, increased plasma renin activity without altering heart rate or plasma norepinephrine. Lisinopril 21-31 renin Homo sapiens 89-94 8751016-1 1995 To investigate the effects of antihypertensive treatment with the angiotensin-converting enzyme (ACE) inhibitor lisinopril on insulin sensitivity and related metabolic variables, the insulin sensitivity index (SI), determined with the Minimal Model Method of Bergman, fasting plasma insulin and glucose concentrations, serum total triglyceride and lipoprotein cholesterol fractions, and blood pressure were assessed in 24 lean, non-diabetic patients with essential hypertension. Lisinopril 112-122 angiotensin I converting enzyme Homo sapiens 97-100 8751016-1 1995 To investigate the effects of antihypertensive treatment with the angiotensin-converting enzyme (ACE) inhibitor lisinopril on insulin sensitivity and related metabolic variables, the insulin sensitivity index (SI), determined with the Minimal Model Method of Bergman, fasting plasma insulin and glucose concentrations, serum total triglyceride and lipoprotein cholesterol fractions, and blood pressure were assessed in 24 lean, non-diabetic patients with essential hypertension. Lisinopril 112-122 insulin Homo sapiens 126-133 8751016-9 1995 These findings demonstrate that the ACE inhibitor lisinopril is neutral with regard to insulin sensitivity, plasma insulin and glucose, and lipoprotein metabolism in patients with essential hypertension. Lisinopril 50-60 angiotensin I converting enzyme Homo sapiens 36-39 8751016-9 1995 These findings demonstrate that the ACE inhibitor lisinopril is neutral with regard to insulin sensitivity, plasma insulin and glucose, and lipoprotein metabolism in patients with essential hypertension. Lisinopril 50-60 insulin Homo sapiens 87-94 8751016-9 1995 These findings demonstrate that the ACE inhibitor lisinopril is neutral with regard to insulin sensitivity, plasma insulin and glucose, and lipoprotein metabolism in patients with essential hypertension. Lisinopril 50-60 insulin Homo sapiens 115-122 7851032-1 1994 The objectives of this study were to evaluate the specific effect of the ACE-inhibitor lisinopril on myocardial mass and diastolic function in uremic patients using a protocol designed to leave blood pressure unchanged. Lisinopril 87-97 angiotensin I converting enzyme Homo sapiens 73-76 7841571-1 1994 OBJECTIVE: This report describes a case of lisinopril overdose managed in part with an infusion of angiotensin II in a patient with dilated cardiomyopathy and reviews other literature reporting angiotensin-converting enzyme (ACE) inhibitor overdose. Lisinopril 43-53 angiotensinogen Homo sapiens 99-113 7841571-1 1994 OBJECTIVE: This report describes a case of lisinopril overdose managed in part with an infusion of angiotensin II in a patient with dilated cardiomyopathy and reviews other literature reporting angiotensin-converting enzyme (ACE) inhibitor overdose. Lisinopril 43-53 angiotensin I converting enzyme Homo sapiens 194-223 7841571-1 1994 OBJECTIVE: This report describes a case of lisinopril overdose managed in part with an infusion of angiotensin II in a patient with dilated cardiomyopathy and reviews other literature reporting angiotensin-converting enzyme (ACE) inhibitor overdose. Lisinopril 43-53 angiotensin I converting enzyme Homo sapiens 225-228 8052664-4 1994 Column chromatography, including modified affinity chromatography on lisinopril-Sepharose, yielded homogeneous ACE after only a 45-fold purification. Lisinopril 69-79 angiotensin I converting enzyme Homo sapiens 111-114 7519541-1 1994 A sprightly 79-year-old woman was treated for high blood pressure with indapamide (2.5 mg/day) and the angiotensin converting enzyme (ACE) inhibitor lisinopril (5 mg/day). Lisinopril 149-159 angiotensin I converting enzyme Homo sapiens 103-132 7519541-1 1994 A sprightly 79-year-old woman was treated for high blood pressure with indapamide (2.5 mg/day) and the angiotensin converting enzyme (ACE) inhibitor lisinopril (5 mg/day). Lisinopril 149-159 angiotensin I converting enzyme Homo sapiens 134-137 7528985-1 1994 To clarify whether angiotensin converting enzyme (ACE) inhibitors prevent progressive renal injury directly by their antihypertensive effect we administered the ACE inhibitor lisinopril to male MWF/Ztm rats as a single daily dose that lowered blood pressure for only 9 of 24 h. We investigated the effects of this treatment in short- and long-term studies and compared them with another antihypertensive drug, the calcium channel blocker nitrendipine, given to partially control blood pressure as done with the ACE inhibitor. Lisinopril 175-185 angiotensin I converting enzyme Rattus norvegicus 161-164 7528985-1 1994 To clarify whether angiotensin converting enzyme (ACE) inhibitors prevent progressive renal injury directly by their antihypertensive effect we administered the ACE inhibitor lisinopril to male MWF/Ztm rats as a single daily dose that lowered blood pressure for only 9 of 24 h. We investigated the effects of this treatment in short- and long-term studies and compared them with another antihypertensive drug, the calcium channel blocker nitrendipine, given to partially control blood pressure as done with the ACE inhibitor. Lisinopril 175-185 angiotensin I converting enzyme Rattus norvegicus 161-164 7995007-6 1994 During angiotensin II infusion, with a similar increase in systemic blood pressure, the change in ERPF, FF, and RVR again was more pronounced during enalapril than during lisinopril (ERPF: -14.6% +/- 2.9% versus -7.8% +/- 3.3%, p = 0.018; FF: 18.3% +/- 5.9% versus 12.8% +/- 6.0%, p = 0.028; RVR: 36.7% +/- 8.1% versus 21.9% +/- 4.3%, p = 0.018). Lisinopril 171-181 angiotensinogen Homo sapiens 7-21 7983291-11 1994 CONCLUSION: The data from this retrospective study confirm the safe and effective use of enalapril and lisinopril, two long-acting ACE inhibitors, in elderly hypertensive patients. Lisinopril 103-113 angiotensin I converting enzyme Homo sapiens 131-134 7955203-8 1994 Neither dose affected LV ACE activity and ACE mRNA levels as determined by competitive polymerase chain reaction, whereas LV ANF mRNA levels were significantly reduced by high-dose lisinopril. Lisinopril 181-191 natriuretic peptide A Rattus norvegicus 125-128 7955203-11 1994 Sustained inhibition of renal ACE during long-term therapy may contribute to the beneficial effect of high-dose lisinopril. Lisinopril 112-122 angiotensin I converting enzyme Rattus norvegicus 30-33 7955203-12 1994 Low-dose lisinopril, although exerting sustained inhibition of the plasma ACE, does not improve survival after myocardial infarction. Lisinopril 9-19 angiotensin I converting enzyme Rattus norvegicus 74-77 7528840-1 1994 To assess the role of angiotensin II (AII) in development of myocardial injury during ischemia and reperfusion, the effects of short-term treatment with the angiotensin-converting enzyme (ACE) inhibitor lisinopril were compared with the effects of short-term treatment with L-158,338, an AII antagonist, in isolated working rat heart. Lisinopril 203-213 angiotensin I converting enzyme Rattus norvegicus 188-191 7837215-1 1994 The present study was performed to investigate the efficacy and safety of the angiotensin converting enzyme (ACE) inhibitor lisinopril compared with those of the calcium channel blocker nifedipine in 293 patients with mild to moderate essential hypertension (supine diastolic blood pressure (DBP) 95-115 mmHg) in a multicentre, randomised, double-blind parallel group study after a two week single-blind placebo run-in period. Lisinopril 124-134 angiotensin I converting enzyme Homo sapiens 109-112 7932518-8 1994 Mean office DBP decreased from baseline -18.1 +/- 8.6 mmHg for lisinopril patients and -15.9 +/- 10.1 mmHg for diltiazem SR patients at week 8. Lisinopril 63-73 D-box binding PAR bZIP transcription factor Homo sapiens 12-15 8136111-8 1994 A significant increase of plasma renin activity and a significant decrease of plasma aldosterone was observed in these patients after treatment with lisinopril. Lisinopril 149-159 renin Homo sapiens 33-38 8206613-9 1994 In contrast, contractions to angiotensin II were augmented by cyclosporin A, lisinopril, and the combination of both but not by D 8731 or D 8731 plus cyclosporin A. Lisinopril 77-87 angiotensinogen Rattus norvegicus 29-43 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. Lisinopril 11-21 angiotensin I converting enzyme Homo sapiens 91-94 8184972-9 1994 The transient endothelium-mediated relaxing phase of the depressor response to systemic injections of endothelin-1 was attenuated by losartan and lisinopril in TG rats. Lisinopril 146-156 endothelin 1 Rattus norvegicus 102-114 8144213-8 1994 Lisinopril also increased aortic bradykinin-(1-9) and bradykinin-(1-7) levels at doses below the threshold for the decrease in the ratio of Ang II to Ang I. Lisinopril 0-10 angiotensinogen Rattus norvegicus 140-146 8144213-8 1994 Lisinopril also increased aortic bradykinin-(1-9) and bradykinin-(1-7) levels at doses below the threshold for the decrease in the ratio of Ang II to Ang I. Lisinopril 0-10 angiogenin Rattus norvegicus 140-143 8174603-4 1994 Reduction in affinity at the amino binding site of somatic angiotensin converting enzyme was related to an increased side chain size (lung KDA (pM): Ro 31-8472 175 +/- 38, lisinopril 2205 +/- 1832, and 351A 2271 +/- 489), or hydrophobicity of the competing unlabelled angiotensin converting enzyme inhibitor (lung KDA (pM): quinaprilat 1267 +/- 629 and perindoprilat 824 +/- 6). Lisinopril 172-182 angiotensin I converting enzyme Rattus norvegicus 59-88 7933808-3 1994 We tested the hypothesis that down-regulation of the Ang II type-1 receptor (AT1-R) gene occurs in UUO in response to Ang II, by examining the effects of an ACE inhibitor [lisinopril (Li), 5 mg/kg/day] and of the specific nonpeptidic AT1-R blocker, losartan (Lo) (10 mg/kg/day). Lisinopril 172-182 angiotensin II receptor, type 1a Rattus norvegicus 77-82 8043942-5 1994 All calcium channel blockers studied have displayed similar metabolic effects, while among the ACE inhibitors studied, lisinopril was associated with the best metabolic responses. Lisinopril 119-129 angiotensin I converting enzyme Homo sapiens 95-98 8165541-0 1994 Both lisinopril and verapamil reduced platelet-derived growth factor-A chain mRNA levels in human saphenous vein endothelial cells stimulated by thrombin. Lisinopril 5-15 coagulation factor II, thrombin Homo sapiens 145-153 8165541-6 1994 PDGF-AA homodimer in conditioned media was measured by ELISA: RESULTS: Lisinopril attenuated the induction by thrombin of PDGF-A chain mRNA levels significantly in human ECs at doses of 10(-6) mol/L and 10(-5) mol/L (p < 0.05) and appeared to decrease PDGF-AA homodimer released in conditioned medium. Lisinopril 71-81 coagulation factor II, thrombin Homo sapiens 110-118 8165541-6 1994 PDGF-AA homodimer in conditioned media was measured by ELISA: RESULTS: Lisinopril attenuated the induction by thrombin of PDGF-A chain mRNA levels significantly in human ECs at doses of 10(-6) mol/L and 10(-5) mol/L (p < 0.05) and appeared to decrease PDGF-AA homodimer released in conditioned medium. Lisinopril 71-81 platelet derived growth factor subunit A Homo sapiens 122-134 8165541-8 1994 CONCLUSIONS: These data suggest that one means by which lisinopril and verapamil both suppress intimal thickening might be inhibition of PDGF-A chain gene expression in ECs regrowing over vessel injury areas that are sites of thrombin generation. Lisinopril 56-66 platelet derived growth factor subunit A Homo sapiens 137-149 8165541-8 1994 CONCLUSIONS: These data suggest that one means by which lisinopril and verapamil both suppress intimal thickening might be inhibition of PDGF-A chain gene expression in ECs regrowing over vessel injury areas that are sites of thrombin generation. Lisinopril 56-66 coagulation factor II, thrombin Homo sapiens 226-234 7743538-9 1994 The message from GISSI-3 was that administration of ACE inhibitors within 24 h of symptom onset will improve survival and left ventricular function provided patients are hemodynamically stable, are not hypotensive and have no renal dysfunction; 76 lives were saved (representing an 11% risk reduction in mortality) after six weeks" lisinopril treatment, 54 of which were saved in the first five days. Lisinopril 332-342 angiotensin I converting enzyme Homo sapiens 52-55 8293771-5 1993 Incubation (24h) with the ACE inhibitors lisinopril 10(-5) M (+28.8%; P < 0.05) and ramiprilat 10(-5) M (+33.7%, P < 0.09) augmented the beta-receptor density in BAEC, but lower ACE inhibitor doses had no affect. Lisinopril 41-51 angiotensin I converting enzyme Bos taurus 26-29 7995322-2 1994 To prevent drug accumulation and adverse effects the dose of hydrophilic angiotensin-converting enzyme (ACE) inhibitors, e.g. lisinopril, must be reduced in patients with renal failure. Lisinopril 126-136 angiotensin I converting enzyme Homo sapiens 73-102 7995322-2 1994 To prevent drug accumulation and adverse effects the dose of hydrophilic angiotensin-converting enzyme (ACE) inhibitors, e.g. lisinopril, must be reduced in patients with renal failure. Lisinopril 126-136 angiotensin I converting enzyme Homo sapiens 104-107 8200499-9 1994 There seems to be no intelligible reason, up to now, to deem that any ACE inhibitor should be considered better than another one in the acute phase of infarction, but still during the first 72 hours after the onset of chest pain the advantages have been shown only with lisinopril and captopril. Lisinopril 270-280 angiotensin I converting enzyme Homo sapiens 70-73 7927959-3 1994 In 16 proteinuric patients with biopsy-proven IgA nephropathy, with normal renal function and blood pressure, maintained at controlled sodium intake < or = 80 mEqII, the efficacy of increasing doses of the ACE inhibitor lisinopril was studied. Lisinopril 223-233 angiotensin I converting enzyme Homo sapiens 209-212 7902354-7 1993 The double mutant also had a 100-fold higher Ki for lisinopril, a competitive inhibitor of ACET, and was 17-fold less sensitive to stimulation by NaCl, an activator of ACET. Lisinopril 52-62 angiotensin I converting enzyme Homo sapiens 91-95 7902354-7 1993 The double mutant also had a 100-fold higher Ki for lisinopril, a competitive inhibitor of ACET, and was 17-fold less sensitive to stimulation by NaCl, an activator of ACET. Lisinopril 52-62 angiotensin I converting enzyme Homo sapiens 168-172 7902354-8 1993 These results directly demonstrate that Tyr-236 and Lys-154 are indeed critical for the catalytic activity, lisinopril inhibition, and NaCl activation of ACET. Lisinopril 108-118 angiotensin I converting enzyme Homo sapiens 154-158 7511728-5 1994 In sham-operated SHR, 2-week treatment with lisinopril decreased blood pressure (BP), left ventricular (LV) weight, and total peripheral resistance (TPR) (p < 0.01 each) and increased RBF and plasma renin activity (PRA) (both p < 0.05); CO and LV end-diastolic pressure (LVEDP) were unchanged. Lisinopril 44-54 renin Rattus norvegicus 202-207 8305779-3 1993 To date, the use of angiotensin-converting enzyme (ACE) inhibitors and development of pancreatitis has been described in the literature with captopril, enalapril maleate, and one case temporally related to lisinopril use. Lisinopril 206-216 angiotensin I converting enzyme Homo sapiens 20-49 8305779-3 1993 To date, the use of angiotensin-converting enzyme (ACE) inhibitors and development of pancreatitis has been described in the literature with captopril, enalapril maleate, and one case temporally related to lisinopril use. Lisinopril 206-216 angiotensin I converting enzyme Homo sapiens 51-54 8301928-8 1993 Lisinopril, a non-sulfhydryl ACE inhibitor, similarly inhibited the gelatinases, but a 100-fold higher concentration of the drug was needed. Lisinopril 0-10 angiotensin I converting enzyme Homo sapiens 29-32 8284265-7 1993 In both WKY and SHR, lisinopril had a greater effect in inhibiting plasma and cerebrospinal fluid ACE, reducing levels of plasma angiotensinogen, and increasing the concentrations of authentic Ang II. Lisinopril 21-31 angiotensin I converting enzyme Rattus norvegicus 98-101 8298535-2 1993 The effect of lisinopril, a potent inhibitor of angiotensin converting enzyme (ACE), injected into the medial preoptic area (MPOA) on water intake was investigated in male Holtzman rats (200-250 g). Lisinopril 14-24 angiotensin I converting enzyme Rattus norvegicus 48-77 8298535-2 1993 The effect of lisinopril, a potent inhibitor of angiotensin converting enzyme (ACE), injected into the medial preoptic area (MPOA) on water intake was investigated in male Holtzman rats (200-250 g). Lisinopril 14-24 angiotensin I converting enzyme Rattus norvegicus 79-82 8284265-7 1993 In both WKY and SHR, lisinopril had a greater effect in inhibiting plasma and cerebrospinal fluid ACE, reducing levels of plasma angiotensinogen, and increasing the concentrations of authentic Ang II. Lisinopril 21-31 angiotensinogen Rattus norvegicus 193-199 8394952-14 1993 However, lisinopril lowered ANF to sham levels in the periventricular preoptic nucleus, the arcuate nucleus, and the perifornical nucleus. Lisinopril 9-19 natriuretic peptide A Rattus norvegicus 28-31 8405086-1 1993 The action of the angiotensin-converting enzyme (ACE) inhibitor lisinopril on the consequences of myocardial reoxygenation and oxidative damage was assessed in cultured chick embryonic ventricular cardiomyocytes. Lisinopril 64-74 angiotensin I converting enzyme Gallus gallus 18-47 8405086-1 1993 The action of the angiotensin-converting enzyme (ACE) inhibitor lisinopril on the consequences of myocardial reoxygenation and oxidative damage was assessed in cultured chick embryonic ventricular cardiomyocytes. Lisinopril 64-74 angiotensin I converting enzyme Gallus gallus 49-52 8405086-9 1993 These data suggest that lisinopril accelerates the recovery of cardiomyocytes during reoxygenation and blunts the effects of oxidative agents through mechanisms involving the endogenous renin angiotensin system and/or a direct cellular action. Lisinopril 24-34 renin Gallus gallus 186-191 8228208-11 1993 The fall in blood pressure with lisinopril was related to baseline plasma renin activity, whereas when amlodipine was given, either alone or in combination, the fall in blood pressure was independent of baseline renin activity. Lisinopril 32-42 renin Homo sapiens 74-79 8228208-14 1993 CONCLUSIONS: The results of the present study indicate that: amlodipine and lisinopril in combination have a marked additional effect on blood pressure compared with either given as a monotherapy; their potentiation of action is long-acting; Black patients tend not to respond to the monotherapy with lisinopril as well as Caucasian patients, although they respond similarly to the combination; the response to amlodipine tends to be greater the higher the initial blood pressure; and, finally, the response to lisinopril is greater the higher the plasma renin activity. Lisinopril 76-86 renin Homo sapiens 555-560 8396158-1 1993 It has been reported that the urinary excretions of chloride (Cl), potassium (K), and magnesium (Mg), but not sodium (Na), after furosemide, a loop diuretic, were decreased by pretreatment with lisinopril, an ACE inhibitor in hypertensive subjects. Lisinopril 194-204 angiotensin I converting enzyme Homo sapiens 209-212 7687717-2 1993 They were then randomly assigned to two distinct oral antihypertensive regimens with either calcium-channel blocker nifedipine (group 1, n = 7) or the angiotensin-converting enzyme (ACE) inhibitor lisinopril (group 2, n = 7). Lisinopril 197-207 angiotensin I converting enzyme Homo sapiens 182-185 8395230-6 1993 The angiotensin-converting enzyme inhibitor, lisinopril (10(-8) mol/l), increased the half-life of bradykinin to 244 +/- 20 minutes; the combination of both inhibitors increased the half-life of bradykinin to 381 +/- 51 minutes. Lisinopril 45-55 kininogen 1 Homo sapiens 99-109 8391095-6 1993 Treatment with lisinopril lowered the PGC to a mean value that was indistinguishable from that for nondiabetic dogs. Lisinopril 15-25 progastricsin Canis lupus familiaris 38-41 8391095-11 1993 We conclude that although treatment of diabetic dogs with either lisinopril or TA-3090 results in differential effects on PGC; each produces a similar decrement in proteinuria. Lisinopril 65-75 progastricsin Canis lupus familiaris 122-125 8395230-6 1993 The angiotensin-converting enzyme inhibitor, lisinopril (10(-8) mol/l), increased the half-life of bradykinin to 244 +/- 20 minutes; the combination of both inhibitors increased the half-life of bradykinin to 381 +/- 51 minutes. Lisinopril 45-55 kininogen 1 Homo sapiens 195-205 8390528-9 1993 CONCLUSIONS: These findings suggest that chronic treatment with the ACE inhibitor lisinopril, but not the diuretic hydrochlorothiazide, may produce favourable effects on blood rheology, but the clinical relevance requires further investigation. Lisinopril 82-92 angiotensin I converting enzyme Homo sapiens 68-71 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). Lisinopril 79-89 angiotensin I converting enzyme Homo sapiens 31-60 8388656-3 1993 Most of the bradykinin-degrading activity in cell monolayers could be inhibited in a concentration-dependent manner by the ACE inhibitors lisinopril, ramiprilat, and captopril. Lisinopril 138-148 kininogen 1 Homo sapiens 12-22 8388656-3 1993 Most of the bradykinin-degrading activity in cell monolayers could be inhibited in a concentration-dependent manner by the ACE inhibitors lisinopril, ramiprilat, and captopril. Lisinopril 138-148 angiotensin I converting enzyme Homo sapiens 123-126 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). Lisinopril 79-89 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). Lisinopril 79-89 low density lipoprotein receptor Homo sapiens 131-163 8392718-3 1993 Bestatin inhibited up to 66%, puromycin about 33%, and lisinopril about 15% of total degrading activity against both ACTH/MSH(4-10) and semax. Lisinopril 55-65 proopiomelanocortin Homo sapiens 117-121 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. Lisinopril 81-91 low density lipoprotein receptor Homo sapiens 120-152 8097091-3 1993 Chronic treatment with ACE inhibitors (captopril or lisinopril) for 25 days, followed by 1 day without treatment, increased plasma ACE, but only slightly modified lung, aorta, heart and kidney specific ACE activity. Lisinopril 52-62 angiotensin I converting enzyme Rattus norvegicus 23-26 8097091-3 1993 Chronic treatment with ACE inhibitors (captopril or lisinopril) for 25 days, followed by 1 day without treatment, increased plasma ACE, but only slightly modified lung, aorta, heart and kidney specific ACE activity. Lisinopril 52-62 angiotensin I converting enzyme Rattus norvegicus 131-134 8097091-3 1993 Chronic treatment with ACE inhibitors (captopril or lisinopril) for 25 days, followed by 1 day without treatment, increased plasma ACE, but only slightly modified lung, aorta, heart and kidney specific ACE activity. Lisinopril 52-62 angiotensin I converting enzyme Rattus norvegicus 131-134 8386065-7 1993 Bradykinin concentrations in the organ bath measured by a specific bradykinin radioimmunoassay remained stable during the addition of lisinopril. Lisinopril 134-144 kininogen 1 Homo sapiens 0-10 8386093-5 1993 Lisinopril attenuated the increase in plasma norepinephrine, and increased plasma renin activity (both P < 0.05). Lisinopril 0-10 renin Rattus norvegicus 82-87 8384939-4 1993 With the ACE inhibitor 125I-351A, a derivative of lisinopril, as a radioligand on coronal sections of LVH and control hearts, in vitro autoradiography demonstrated ACE binding in aorta, coronary arteries, atria, and ventricles of both groups. Lisinopril 50-60 angiotensin I converting enzyme Rattus norvegicus 9-12 8384939-4 1993 With the ACE inhibitor 125I-351A, a derivative of lisinopril, as a radioligand on coronal sections of LVH and control hearts, in vitro autoradiography demonstrated ACE binding in aorta, coronary arteries, atria, and ventricles of both groups. Lisinopril 50-60 angiotensin I converting enzyme Rattus norvegicus 164-167 8386065-11 1993 Endothelium dependent relaxation to lisinopril and captopril was also observed in human coronary arteries treated with bradykinin (> or = 10(-7) M), but not in those treated with substance P (10(-8) M). Lisinopril 36-46 kininogen 1 Homo sapiens 119-129 8392403-0 1993 Rapid reversal of a motor nerve conduction deficit in streptozotocin-diabetic rats by the angiotensin converting enzyme inhibitor lisinopril. Lisinopril 130-140 angiotensin I converting enzyme Rattus norvegicus 90-119 8392403-1 1993 The effect of treatment of rats with the angiotensin converting enzyme inhibitor lisinopril after 5 weeks of untreated streptozotocin-diabetes was examined by daily monitoring of sciatic motor conduction velocity to tibialis anterior muscle. Lisinopril 81-91 angiotensin I converting enzyme Rattus norvegicus 41-70 1366257-11 1992 The ACE activity in serum 24 h post-dose was lower (p < 0.001) after treatment with lisinopril 8.0 (SD 3.3) mumol/min/1 than with enalapril 16.1 (SD 6.0). Lisinopril 87-97 angiotensin I converting enzyme Homo sapiens 4-7 8281528-5 1993 ), sodium excretion was significantly increased during therapy with lisinopril but only slightly during nitrendipine, indicating that angiotensin-converting enzyme inhibition may improve the sodium-retaining state of heart transplant recipients associated with ciclosporin A. Lisinopril 68-78 angiotensin I converting enzyme Homo sapiens 134-163 8385525-1 1993 Although lisinopril and enalapril are equipotent angiotensin converting enzyme (ACE) inhibitors lisinopril has been reported to produce greater inhibition of plasma ACE 24 hours after single doses. Lisinopril 96-106 angiotensin I converting enzyme Homo sapiens 49-78 8385525-1 1993 Although lisinopril and enalapril are equipotent angiotensin converting enzyme (ACE) inhibitors lisinopril has been reported to produce greater inhibition of plasma ACE 24 hours after single doses. Lisinopril 96-106 angiotensin I converting enzyme Homo sapiens 80-83 8385525-1 1993 Although lisinopril and enalapril are equipotent angiotensin converting enzyme (ACE) inhibitors lisinopril has been reported to produce greater inhibition of plasma ACE 24 hours after single doses. Lisinopril 96-106 angiotensin I converting enzyme Homo sapiens 165-168 8385525-3 1993 Lisinopril lowered mean 24 hour systolic blood pressure significantly more than enalapril after 4 weeks of treatment (14/7 +/- 2/1mmHg & 9/6 +/- 2/1mmHg, respectively, adjusted SBP difference 4.8mmHg, P < 0.01). Lisinopril 0-10 selenium binding protein 1 Homo sapiens 181-184 1329541-2 1992 In the current study, we examined the effects of the active site-directed ACE inhibitors lisinopril and captopril on ACE gene expression and activity in cultured porcine pulmonary artery endothelial cells. Lisinopril 89-99 angiotensin I converting enzyme Homo sapiens 74-77 1329541-2 1992 In the current study, we examined the effects of the active site-directed ACE inhibitors lisinopril and captopril on ACE gene expression and activity in cultured porcine pulmonary artery endothelial cells. Lisinopril 89-99 angiotensin I converting enzyme Homo sapiens 117-120 1329541-3 1992 Exposure of endothelial cells to both lisinopril and captopril was associated with increased ACE mRNA levels and concomitant increases in ACE activity. Lisinopril 38-48 angiotensin I converting enzyme Homo sapiens 93-96 1329541-3 1992 Exposure of endothelial cells to both lisinopril and captopril was associated with increased ACE mRNA levels and concomitant increases in ACE activity. Lisinopril 38-48 angiotensin I converting enzyme Homo sapiens 138-141 1329541-6 1992 Nuclear runoff assays indicated that 48 h of exposure to 100 microM of either captopril or lisinopril increased ACE gene transcription approximately threefold relative to a tubulin control, a level comparable to the increases in ACE mRNA levels and activity observed during ACE inhibitor exposure. Lisinopril 91-101 angiotensin I converting enzyme Homo sapiens 112-115 1329541-6 1992 Nuclear runoff assays indicated that 48 h of exposure to 100 microM of either captopril or lisinopril increased ACE gene transcription approximately threefold relative to a tubulin control, a level comparable to the increases in ACE mRNA levels and activity observed during ACE inhibitor exposure. Lisinopril 91-101 angiotensin I converting enzyme Homo sapiens 229-232 1329541-6 1992 Nuclear runoff assays indicated that 48 h of exposure to 100 microM of either captopril or lisinopril increased ACE gene transcription approximately threefold relative to a tubulin control, a level comparable to the increases in ACE mRNA levels and activity observed during ACE inhibitor exposure. Lisinopril 91-101 angiotensin I converting enzyme Homo sapiens 229-232 1324678-0 1992 Mixed-type inhibition of bovine lung angiotensin converting enzyme by lisinopril and its dansyl derivative. Lisinopril 70-80 angiotensin I converting enzyme Bos taurus 37-66 1324678-1 1992 The steady-state inhibition of bovine lung angiotensin converting enzyme (ACE; EC 3.4.15.1) by the slow-binding inhibitor lisinopril and its dansyl derivative conformed to a linear mixed inhibition model with inhibitor binding to ES as well as to E. Studied at pH8, 35 degrees, and using N-(3-[2-furyl]-acryloyl)phe-gly-gly as substrate, the approach to steady-state activity at different substrate concentrations pointed to slow isomerizations in both EI and EIS. Lisinopril 122-132 angiotensin I converting enzyme Bos taurus 43-72 1324678-1 1992 The steady-state inhibition of bovine lung angiotensin converting enzyme (ACE; EC 3.4.15.1) by the slow-binding inhibitor lisinopril and its dansyl derivative conformed to a linear mixed inhibition model with inhibitor binding to ES as well as to E. Studied at pH8, 35 degrees, and using N-(3-[2-furyl]-acryloyl)phe-gly-gly as substrate, the approach to steady-state activity at different substrate concentrations pointed to slow isomerizations in both EI and EIS. Lisinopril 122-132 angiotensin I converting enzyme Bos taurus 74-77 1326422-0 1992 Circulating angiotensin II levels under repeated administration of lisinopril in normal subjects. Lisinopril 67-77 angiotensinogen Homo sapiens 12-26 1326422-7 1992 Plasma AII concentration measured by an established method using high performance liquid chromatography combined with a radioimmunoassay, however, was maintained at approximately the pretreatment level when it was measured at 24 h intervals after each administration of lisinopril. Lisinopril 270-280 angiotensinogen Homo sapiens 7-10 8281530-6 1993 The changes in daylong plasma glucose and insulin-stimulated glucose uptake increased after hydrochlorothiazide treatment and decreased following lisinopril. Lisinopril 146-156 insulin Homo sapiens 42-49 1335236-1 1992 Angiotensin converting enzyme (ACE; EC 3.4.15.1) was purified from porcine kidney and lung (endothelial isoenzyme) and testis (testicular isoenzyme) by affinity chromatography on lisinopril-2.8 nm-Sepharose. Lisinopril 179-189 angiotensin-converting enzyme Sus scrofa 0-29 1335236-1 1992 Angiotensin converting enzyme (ACE; EC 3.4.15.1) was purified from porcine kidney and lung (endothelial isoenzyme) and testis (testicular isoenzyme) by affinity chromatography on lisinopril-2.8 nm-Sepharose. Lisinopril 179-189 angiotensin-converting enzyme Sus scrofa 31-34 1329475-7 1992 Moreover, administration of once-daily lisinopril 10 mg resulted in a decrease in plasma concentrations of angiotensin II, aldosterone, and atrial natriuretic peptide, and an increase in plasma concentrations of active renin. Lisinopril 39-49 angiotensinogen Homo sapiens 107-121 1329475-7 1992 Moreover, administration of once-daily lisinopril 10 mg resulted in a decrease in plasma concentrations of angiotensin II, aldosterone, and atrial natriuretic peptide, and an increase in plasma concentrations of active renin. Lisinopril 39-49 renin Homo sapiens 219-224 1329481-5 1992 The suppression of such neurohormonal activity through the use of long-acting angiotensin-converting enzyme (ACE) inhibitors, such as lisinopril, provides a means of controlling such symptoms. Lisinopril 134-144 angiotensin I converting enzyme Homo sapiens 109-112 1330096-1 1992 OBJECTIVE: To report a case of fatal angioedema associated with the use of lisinopril, a long-acting angiotensin-converting enzyme (ACE) inhibitor. Lisinopril 75-85 angiotensin I converting enzyme Homo sapiens 101-130 1330096-1 1992 OBJECTIVE: To report a case of fatal angioedema associated with the use of lisinopril, a long-acting angiotensin-converting enzyme (ACE) inhibitor. Lisinopril 75-85 angiotensin I converting enzyme Homo sapiens 132-135 1366257-11 1992 The ACE activity in serum 24 h post-dose was lower (p < 0.001) after treatment with lisinopril 8.0 (SD 3.3) mumol/min/1 than with enalapril 16.1 (SD 6.0). Lisinopril 87-97 CD59 molecule (CD59 blood group) Homo sapiens 117-122 1320075-5 1992 We then determined the effect of short-term incubation of PNC with captopril or lisinopril upon angiotensin II binding kinetics. Lisinopril 80-90 angiotensinogen Rattus norvegicus 96-110 1321187-9 1992 The ACE inhibitors lisinopril and perindoprilat displayed similar high affinities in competing for the binding of 125I-351A to the endothelium and adventitia of the sheep aorta, suggesting that at these two sites the radioligand was binding to ACE. Lisinopril 19-29 angiotensin-converting enzyme Ovis aries 4-7 1376812-1 1992 The antihypertensive effect of the angiotensin-converting enzyme (ACE) inhibitor lisinopril administered in a single dose of 20 mg was evaluated by ambulatory blood pressure monitoring (ABPM) in a double-blind, placebo-controlled, cross-over study. Lisinopril 81-91 angiotensin I converting enzyme Homo sapiens 35-64 1376812-1 1992 The antihypertensive effect of the angiotensin-converting enzyme (ACE) inhibitor lisinopril administered in a single dose of 20 mg was evaluated by ambulatory blood pressure monitoring (ABPM) in a double-blind, placebo-controlled, cross-over study. Lisinopril 81-91 angiotensin I converting enzyme Homo sapiens 66-69 1325031-4 1992 Analysis of displacement of 125I-Ro 31-8472 binding from ACE by ACE inhibitors 351A and lisinopril yielded biphasic curves for pulmonary, renal, and plasma ACE and a monophasic curve for ACE from the testis. Lisinopril 88-98 angiotensin I converting enzyme Rattus norvegicus 57-60 1325031-4 1992 Analysis of displacement of 125I-Ro 31-8472 binding from ACE by ACE inhibitors 351A and lisinopril yielded biphasic curves for pulmonary, renal, and plasma ACE and a monophasic curve for ACE from the testis. Lisinopril 88-98 angiotensin I converting enzyme Rattus norvegicus 64-67 1325031-4 1992 Analysis of displacement of 125I-Ro 31-8472 binding from ACE by ACE inhibitors 351A and lisinopril yielded biphasic curves for pulmonary, renal, and plasma ACE and a monophasic curve for ACE from the testis. Lisinopril 88-98 angiotensin I converting enzyme Rattus norvegicus 64-67 1325031-4 1992 Analysis of displacement of 125I-Ro 31-8472 binding from ACE by ACE inhibitors 351A and lisinopril yielded biphasic curves for pulmonary, renal, and plasma ACE and a monophasic curve for ACE from the testis. Lisinopril 88-98 angiotensin I converting enzyme Rattus norvegicus 64-67 1321247-1 1992 To determine the haemodynamic profile of angiotensin converting enzyme (ACE) inhibitors during stress, the cardiovascular response to various stress tests was examined in patients with essential hypertension before and after three months of therapy with lisinopril. Lisinopril 254-264 angiotensin I converting enzyme Homo sapiens 72-75 1629885-6 1992 All the ACE inhibitors studied had similar cardiovascular responses but lisinopril displayed the larger metabolic response. Lisinopril 72-82 angiotensin I converting enzyme Homo sapiens 8-11 1321247-3 1992 ACE inhibition with lisinopril effectively reduced systolic and diastolic pressure in the office (P less than 0.001), at rest (P less than 0.002), during mental stress (P less than 0.003), cold pressor test (P less than 0.003), and reaction time task (P less than 0.05). Lisinopril 20-30 angiotensin I converting enzyme Homo sapiens 0-3 1321247-10 1992 This response pattern to ACE inhibition with lisinopril may reduce the impact of recurring stress-induced increases of blood pressure and of exaggerated vasoconstrictive stimuli on the cardiovascular system. Lisinopril 45-55 angiotensin I converting enzyme Homo sapiens 25-28 1575176-8 1992 A recent double-blind randomized study comparing a new sustained release nifedipine formulation and the ACE inhibitor lisinopril found the 2 drugs equivalent in efficacy with no differences in the rate of adverse events. Lisinopril 118-128 angiotensin I converting enzyme Homo sapiens 104-107 1319250-0 1992 Rapid reversal of angiotensin converting enzyme inhibition by lisinopril in the perfused rabbit lung. Lisinopril 62-72 angiotensin-converting enzyme Oryctolagus cuniculus 18-47 1319250-1 1992 Lisinopril is a potent competitive inhibitor of purified rabbit lung ACE (dissociation t1/2 = 105 min). Lisinopril 0-10 angiotensin-converting enzyme Oryctolagus cuniculus 69-72 1325885-6 1992 There was marked variation in ACE inhibitor binding affinity at the two binding sites of lung ACE across the panel of ACE inhibitors studied (equilibrium dissociation constant; Kd; pmol/L) for site one vs site two: cilazaprilat 40 +/- 3 vs 430 +/- 92*; lisinopril 25 +/- 1 vs 848 +/- 107**; and quinaprilat 4 +/- 1 vs 1869 +/- 720; *P less than 0.05; **P less than 0.005, t-test, n = 3). Lisinopril 253-263 angiotensin I converting enzyme Rattus norvegicus 30-33 1325885-6 1992 There was marked variation in ACE inhibitor binding affinity at the two binding sites of lung ACE across the panel of ACE inhibitors studied (equilibrium dissociation constant; Kd; pmol/L) for site one vs site two: cilazaprilat 40 +/- 3 vs 430 +/- 92*; lisinopril 25 +/- 1 vs 848 +/- 107**; and quinaprilat 4 +/- 1 vs 1869 +/- 720; *P less than 0.05; **P less than 0.005, t-test, n = 3). Lisinopril 253-263 angiotensin I converting enzyme Rattus norvegicus 94-97 1325885-6 1992 There was marked variation in ACE inhibitor binding affinity at the two binding sites of lung ACE across the panel of ACE inhibitors studied (equilibrium dissociation constant; Kd; pmol/L) for site one vs site two: cilazaprilat 40 +/- 3 vs 430 +/- 92*; lisinopril 25 +/- 1 vs 848 +/- 107**; and quinaprilat 4 +/- 1 vs 1869 +/- 720; *P less than 0.05; **P less than 0.005, t-test, n = 3). Lisinopril 253-263 angiotensin I converting enzyme Rattus norvegicus 94-97 1314588-5 1992 Instead, the effect on kcat together with a 100-fold decrease in affinity for the ACE inhibitor lisinopril indicates that Tyr-200 may participate in catalysis by stabilizing the transition state complex. Lisinopril 96-106 angiotensin I converting enzyme Homo sapiens 82-85 1350796-2 1992 Eight weeks" treatment with the combination of ACE inhibitor and beta-blocker or the diuretic and beta-blocker produced falls in blood pressure (lying: -8.4 +/- 15.4/ -7.3 +/- 80 mmHg and -6.1 +/- 15.3/ -5.2 +/- 8.8 mmHg [mean +/- SD] for lisinopril and hydrochlorothiazide respectively; standing: -10.2 +/- 14.2/8.2 +/- 9.2 mmHg and -6.8 +/- 14/ -6.3 +/- 10.3 mmHg for lisinopril and hydrochlorothiazide respectively) which were not statistically significantly different. Lisinopril 239-249 angiotensin I converting enzyme Homo sapiens 47-50 1350796-2 1992 Eight weeks" treatment with the combination of ACE inhibitor and beta-blocker or the diuretic and beta-blocker produced falls in blood pressure (lying: -8.4 +/- 15.4/ -7.3 +/- 80 mmHg and -6.1 +/- 15.3/ -5.2 +/- 8.8 mmHg [mean +/- SD] for lisinopril and hydrochlorothiazide respectively; standing: -10.2 +/- 14.2/8.2 +/- 9.2 mmHg and -6.8 +/- 14/ -6.3 +/- 10.3 mmHg for lisinopril and hydrochlorothiazide respectively) which were not statistically significantly different. Lisinopril 370-380 angiotensin I converting enzyme Homo sapiens 47-50 1315560-11 1992 Six healthy volunteers received 20 mg lisinopril, a long-acting ACE-inhibitor. Lisinopril 38-48 angiotensin I converting enzyme Homo sapiens 64-67 1376274-0 1992 Nitric oxide participation in renal hemodynamic effect of angiotensin converting enzyme inhibitor lisinopril. Lisinopril 98-108 angiotensin-converting enzyme Oryctolagus cuniculus 58-87 1333254-2 1992 In the ex vivo- and in vitro-experiments using isolated rat aorta, vascular prostacyclin (PGI2) production is dose-dependently stimulated by the ACE inhibitors captopril, lisinopril, and ramipril. Lisinopril 171-181 angiotensin I converting enzyme Rattus norvegicus 145-148 1327597-4 1992 Following acute administration of lisinopril, perindopril or benazepril, ACE was markedly inhibited in the lung, kidney and blood vessels but not in the testis. Lisinopril 34-44 angiotensin I converting enzyme Homo sapiens 73-76 1327597-11 1992 After chronic administration of lisinopril or perindopril for 14 days, a similar pattern of ACE inhibition was observed in the kidney, lung and blood vessels. Lisinopril 32-42 angiotensin I converting enzyme Homo sapiens 92-95 1327597-12 1992 In the lung, however, lisinopril was found to increase total ACE by 30%, while plasma ACE was increased two-threefold by both lisinopril and perindopril. Lisinopril 22-32 angiotensin I converting enzyme Homo sapiens 61-64 1327597-12 1992 In the lung, however, lisinopril was found to increase total ACE by 30%, while plasma ACE was increased two-threefold by both lisinopril and perindopril. Lisinopril 126-136 angiotensin I converting enzyme Homo sapiens 86-89 1282632-4 1992 Lisinopril and captopril alone did not affect vascular tone; however, in rings with endothelium partially relaxed with bradykinin (> or = 10(-10) M), all ACE inhibitors caused further relaxations. Lisinopril 0-10 angiotensin I converting enzyme Homo sapiens 157-160 1282632-6 1992 Mechanical removal of the endothelium or incubation with nitro-L-arginine or the bradykinin2-receptor antagonist Hoe 140 prevented the relaxations to bradykinin and lisinopril. Lisinopril 165-175 kininogen 1 Homo sapiens 81-91 1282632-8 1992 Endothelium-dependent relaxations to lisinopril were also observed in human coronary arteries treated with bradykinin (> or = 10(-7) M). Lisinopril 37-47 kininogen 1 Homo sapiens 107-117 1660550-5 1991 Ang II infusion induced typical effects which appeared to be similar before and during lisinopril treatment: a dose-related fall in renal plasma flow and rise in systemic blood pressure, renal vascular resistance and filtration fraction, while the glomerular filtration rate remained relatively stable. Lisinopril 87-97 angiotensinogen Homo sapiens 0-6 1317477-2 1992 The renal and systemic hemodynamic response to lisinopril, an angiotension converting enzyme (ACE) inhibitor, in patients with ADPKD without renal failure was compared with the response in matched unaffected family members. Lisinopril 47-57 angiotensin I converting enzyme Homo sapiens 62-92 1317477-2 1992 The renal and systemic hemodynamic response to lisinopril, an angiotension converting enzyme (ACE) inhibitor, in patients with ADPKD without renal failure was compared with the response in matched unaffected family members. Lisinopril 47-57 angiotensin I converting enzyme Homo sapiens 94-97 1312233-10 1992 The LIS + HCTZ association caused a significant reduction of DBP in comparison to the other combined treatment (88.1 +/- 0.7 vs 90.3 +/- 0.7; p = 0.026). Lisinopril 4-7 D-box binding PAR bZIP transcription factor Homo sapiens 61-64 1312233-12 1992 At the end of the study 79.5% of patients treated with LIS + HCTZ presented normal results (DBP less than or equal to 90 mmHg), whereas the percentage of similar results in the comparison group was 72%. Lisinopril 55-58 D-box binding PAR bZIP transcription factor Homo sapiens 92-95 1662562-0 1991 Different hemodynamic (24-h ambulatory blood pressure monitoring) and renin-inhibiting effect of a 1-week treatment with enalapril and lisinopril. Lisinopril 135-145 renin Homo sapiens 70-75 1662562-6 1991 Both drugs inhibited ACE activity to a highly significant extent, but in this regard lisinopril was more effective than enalapril. Lisinopril 85-95 angiotensin I converting enzyme Homo sapiens 21-24 1662562-7 1991 However, lisinopril"s greater ACE inhibition was not accompanied by a greater hypotensive effect. Lisinopril 9-19 angiotensin I converting enzyme Homo sapiens 30-33 1370299-2 1992 Inhibition of the endothelial cell autocrine angiotensin system, with either the angiotensin-converting enzyme inhibitor lisinopril or the angiotensin II receptor antagonist sar1, ile8-angiotensin II, leads to increased endothelial cell migration and urokinase-like plasminogen activator (u-PA) activity (Bell, L., and J. Lisinopril 121-131 plasminogen activator, urokinase Bos taurus 251-287 1370299-2 1992 Inhibition of the endothelial cell autocrine angiotensin system, with either the angiotensin-converting enzyme inhibitor lisinopril or the angiotensin II receptor antagonist sar1, ile8-angiotensin II, leads to increased endothelial cell migration and urokinase-like plasminogen activator (u-PA) activity (Bell, L., and J. Lisinopril 121-131 plasminogen activator, urokinase Bos taurus 289-293 1658975-0 1991 [Treatment of hypertension with the ACE inhibitor lisinopril. Lisinopril 50-60 angiotensin I converting enzyme Homo sapiens 36-39 1724523-0 1991 Angiotensin converting enzyme inhibition in heart, kidney, and serum studied ex vivo after administration of zofenopril, captopril, and lisinopril. Lisinopril 136-146 angiotensin I converting enzyme Rattus norvegicus 0-29 1724523-2 1991 ACE activity in all regions of the heart, kidney, and serum was markedly reduced 4 h after administration of lisinopril and zofenopril and only partially recovered toward control levels at 24 h. After captopril treatment, ACE activity was partially inhibited in heart, kidney, and serum at 1 h and fully recovered toward control levels in most regions at 24 h. These results suggest that these inhibitors reduce ACE in all regions of the heart and kidney without regional selective inhibition. Lisinopril 109-119 angiotensin I converting enzyme Rattus norvegicus 0-3 1724523-2 1991 ACE activity in all regions of the heart, kidney, and serum was markedly reduced 4 h after administration of lisinopril and zofenopril and only partially recovered toward control levels at 24 h. After captopril treatment, ACE activity was partially inhibited in heart, kidney, and serum at 1 h and fully recovered toward control levels in most regions at 24 h. These results suggest that these inhibitors reduce ACE in all regions of the heart and kidney without regional selective inhibition. Lisinopril 109-119 angiotensin I converting enzyme Rattus norvegicus 222-225 1724523-2 1991 ACE activity in all regions of the heart, kidney, and serum was markedly reduced 4 h after administration of lisinopril and zofenopril and only partially recovered toward control levels at 24 h. After captopril treatment, ACE activity was partially inhibited in heart, kidney, and serum at 1 h and fully recovered toward control levels in most regions at 24 h. These results suggest that these inhibitors reduce ACE in all regions of the heart and kidney without regional selective inhibition. Lisinopril 109-119 angiotensin I converting enzyme Rattus norvegicus 222-225 1724523-3 1991 Lisinopril and zofenopril at these doses produced longer-lasting ACE inhibition than captopril. Lisinopril 0-10 angiotensin I converting enzyme Rattus norvegicus 65-68 1660550-7 1991 We conclude that the long-term antiproteinuric effect of the ACE inhibitor, lisinopril, is neither mediated through changes in circulatory Ang II levels nor influenced by acute changes in systemic and renal hemodynamics, suggesting a non-hemodynamic mechanism of action. Lisinopril 76-86 angiotensin I converting enzyme Homo sapiens 61-64 1668266-7 1991 The catalytic activity of recombinant angiotensin-converting enzyme, in terms of angiotensin I and 2-furanacryloyl-Phe-Gly-Gly hydrolysis, chloride activation, and lisinopril inhibition, was essentially identical to that of the native enzyme. Lisinopril 164-174 angiotensin-converting enzyme Cricetulus griseus 38-67 1649623-5 1991 We find that the somatic isozyme in fact contains 2 mol of Zn2+ and binds 2 mol of lisinopril (an ACE inhibitor) per mol of enzyme, whereas the testis isozyme contains 1 mol of Zn2+ and binds 1 mol of lisinopril. Lisinopril 83-93 angiotensin I converting enzyme Homo sapiens 98-101 1649623-7 1991 However, active site titration with lisinopril assayed by hydrolysis of furanacryloyl-Phe-Gly-Gly revealed that 1 mol of inhibitor/mol of enzyme abolished the activity of either isozyme, indicating that the principal angiotensin-converting site likely resides in the C-terminal (testicular) domain of somatic ACE and that binding of inhibitor to this site is stronger than to the second site. Lisinopril 36-46 angiotensin I converting enzyme Homo sapiens 309-312 1660796-0 1991 Acute effects of the ACE inhibitor lisinopril on cardiac electrophysiological parameters of isolated guinea pig hearts. Lisinopril 35-45 LOW QUALITY PROTEIN: angiotensin-converting enzyme Cavia porcellus 21-24 1653792-0 1991 Measurement of angiotensin converting enzyme induction and inhibition using quantitative in vitro autoradiography: tissue selective induction after chronic lisinopril treatment. Lisinopril 156-166 angiotensin I converting enzyme Rattus norvegicus 15-44 1653792-11 1991 Despite this, during chronic treatment with lisinopril, ACE activity in all of these organs was inhibited with low levels of free ACE. Lisinopril 44-54 angiotensin I converting enzyme Rattus norvegicus 56-59 1653792-11 1991 Despite this, during chronic treatment with lisinopril, ACE activity in all of these organs was inhibited with low levels of free ACE. Lisinopril 44-54 angiotensin I converting enzyme Rattus norvegicus 130-133 1846675-8 1991 The inhibition of AI stimulation of aldosterone release by lisinopril is mostly due to lisinopril inhibition of ACE and resulting decreased conversion of AI to AII. Lisinopril 59-69 angiotensin I converting enzyme Rattus norvegicus 112-115 1846675-8 1991 The inhibition of AI stimulation of aldosterone release by lisinopril is mostly due to lisinopril inhibition of ACE and resulting decreased conversion of AI to AII. Lisinopril 59-69 angiotensinogen Rattus norvegicus 160-163 1846675-8 1991 The inhibition of AI stimulation of aldosterone release by lisinopril is mostly due to lisinopril inhibition of ACE and resulting decreased conversion of AI to AII. Lisinopril 87-97 angiotensin I converting enzyme Rattus norvegicus 112-115 2164777-14 1990 These results indicate that lisinopril interrupts an autocrine pathway in endothelial cells, in which endothelial cell-derived angiotensin I is converted to angiotensin II by ACE, and imply that angiotensin-converting enzyme inhibitors in vivo would act to reduce vessel wall injury by directly increasing the rate of endothelial cell wound closure; by increasing the antithrombotic tendency of the endothelium via enhanced u-PA; and indirectly, by decreasing production of angiotensin II and thereby the rate of smooth muscle cell migration into the intima. Lisinopril 28-38 angiotensin I converting enzyme Bos taurus 175-178 1963909-0 1990 A comparison of lisinopril with enalapril by monitoring plasma angiotensin II levels in humans. Lisinopril 16-26 angiotensinogen Homo sapiens 63-77 1963909-7 1990 The results indicate that a single administration of 20 mg lisinopril and 10 mg enalapril show similar potency for lowering the circulating ANG II level, although lisinopril exerts a more sustained inhibition of serum ACE activity. Lisinopril 163-173 angiotensin I converting enzyme Homo sapiens 218-221 2164777-8 1990 Lisinopril increased cell-associated u-plasminogen activator (u-PA) 23% +/- 3% (P less than 0.001) in migrating BAEC and angiotensin II abolished this increase. Lisinopril 0-10 plasminogen activator, urokinase Bos taurus 62-66 1847721-4 1991 Lisinopril reduced albumin excretion from 1343 +/- 337 micrograms min-1 to 879 +/- 299 micrograms min-1 (P less than 0.01), whereas nifedipine was without effect, 1436 +/- 336 micrograms min-1 vs. 1319 +/- 342 micrograms min-1. Lisinopril 0-10 CD59 molecule (CD59 blood group) Homo sapiens 66-71 1847721-4 1991 Lisinopril reduced albumin excretion from 1343 +/- 337 micrograms min-1 to 879 +/- 299 micrograms min-1 (P less than 0.01), whereas nifedipine was without effect, 1436 +/- 336 micrograms min-1 vs. 1319 +/- 342 micrograms min-1. Lisinopril 0-10 CD59 molecule (CD59 blood group) Homo sapiens 98-103 1847721-4 1991 Lisinopril reduced albumin excretion from 1343 +/- 337 micrograms min-1 to 879 +/- 299 micrograms min-1 (P less than 0.01), whereas nifedipine was without effect, 1436 +/- 336 micrograms min-1 vs. 1319 +/- 342 micrograms min-1. Lisinopril 0-10 CD59 molecule (CD59 blood group) Homo sapiens 98-103 1847721-4 1991 Lisinopril reduced albumin excretion from 1343 +/- 337 micrograms min-1 to 879 +/- 299 micrograms min-1 (P less than 0.01), whereas nifedipine was without effect, 1436 +/- 336 micrograms min-1 vs. 1319 +/- 342 micrograms min-1. Lisinopril 0-10 CD59 molecule (CD59 blood group) Homo sapiens 98-103 2172073-3 1990 Continuation of lisinopril administration for 3 weeks after the onset of jaundice was associated with the development of grade III encephalopathy and a marked decrease in prothrombin and proaccelerin levels. Lisinopril 16-26 coagulation factor II, thrombin Homo sapiens 171-182 1706800-1 1990 The antihypertensive effects and pharmacokinetic properties of lisinopril, an angiotensin-converting enzyme (ACE) inhibitor, were investigated in hypertensive patients with normal renal function (NRF, mean serum creatinine 1.0 mg/dl, n = 9) and those with impaired renal function (IRF, mean serum creatinine 1.7 mg/dl, n = 8). Lisinopril 63-73 angiotensin I converting enzyme Homo sapiens 78-107 1706800-1 1990 The antihypertensive effects and pharmacokinetic properties of lisinopril, an angiotensin-converting enzyme (ACE) inhibitor, were investigated in hypertensive patients with normal renal function (NRF, mean serum creatinine 1.0 mg/dl, n = 9) and those with impaired renal function (IRF, mean serum creatinine 1.7 mg/dl, n = 8). Lisinopril 63-73 angiotensin I converting enzyme Homo sapiens 109-112 1706800-5 1990 Serum ACE activity was markedly suppressed for 24 h. Plasma levels of lisinopril in the IRF group were higher than those in NRF with significant differences in the peak levels and areas under the plasma concentration time curve (AUC). Lisinopril 70-80 angiotensin I converting enzyme Homo sapiens 6-9 2164777-5 1990 The angiotensin-converting enzyme (ACE) inhibitor lisinopril increased BAEC migration 41% +/- 3% (P less than 0.001), as did the specific angiotensin II antagonist sar1, ile8-angiotensin II (SAR) (41% +/- 3% (P less than 0.001). Lisinopril 50-60 angiotensin I converting enzyme Bos taurus 35-38 2164777-8 1990 Lisinopril increased cell-associated u-plasminogen activator (u-PA) 23% +/- 3% (P less than 0.001) in migrating BAEC and angiotensin II abolished this increase. Lisinopril 0-10 plasminogen activator, urokinase Bos taurus 37-60 2164777-14 1990 These results indicate that lisinopril interrupts an autocrine pathway in endothelial cells, in which endothelial cell-derived angiotensin I is converted to angiotensin II by ACE, and imply that angiotensin-converting enzyme inhibitors in vivo would act to reduce vessel wall injury by directly increasing the rate of endothelial cell wound closure; by increasing the antithrombotic tendency of the endothelium via enhanced u-PA; and indirectly, by decreasing production of angiotensin II and thereby the rate of smooth muscle cell migration into the intima. Lisinopril 28-38 plasminogen activator, urokinase Bos taurus 424-428 2155615-1 1990 Two biotinylated derivatives of the angiotensin-converting enzyme (ACE) inhibitor, lisinopril, were synthesized. Lisinopril 83-93 angiotensin I converting enzyme (peptidyl-dipeptidase A) 1 Mus musculus 67-70 2207707-2 1990 ACE inhibitors and thiorphan competed to a similar level for the [3H]SQ29,852 binding site in the human temporal cortex with a rank order of affinity (pKi values mean +/- S.E.M., n = 3), lisinopril (9.49 +/- 0.02), captopril (9.16 +/- 0.08), SQ29,852 (8.58 +/- 0.04), epicaptopril (7.09 +/- 0.08), fosinopril (7.08 +/- 0.05) and thiorphan (6.40 +/- 0.04). Lisinopril 187-197 angiotensin I converting enzyme Homo sapiens 0-3 2164644-0 1990 Lisinopril: a new ACE inhibitor for the treatment of hypertension and congestive heart failure. Lisinopril 0-10 angiotensin I converting enzyme Homo sapiens 18-21 2189445-2 1990 Specifically discussed are: proposed mechanisms of action, the pharmacology of the commercially available ACE inhibitors (captopril, enalapril, and lisinopril), their renal effects, and their safety and efficacy. Lisinopril 148-158 angiotensin I converting enzyme Homo sapiens 106-109 2167741-10 1990 The rank order of potency of the ACE inhibitors was quinaprilat = benazeprilat greater than perindoprilat greater than 351A greater than lisinopril greater than fosinoprilat. Lisinopril 137-147 angiotensin I converting enzyme Rattus norvegicus 33-36 2158900-4 1990 The captopril- and lisinopril-induced stimulation of vascular 6-keto-PGF1 alpha production was also significantly decreased when the BK antagonist was added to the incubation medium together with the ACE inhibitors. Lisinopril 19-29 angiotensin I converting enzyme Rattus norvegicus 200-203 2155615-6 1990 These results indicate that the bound determinant of lisinopril must lie at least 11 A below the outer surface of the ACE molecule. Lisinopril 53-63 angiotensin I converting enzyme (peptidyl-dipeptidase A) 1 Mus musculus 118-121 33779339-0 2021 Time-Dependent Effects of Individual and Combined Treatments With Nebivolol, Lisinopril, and Valsartan on Blood Pressure and Vascular Reactivity to Angiotensin II and Norepinephrine. Lisinopril 77-87 angiotensinogen Rattus norvegicus 148-162 2173313-4 1990 Lisinopril monotherapy in the 1902 patients completing the trial resulted in marked reductions of systolic (SBP) and DBP from 172.5/102.4 mm Hg at baseline to 147.4/86.6 mm Hg by week 8. Lisinopril 0-10 selenium binding protein 1 Homo sapiens 108-111 2285612-4 1990 Enalapril and lisinopril are potent nonsulfhydryl inhibitors of ACE characterized by weak chelating properties. Lisinopril 14-24 angiotensin I converting enzyme Homo sapiens 64-67 2175149-0 1990 Additive antiproteinuric effect of the NSAID indomethacin and the ACE inhibitor lisinopril. Lisinopril 80-90 angiotensin I converting enzyme Homo sapiens 66-69 2175149-1 1990 Both angiotensin-converting enzyme (ACE) inhibitors like lisinopril and nonsteroidal anti-inflammatory drugs (NSAIDs) like indomethacin have been shown to lower urinary protein excretion in renal disease. Lisinopril 57-67 angiotensin I converting enzyme Homo sapiens 5-34 2175149-1 1990 Both angiotensin-converting enzyme (ACE) inhibitors like lisinopril and nonsteroidal anti-inflammatory drugs (NSAIDs) like indomethacin have been shown to lower urinary protein excretion in renal disease. Lisinopril 57-67 angiotensin I converting enzyme Homo sapiens 36-39 34339022-2 2021 Coenzyme Q10 (Q10) as a powerful antioxidant and lisinopril (LIS) as an angiotensin-converting enzyme inhibitor seem to provide protection against DOX-induced cardiotoxicity. Lisinopril 49-59 angiotensin I converting enzyme Rattus norvegicus 72-101 34975523-8 2021 Additionally, nephrin excretion was significantly elevated in SSLepRmutant rats versus SS rats, and lisinopril reduced nephrin excretion in both strains. Lisinopril 100-110 NPHS1 adhesion molecule, nephrin Rattus norvegicus 119-126 34330145-14 2021 In conclusion, the results of this study showed that radiation greatly increased miRNA34-a in rat kidneys, while lisinopril mitigated radiation-induced decrease of the Notch ligand, Jagged1, a molecular target of miRNA34-a. Lisinopril 113-123 jagged canonical Notch ligand 1 Rattus norvegicus 182-189 33769277-6 2021 SNVs in AGT (p = 0.0141), REN (p = 0.0192), and ACE2 (p = 0.0002) were found to be associated with successful treatment on lisinopril. Lisinopril 123-133 angiotensinogen Homo sapiens 8-11 33769277-6 2021 SNVs in AGT (p = 0.0141), REN (p = 0.0192), and ACE2 (p = 0.0002) were found to be associated with successful treatment on lisinopril. Lisinopril 123-133 renin Homo sapiens 26-29 33769277-6 2021 SNVs in AGT (p = 0.0141), REN (p = 0.0192), and ACE2 (p = 0.0002) were found to be associated with successful treatment on lisinopril. Lisinopril 123-133 angiotensin converting enzyme 2 Homo sapiens 48-52 34144158-6 2021 High levels of plasma angiotensin II (Ang II) and upregulated nicotinamide adenine dinucleotide phosphate oxidase 4 (Nox4) protein expression in the kidneys induced by L-NAME were alleviated by CT flower extract or lisinopril co-treatment (p < 0.05). Lisinopril 215-225 NADPH oxidase 4 Rattus norvegicus 117-121 34339022-2 2021 Coenzyme Q10 (Q10) as a powerful antioxidant and lisinopril (LIS) as an angiotensin-converting enzyme inhibitor seem to provide protection against DOX-induced cardiotoxicity. Lisinopril 61-64 angiotensin I converting enzyme Rattus norvegicus 72-101 34769093-9 2021 This dual activity distinguishes these ACE inhibitory peptides from synthetic drugs, such as Captopril and Lisinopril which were not shown to inhibit ACE2 activity, and may represent a potential strategy in the treatment of COVID-19. Lisinopril 107-117 angiotensin I converting enzyme Homo sapiens 39-42 34321400-9 2021 Although lisinopril reduced systolic and diastolic blood pressure, UACR, hsCRP and fibrinogen in both study groups, these effects were stronger in group B than in group A. Lisinopril 9-19 fibrinogen beta chain Homo sapiens 83-93 34321400-11 2021 The impact of lisinopril on uric acid, hsCRP, fibrinogen, homocysteine and UACR correlated weakly with its hypotensive properties, androgen levels and insulin sensitivity. Lisinopril 14-24 fibrinogen beta chain Homo sapiens 46-56 34282598-12 2021 Lisinopril/verapamil combination enhanced glycemic control and kidney function via diminishing EST and Ang-2. Lisinopril 0-10 angiopoietin 2 Homo sapiens 103-108 34082361-4 2021 Computational (DFT) methods are applied on simplified models of Zn2+-HEXXH binding motif without/with bound inhibitors in order to assess the ability of two pharmaceutical drugs (Captopril and Lisinopril) and Val-Pro-Pro to coordinate with Zn2+-HEXXH binding motif of ACE. Lisinopril 193-203 angiotensin I converting enzyme Homo sapiens 268-271 34440554-3 2021 METHODS: We have investigated the influence of the ACE inhibitors (lisinopril, captopril) and the AT1 antagonists (telmisartan, olmesartan) on the level of ACE2 mRNA and protein expression as well as their influence on the cytopathic effect of SARS-CoV-2 and on the cell barrier integrity in a Caco-2 cell model. Lisinopril 67-77 angiotensin I converting enzyme Homo sapiens 51-54 34440554-3 2021 METHODS: We have investigated the influence of the ACE inhibitors (lisinopril, captopril) and the AT1 antagonists (telmisartan, olmesartan) on the level of ACE2 mRNA and protein expression as well as their influence on the cytopathic effect of SARS-CoV-2 and on the cell barrier integrity in a Caco-2 cell model. Lisinopril 67-77 angiotensin converting enzyme 2 Homo sapiens 156-160 34292730-0 2021 Self-Assembly of Angiotensin-Converting Enzyme Inhibitors Captopril and Lisinopril and Their Crystal Structures. Lisinopril 72-82 angiotensin I converting enzyme Homo sapiens 17-46 34292730-1 2021 The peptide angiotensin-converting enzyme inhibitors captopril and lisinopril are unexpectedly shown to exhibit critical aggregation concentration (CAC) behavior through measurements of surface tension, electrical conductivity, and dye probe fluorescence. Lisinopril 67-77 angiotensin I converting enzyme Homo sapiens 12-41 34352275-8 2021 ACE inhibitors lisinopril, captopril, fosinopril, and diuretic triamterene demonstrated an inhibition effect on ACE activity. Lisinopril 15-25 angiotensin I converting enzyme Bos taurus 0-3 34352275-8 2021 ACE inhibitors lisinopril, captopril, fosinopril, and diuretic triamterene demonstrated an inhibition effect on ACE activity. Lisinopril 15-25 angiotensin I converting enzyme Bos taurus 112-115 34352275-12 2021 Captopril, fosinopril, lisinopril, and triamterene demonstrated a non-competitive inhibition effect on ACE activity. Lisinopril 23-33 angiotensin I converting enzyme Bos taurus 103-106 34304582-3 2021 Here, we aimed to determine whether lisinopril-tryptophan (lisW-S), a C-domain specific ACE inhibitor that preserves the N-domain catalytic activity, together with sacubitril (NEP inhibitor), differentially influences cardiovascular function and vascular permeability in hypertension compared with omapatrilat and lisinopril+sacubitril which inhibits both the ACE C- and N-domains. Lisinopril 36-46 angiotensin I converting enzyme (peptidyl-dipeptidase A) 1 Mus musculus 88-91 34304582-3 2021 Here, we aimed to determine whether lisinopril-tryptophan (lisW-S), a C-domain specific ACE inhibitor that preserves the N-domain catalytic activity, together with sacubitril (NEP inhibitor), differentially influences cardiovascular function and vascular permeability in hypertension compared with omapatrilat and lisinopril+sacubitril which inhibits both the ACE C- and N-domains. Lisinopril 36-46 angiotensin I converting enzyme (peptidyl-dipeptidase A) 1 Mus musculus 360-363 34077352-11 2022 For ramipril and lisinopril, only a high dose of lisinopril was able to produce a modest reduction of the DPP-4 activity, but it was not enough to inhibit the inactivation of GLP-1. Lisinopril 49-59 dipeptidylpeptidase 4 Rattus norvegicus 106-111 35093482-10 2022 Lisinopril abrogated radiation-induced increases in BALF MCP-1 (CCL2) and MIP-1alpha cytokine levels (p < 0.0001). Lisinopril 0-10 C-C motif chemokine ligand 2 Homo sapiens 57-62 35093482-5 2022 Mitigation of radiation-induced pneumonitis with the ACE-inhibitor lisinopril was evaluated in the 13.5 Gy rat PBI model. Lisinopril 67-77 angiotensin I converting enzyme Rattus norvegicus 53-56 35093482-10 2022 Lisinopril abrogated radiation-induced increases in BALF MCP-1 (CCL2) and MIP-1alpha cytokine levels (p < 0.0001). Lisinopril 0-10 C-C motif chemokine ligand 2 Homo sapiens 64-68 35093482-10 2022 Lisinopril abrogated radiation-induced increases in BALF MCP-1 (CCL2) and MIP-1alpha cytokine levels (p < 0.0001). Lisinopril 0-10 C-C motif chemokine ligand 3 Homo sapiens 74-84 35093482-11 2022 Treatment with lisinopril reduced both ACE expression (p=0.006) and frequency of CD45+CD11b+ lung myeloid cells (p=0.004). Lisinopril 15-25 angiotensin I converting enzyme Homo sapiens 39-42 35093482-11 2022 Treatment with lisinopril reduced both ACE expression (p=0.006) and frequency of CD45+CD11b+ lung myeloid cells (p=0.004). Lisinopril 15-25 integrin subunit alpha M Homo sapiens 86-91 35093482-12 2022 In vitro, radiation injury acutely increased ACE activity (p=0.045) and reactive oxygen species (ROS) generation (p=0.004) in human monocytes, whereas treatment with lisinopril blocked radiation-induced increases in both ACE and ROS. Lisinopril 166-176 angiotensin I converting enzyme Homo sapiens 45-48 35093482-12 2022 In vitro, radiation injury acutely increased ACE activity (p=0.045) and reactive oxygen species (ROS) generation (p=0.004) in human monocytes, whereas treatment with lisinopril blocked radiation-induced increases in both ACE and ROS. Lisinopril 166-176 angiotensin I converting enzyme Homo sapiens 221-224 35359831-0 2022 Oral Lisinopril Raises Tissue Levels of ACE2, the SARS-CoV-2 Receptor, in Healthy Male and Female Mice. Lisinopril 5-15 angiotensin converting enzyme 2 Homo sapiens 40-44 35359831-2 2022 However, it is unclear whether ACE1 inhibitors (e.g., lisinopril) or angiotensin receptor blockers (e.g., losartan) alter tissue ACE2 expression. Lisinopril 54-64 angiotensin converting enzyme 2 Homo sapiens 129-133 35359831-3 2022 This study sought to determine whether lisinopril or losartan, as monotherapies or in combination, changes tissue levels of ACE2 in healthy male and female mice. Lisinopril 39-49 angiotensin I converting enzyme (peptidyl-dipeptidase A) 2 Mus musculus 124-128 35359831-7 2022 Oral lisinopril increased the ACE2 protein index across all tissues (p < 0.0001 vs. control). Lisinopril 5-15 angiotensin I converting enzyme (peptidyl-dipeptidase A) 2 Mus musculus 30-34 35359831-8 2022 In contrast, the combination of lisinopril plus losartan did not increase ACE2 levels in any tissue (p = 0.89 vs. control) and even decreased tissue expression of the Ace2 gene (p < 0.001 vs. control). Lisinopril 32-42 angiotensin I converting enzyme (peptidyl-dipeptidase A) 2 Mus musculus 167-171 35359831-9 2022 Tissue ACE2 remained elevated in the mice 21 days after cessation of lisinopril (p = 0.02). Lisinopril 69-79 angiotensin I converting enzyme (peptidyl-dipeptidase A) 2 Mus musculus 7-11 35359831-12 2022 Oral lisinopril increases ACE2, the cellular receptor for SARS-CoV-2, in tissues that are relevant to the transmission and pathogenesis of COVID-19. Lisinopril 5-15 angiotensin converting enzyme 2 Homo sapiens 26-30 35359831-13 2022 Remarkably, the addition of losartan prevented lisinopril-induced increases in ACE2 across tissues. Lisinopril 47-57 angiotensin converting enzyme 2 Homo sapiens 79-83 35052483-7 2022 Genetic knockdown of genes in the WNT signaling pathway, Axin, frizzled, nemo, and wingless, diminished or abolished the effects of Lisinopril treatment on climbing speed traits. Lisinopril 132-142 axin 1 Homo sapiens 57-61 35146537-6 2022 Meanwhile, we found several VIP variants that might alter the drug metabolism of cisplatin-cyclophosphamide (CYP2E1), vitamin E (CYP4F2), asthma amlodipine, chlorthalidone, and lisinopril (ACE) through PharmGKB. Lisinopril 177-187 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 109-115 35311118-5 2022 One irradiated group was treated with the ACE-inhibitor lisinopril, and a separate group in each strain served as nonirradiated controls. Lisinopril 56-66 angiotensin I converting enzyme Rattus norvegicus 42-45 2550029-7 1989 We conclude (1) there is a heterogeneous response to lisinopril in patients with chronic renal disease and hypertension, (2) lisinopril monotherapy may result in effective blood pressure control without renal hemodynamic compromise, and (3) an increase in PRA following converting enzyme inhibition may identify those in whom the circulating renin angiotensin system is participating in systemic hypertension and intrarenal hemodynamic changes. Lisinopril 125-135 renin Homo sapiens 342-347 2559191-0 1989 Intestinal absorption mechanism of dipeptide angiotensin converting enzyme inhibitors of the lysyl-proline type: lisinopril and SQ 29,852. Lisinopril 113-123 angiotensin I converting enzyme Rattus norvegicus 45-74 2552823-3 1989 The distribution of ACE was mapped using an iodinated derivative of lisinopril. Lisinopril 68-78 angiotensin I converting enzyme Rattus norvegicus 20-23 2550696-0 1989 Efficacy and variability of the antiproteinuric effect of ACE inhibition by lisinopril. Lisinopril 76-86 angiotensin I converting enzyme Homo sapiens 58-61 2550696-1 1989 We studied the efficacy of the ACE inhibitor lisinopril in treating overt proteinuria in comparison with the NSAID indomethacin, and evaluated some of the conditions that could influence this antiproteinuric effect. Lisinopril 45-55 angiotensin I converting enzyme Homo sapiens 31-34 2550696-7 1989 Thus, the antiproteinuric effect of the ACE inhibitor lisinopril appears to be dose and time related, and is strongly dependent on dietary sodium restriction, whereas it does not depend on initial proteinuria, BP, or GFR. Lisinopril 54-64 angiotensin I converting enzyme Homo sapiens 40-43 2544410-5 1989 Both aldosterone and angiotensin II production could be attenuated by adding the angiotensin converting enzyme inhibitor lisinopril to the culture medium (0.1 mM). Lisinopril 121-131 angiotensinogen Rattus norvegicus 21-35 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. Lisinopril 39-49 angiotensin I converting enzyme Homo sapiens 126-129 2544410-5 1989 Both aldosterone and angiotensin II production could be attenuated by adding the angiotensin converting enzyme inhibitor lisinopril to the culture medium (0.1 mM). Lisinopril 121-131 angiotensin I converting enzyme Rattus norvegicus 81-110 2546289-0 1989 [Lisinopril (Zestril)--a new ACE inhibitor]. Lisinopril 1-11 angiotensin I converting enzyme Homo sapiens 29-32 2546289-0 1989 [Lisinopril (Zestril)--a new ACE inhibitor]. Lisinopril 13-20 angiotensin I converting enzyme Homo sapiens 29-32 2558510-5 1989 We purified one ACE from the soluble fraction by lisinopril-linked Sepharose 6B affinity column chromatography and Cellulofine GCL-200 gel filteration. Lisinopril 49-59 angiotensin I converting enzyme Homo sapiens 16-19 2550634-3 1989 Lisinopril treatment reduced supine and standing cuff clinic measurements of BP 24 h after dosing by (systolic/diastolic) 21.1/11.8 and 16.7/10.1 mmHg, respectively. Lisinopril 0-10 BP24 Homo sapiens 77-82 2550640-7 1989 Lisinopril is a novel ACE inhibitor that does not contain a sulphydryl group. Lisinopril 0-10 angiotensin I converting enzyme Homo sapiens 22-25 2550642-7 1989 The larger fall in SBP with lisinopril was statistically significant (lying SBP, P = 0.01; standing SBP, P = 0.0001). Lisinopril 28-38 selenium binding protein 1 Homo sapiens 19-22 2550642-7 1989 The larger fall in SBP with lisinopril was statistically significant (lying SBP, P = 0.01; standing SBP, P = 0.0001). Lisinopril 28-38 selenium binding protein 1 Homo sapiens 76-79 2550642-7 1989 The larger fall in SBP with lisinopril was statistically significant (lying SBP, P = 0.01; standing SBP, P = 0.0001). Lisinopril 28-38 selenium binding protein 1 Homo sapiens 76-79 2550642-8 1989 In addition, a significantly larger proportion of patients achieved BP control (DBP less than 95 mmHg) with lisinopril than with captopril (79% versus 67%; P = 0.02). Lisinopril 108-118 D-box binding PAR bZIP transcription factor Homo sapiens 80-83 2550644-4 1989 The fall in ACE activity at 24 h was 18.5 (8.2-28.8) U/l greater for lisinopril. Lisinopril 69-79 angiotensin I converting enzyme Homo sapiens 12-15 2550647-1 1989 In a series of studies, lisinopril, a new, once-daily, non-sulphydryl-containing ACE inhibitor, has been evaluated for the treatment of congestive heart failure (CHF). Lisinopril 24-34 angiotensin I converting enzyme Homo sapiens 81-84 2550647-10 1989 These results confirm those of previous studies, from which it is concluded that lisinopril is an important addition to the ACE inhibitor class for the treatment of CHF. Lisinopril 81-91 angiotensin I converting enzyme Homo sapiens 124-127 2562398-0 1989 Lisinopril--another ACE inhibitor. Lisinopril 0-10 angiotensin I converting enzyme Homo sapiens 20-23 2545394-11 1989 Rank order of potency of the ACE inhibitors tested was CI906 = CGS14831 greater than S9780 greater than 351A greater than MK521 greater than SQ27519 Lisinopril 122-127 angiotensin I converting enzyme Rattus norvegicus 29-32 2540224-6 1989 Lisinopril administration resulted in a rise in plasma renin activity and a fall in plasma aldosterone concentrations which were similar in both groups and which returned over time toward the baseline. Lisinopril 0-10 renin Homo sapiens 55-60 2557876-8 1989 Following oral administration of the drugs to SHR, the degree and duration of ACE inhibition in aorta and lung correlated with the antihypertensive actions, with ramipril, lisinopril, and zofenopril producing effects of the greatest magnitude and duration. Lisinopril 172-182 angiotensin I converting enzyme Rattus norvegicus 78-81 2540224-8 1989 Lisinopril alone or in combination with hydrochlorothiazide produces favorable antihypertensive effects in both younger and older predominantly black, low-renin patients with essential hypertension. Lisinopril 0-10 renin Homo sapiens 155-160 2550712-1 1989 A change has been made in the commonly used lisinopril affinity gel procedure for purifying angiotensin converting enzyme. Lisinopril 44-54 angiotensin I converting enzyme Bos taurus 92-121 2846685-0 1988 Effects of the angiotensin converting enzyme inhibitor, lisinopril, on normal and diabetic rats. Lisinopril 56-66 angiotensin I converting enzyme Rattus norvegicus 15-44 2853724-3 1988 Thereafter the rats were further separated randomly to receive the ACE inhibitor lisinopril (3-8 mg/kg per day) or no drug treatment for 11 weeks. Lisinopril 81-91 angiotensin I converting enzyme Rattus norvegicus 67-70 2853724-7 1988 Plasma renin activity increased on lisinopril treatment in all groups except DS rats on the high-salt diet. Lisinopril 35-45 renin Rattus norvegicus 7-12 2853660-2 1988 Lisinopril, a new nonsulfhydryl angiotensin-converting-enzyme (ACE) inhibitor, is absorbed in its active form. Lisinopril 0-10 angiotensin I converting enzyme Homo sapiens 32-61 2853660-2 1988 Lisinopril, a new nonsulfhydryl angiotensin-converting-enzyme (ACE) inhibitor, is absorbed in its active form. Lisinopril 0-10 angiotensin I converting enzyme Homo sapiens 63-66 2854271-5 1988 A method is proposed for the elimination of this disturbances in the NEP-determination with a phosphate-free buffer using two comparison tests with Lisinopril and o-Phenanthroline. Lisinopril 148-158 membrane metalloendopeptidase Homo sapiens 69-72 2844082-7 1988 However, recent studies with lisinopril, a new long-acting, nonsulfhydryl angiotensin-converting enzyme inhibitor, indicate that reductions in systolic and diastolic blood pressure in older hypertensive patients receiving either angiotensin-converting enzyme inhibitor or hydrochlorothiazide monotherapy were not significantly different. Lisinopril 29-39 angiotensin I converting enzyme Homo sapiens 74-103 2844082-7 1988 However, recent studies with lisinopril, a new long-acting, nonsulfhydryl angiotensin-converting enzyme inhibitor, indicate that reductions in systolic and diastolic blood pressure in older hypertensive patients receiving either angiotensin-converting enzyme inhibitor or hydrochlorothiazide monotherapy were not significantly different. Lisinopril 29-39 angiotensin I converting enzyme Homo sapiens 229-258 2844085-3 1988 Lisinopril, a new long-acting angiotensin-converting enzyme inhibitor, also has been shown to be an effective antihypertensive agent in older patients. Lisinopril 0-10 angiotensin I converting enzyme Homo sapiens 30-59 2844087-11 1988 The improvement in left ventricular ejection fraction with lisinopril may be indicative of a more favorable prognosis in patients with CHF, since another long-acting ACE inhibitor, enalapril, reduces the rate of mortality associated with CHF. Lisinopril 59-69 angiotensin I converting enzyme Homo sapiens 166-169 2846685-5 1988 Lisinopril reduced systolic blood pressure and inhibited serum ACE activity in both normal and diabetic rats in a dose-response fashion. Lisinopril 0-10 angiotensin I converting enzyme Rattus norvegicus 63-66 2846685-8 1988 Plasma renin activity (PRA) increased sharply in both groups of rats treated with the lower doses of lisinopril, only to decrease at the 5 mg/kg level. Lisinopril 101-111 renin Rattus norvegicus 7-12 2846685-10 1988 Formation of angiotensin II (Ang II) in both normal and diabetic rats was maximally inhibited at doses of 1.0 and 0.1 mg/kg of lisinopril, respectively without a significantly greater effect at the higher doses of the drug. Lisinopril 127-137 angiotensinogen Rattus norvegicus 13-27 2846685-10 1988 Formation of angiotensin II (Ang II) in both normal and diabetic rats was maximally inhibited at doses of 1.0 and 0.1 mg/kg of lisinopril, respectively without a significantly greater effect at the higher doses of the drug. Lisinopril 127-137 angiotensinogen Rattus norvegicus 29-35 2843195-3 1988 All three angiotensin-converting enzyme (ACE) inhibitors reduced arterial pressure to about the same extent: captopril by 14%, enalapril by 18%, and lisinopril by 13%. Lisinopril 149-159 angiotensin I converting enzyme Homo sapiens 41-44 2833813-5 1988 In 11 patients with renovascular hypertension, treatment with the angiotensin-converting enzyme (ACE) inhibitor, lisinopril, resulted in a significant increase in PRA, accompanied by a decrease in RS measured by the enzymatic assay. Lisinopril 113-123 angiotensin I converting enzyme Homo sapiens 66-95 2844497-2 1988 Lisinopril is an orally active angiotensin-converting enzyme (ACE) inhibitor which at dosages of 20 to 80 mg once daily is effective in lowering blood pressure in all grades of essential hypertension. Lisinopril 0-10 angiotensin I converting enzyme Homo sapiens 31-60 2844497-2 1988 Lisinopril is an orally active angiotensin-converting enzyme (ACE) inhibitor which at dosages of 20 to 80 mg once daily is effective in lowering blood pressure in all grades of essential hypertension. Lisinopril 0-10 angiotensin I converting enzyme Homo sapiens 62-65 2844497-8 1988 If additional studies confirm these preliminary findings, then lisinopril will have a similar profile of indications to other ACE inhibitors, and like some other drugs in this class it offers the convenience of once daily administration. Lisinopril 63-73 angiotensin I converting enzyme Homo sapiens 126-129 2838262-1 1988 Angiotensin converting enzyme (ACE) was characterized by radioligand studies utilizing the potent ACE inhibitor 351A, a derivative of lisinopril. Lisinopril 134-144 angiotensin I converting enzyme Rattus norvegicus 0-29 2838262-1 1988 Angiotensin converting enzyme (ACE) was characterized by radioligand studies utilizing the potent ACE inhibitor 351A, a derivative of lisinopril. Lisinopril 134-144 angiotensin I converting enzyme Rattus norvegicus 31-34 2833813-5 1988 In 11 patients with renovascular hypertension, treatment with the angiotensin-converting enzyme (ACE) inhibitor, lisinopril, resulted in a significant increase in PRA, accompanied by a decrease in RS measured by the enzymatic assay. Lisinopril 113-123 angiotensin I converting enzyme Homo sapiens 97-100 2832327-2 1988 Inhibition of angiotensin converting enzyme (ACE) in serum and tissues of rats was studied after administration of lisinopril, an ACE inhibitor. Lisinopril 115-125 angiotensin I converting enzyme Rattus norvegicus 14-43 2832327-2 1988 Inhibition of angiotensin converting enzyme (ACE) in serum and tissues of rats was studied after administration of lisinopril, an ACE inhibitor. Lisinopril 115-125 angiotensin I converting enzyme Rattus norvegicus 45-48 2832327-4 1988 Following oral administration of lisinopril (10 mg/kg), serum ACE activity was acutely reduced but recovered gradually over 24 hours. Lisinopril 33-43 angiotensin I converting enzyme Rattus norvegicus 62-65 2832327-5 1988 Four hours after lisinopril administration, ACE activity was markedly inhibited in kidney (11% of control level), adrenal (8%), duodenum (8%), and lung (33%; p less than 0.05). Lisinopril 17-27 angiotensin I converting enzyme Rattus norvegicus 44-47 2832327-7 1988 In brain, ACE activity was markedly reduced 4 hours after lisinopril administration in the circumventricular organs, including the subfornical organ (16-22%) and organum vasculosum of the lamina terminalis (7%; p less than 0.05). Lisinopril 58-68 angiotensin I converting enzyme Rattus norvegicus 10-13 2832327-10 1988 These results establish that lisinopril has differential effects on inhibiting ACE in different tissues and suggest that the prolonged tissue ACE inhibition after a single oral dose of lisinopril may reflect targets involved in the hypotensive action of ACE inhibitors. Lisinopril 29-39 angiotensin I converting enzyme Rattus norvegicus 79-82 2832327-10 1988 These results establish that lisinopril has differential effects on inhibiting ACE in different tissues and suggest that the prolonged tissue ACE inhibition after a single oral dose of lisinopril may reflect targets involved in the hypotensive action of ACE inhibitors. Lisinopril 185-195 angiotensin I converting enzyme Rattus norvegicus 142-145 2832327-10 1988 These results establish that lisinopril has differential effects on inhibiting ACE in different tissues and suggest that the prolonged tissue ACE inhibition after a single oral dose of lisinopril may reflect targets involved in the hypotensive action of ACE inhibitors. Lisinopril 185-195 angiotensin I converting enzyme Rattus norvegicus 142-145 2835538-3 1988 Enzymatically active ACE was isolated from renal homogenates by chromatography using an affinity column constructed by linking an ACE inhibitor, lisinopril, to Affi-Gel 15. Lisinopril 145-155 angiotensin I converting enzyme (peptidyl-dipeptidase A) 1 Mus musculus 21-24 2835538-3 1988 Enzymatically active ACE was isolated from renal homogenates by chromatography using an affinity column constructed by linking an ACE inhibitor, lisinopril, to Affi-Gel 15. Lisinopril 145-155 angiotensin I converting enzyme (peptidyl-dipeptidase A) 1 Mus musculus 130-133 3208727-5 1988 Lung vascular ACE content was quantitated by measuring the single pass binding of an iodinated-converting enzyme inhibitor, 125I-MK351A, a derivative of lisinopril. Lisinopril 153-163 angiotensin I converting enzyme Rattus norvegicus 14-17 3063490-1 1988 This review will discuss the safety profiles of the angiotensin-converting enzyme (ACE) inhibitors captopril, enalapril and lisinopril in patients with hypertension. Lisinopril 124-134 angiotensin I converting enzyme Homo sapiens 83-86 2853446-1 1988 Influence of angiotensin converting enzyme inhibition by lisinopril. Lisinopril 57-67 angiotensin I converting enzyme Homo sapiens 13-42 2904396-1 1988 Further development of ACE inhibitors: from captopril to lisinopril]. Lisinopril 57-67 angiotensin I converting enzyme Homo sapiens 23-26 2849698-5 1988 Lung ACE content was quantitated by measuring the single-pass binding of an iodinated ACE inhibitor, 125I-MK 351A, a derivative of lisinopril. Lisinopril 131-141 angiotensin I converting enzyme Rattus norvegicus 5-8 2849698-5 1988 Lung ACE content was quantitated by measuring the single-pass binding of an iodinated ACE inhibitor, 125I-MK 351A, a derivative of lisinopril. Lisinopril 131-141 angiotensin I converting enzyme Rattus norvegicus 86-89 3041097-11 1987 We conclude that the ACE inhibitor lisinopril effectively reduces blood pressure and proteinuria in renal disease. Lisinopril 35-45 angiotensin I converting enzyme Homo sapiens 21-24 2822313-0 1987 Pharmacokinetics of angiotensin converting enzyme inhibition in tissues following oral lisinopril: studies in the rat using quantitative radioinhibitor binding. Lisinopril 87-97 angiotensin I converting enzyme Rattus norvegicus 20-49 3036166-3 1987 Binding of 125I MK351A to rat serum ACE was reduced in a concentration dependent manner in vitro by the ACE inhibitors MK521 (lisinopril), S9780, and Ro 31-3113-000 (Cilazapril diacid). Lisinopril 119-124 angiotensin I converting enzyme Homo sapiens 36-39 3036166-3 1987 Binding of 125I MK351A to rat serum ACE was reduced in a concentration dependent manner in vitro by the ACE inhibitors MK521 (lisinopril), S9780, and Ro 31-3113-000 (Cilazapril diacid). Lisinopril 119-124 angiotensin I converting enzyme Homo sapiens 104-107 3036166-3 1987 Binding of 125I MK351A to rat serum ACE was reduced in a concentration dependent manner in vitro by the ACE inhibitors MK521 (lisinopril), S9780, and Ro 31-3113-000 (Cilazapril diacid). Lisinopril 126-136 angiotensin I converting enzyme Homo sapiens 36-39 3036166-3 1987 Binding of 125I MK351A to rat serum ACE was reduced in a concentration dependent manner in vitro by the ACE inhibitors MK521 (lisinopril), S9780, and Ro 31-3113-000 (Cilazapril diacid). Lisinopril 126-136 angiotensin I converting enzyme Homo sapiens 104-107 2822313-10 1987 Individual tissues in the rat had differences in time course and degree of ACE inhibition after a single dose of lisinopril. Lisinopril 113-123 angiotensin I converting enzyme Rattus norvegicus 75-78 2439065-1 1987 Peptidyl-dipeptidase A (angiotensin converting enzyme; ACE, EC 3.4.15.1), has been purified from pig kidney and striatum by affinity chromatography employing the selective inhibitor lisinopril as ligand. Lisinopril 182-192 angiotensin-converting enzyme Sus scrofa 24-53 2822304-0 1987 Blockade of angiotensin converting enzyme in circumventricular organs of the brain after oral lisinopril administration demonstrated by quantitative in vitro autoradiography. Lisinopril 94-104 angiotensin I converting enzyme Rattus norvegicus 12-41 2822304-2 1987 To elucidate the central effect of lisinopril, a new angiotensin converting enzyme (ACE) inhibitor, ACE localization and levels were followed in the brain of Sprague-Dawley rats by quantitative in vitro autoradiography after administration of the drug. Lisinopril 35-45 angiotensin I converting enzyme Rattus norvegicus 53-82 2822304-2 1987 To elucidate the central effect of lisinopril, a new angiotensin converting enzyme (ACE) inhibitor, ACE localization and levels were followed in the brain of Sprague-Dawley rats by quantitative in vitro autoradiography after administration of the drug. Lisinopril 35-45 angiotensin I converting enzyme Rattus norvegicus 84-87 2822304-7 1987 Lisinopril inhibited brain ACE in the subfornical organ and organum vasculosum of the lamina terminalis, circumventricular organs, where the blood brain barrier is deficient. Lisinopril 0-10 angiotensin I converting enzyme Rattus norvegicus 27-30 3027262-5 1987 Enzyme activity was inhibited by classical angiotensin converting enzyme inhibitors, including captopril, enalaprilat (MK422), and lisinopril (MK521). Lisinopril 131-141 angiotensin-converting enzyme Sus scrofa 43-72 3027262-5 1987 Enzyme activity was inhibited by classical angiotensin converting enzyme inhibitors, including captopril, enalaprilat (MK422), and lisinopril (MK521). Lisinopril 143-148 angiotensin-converting enzyme Sus scrofa 43-72 2439065-1 1987 Peptidyl-dipeptidase A (angiotensin converting enzyme; ACE, EC 3.4.15.1), has been purified from pig kidney and striatum by affinity chromatography employing the selective inhibitor lisinopril as ligand. Lisinopril 182-192 angiotensin-converting enzyme Sus scrofa 55-58 2856460-1 1987 The effects of orally administered captopril, enalapril and lisinopril on plasma concentrations of angiotensin converting enzyme (ACE), angiotensin II (ANGII) and renin (PRC) were studied over a period of 6 hours in 6 normal subjects. Lisinopril 60-70 angiotensin I converting enzyme Homo sapiens 99-128 3038391-4 1987 Plasma lisinopril concentrations of 30-70 ng/ml were required for 50% inhibition of plasma ACE activity in vivo. Lisinopril 7-17 angiotensin I converting enzyme Homo sapiens 91-94 2831115-1 1987 Lisinopril is a new, long-acting, nonsulfhydryl angiotension-converting enzyme (ACE) inhibitor that is excreted unchanged by the kidney. Lisinopril 0-10 angiotensin I converting enzyme Homo sapiens 80-83 2822521-0 1987 Increase in vasoactive intestinal polypeptides (VIP) by the angiotensin converting enzyme (ACE) inhibitor lisinopril in congestive heart failure. Lisinopril 106-116 vasoactive intestinal peptide Homo sapiens 48-51 2822521-0 1987 Increase in vasoactive intestinal polypeptides (VIP) by the angiotensin converting enzyme (ACE) inhibitor lisinopril in congestive heart failure. Lisinopril 106-116 angiotensin I converting enzyme Homo sapiens 60-89 2822521-0 1987 Increase in vasoactive intestinal polypeptides (VIP) by the angiotensin converting enzyme (ACE) inhibitor lisinopril in congestive heart failure. Lisinopril 106-116 angiotensin I converting enzyme Homo sapiens 91-94 2822521-10 1987 Plasma VIP was significantly increased by a mean of 20.3% (P less than 0.01) on the lisinopril treatment days compared with the control days, whereas circulating catecholamines showed no significant pattern of change. Lisinopril 84-94 vasoactive intestinal peptide Homo sapiens 7-10 3016431-0 1986 Effects of lisinopril, a new angiotensin converting enzyme inhibitor in a cryo-injury model of chronic left ventricular failure. Lisinopril 11-21 angiotensin I converting enzyme Homo sapiens 29-58 3014850-1 1986 The acute hemodynamic and hormonal effects of the oral angiotensin-converting enzyme (ACE) inhibitor lisinopril (MK-521) were assessed over a period of 96 hours in 12 patients with heart failure. Lisinopril 101-111 angiotensin I converting enzyme Homo sapiens 55-84 3014850-1 1986 The acute hemodynamic and hormonal effects of the oral angiotensin-converting enzyme (ACE) inhibitor lisinopril (MK-521) were assessed over a period of 96 hours in 12 patients with heart failure. Lisinopril 101-111 angiotensin I converting enzyme Homo sapiens 86-89 2442549-1 1987 Lisinopril is an orally active, nonsulfhydryl angiotensin-converting-enzyme (ACE) inhibitor that is not metabolized or bound to protein. Lisinopril 0-10 angiotensin I converting enzyme Homo sapiens 46-75 2442549-1 1987 Lisinopril is an orally active, nonsulfhydryl angiotensin-converting-enzyme (ACE) inhibitor that is not metabolized or bound to protein. Lisinopril 0-10 angiotensin I converting enzyme Homo sapiens 77-80 2442549-7 1987 Lisinopril inhibits ACE activity, thereby reducing plasma angiotensin II and aldosterone and increasing plasma renin activity. Lisinopril 0-10 angiotensin I converting enzyme Homo sapiens 20-23 2442549-7 1987 Lisinopril inhibits ACE activity, thereby reducing plasma angiotensin II and aldosterone and increasing plasma renin activity. Lisinopril 0-10 angiotensinogen Homo sapiens 58-72 2442549-7 1987 Lisinopril inhibits ACE activity, thereby reducing plasma angiotensin II and aldosterone and increasing plasma renin activity. Lisinopril 0-10 renin Homo sapiens 111-116 2442555-1 1987 Eleven patients (five women and six men), aged 24-60 years, were treated with the angiotensin-converting enzyme (ACE) inhibitor, lisinopril, with a once-daily dose as the only antihypertensive treatment. Lisinopril 129-139 angiotensin I converting enzyme Homo sapiens 82-111 2442555-1 1987 Eleven patients (five women and six men), aged 24-60 years, were treated with the angiotensin-converting enzyme (ACE) inhibitor, lisinopril, with a once-daily dose as the only antihypertensive treatment. Lisinopril 129-139 angiotensin I converting enzyme Homo sapiens 113-116 2442558-1 1987 The acute hemodynamic, hormonal, and pharmacokinetic aspects of treatment with the angiotensin-converting enzyme (ACE) inhibitor lisinopril were assessed in two studies in 24 patients with chronic stable congestive heart failure (CHF). Lisinopril 129-139 angiotensin I converting enzyme Homo sapiens 83-112 2442558-1 1987 The acute hemodynamic, hormonal, and pharmacokinetic aspects of treatment with the angiotensin-converting enzyme (ACE) inhibitor lisinopril were assessed in two studies in 24 patients with chronic stable congestive heart failure (CHF). Lisinopril 129-139 angiotensin I converting enzyme Homo sapiens 114-117 2442558-7 1987 The analysis of the hormonal parameters indicate potent inhibition of the renin-angiotensin-aldosterone system for a period exceeding 24 h. In the pharmacokinetic study, 12 hospitalized patients with chronic CHF received lisinopril both orally and intravenously, with each dose followed by a 72-h arterial blood and urine sampling schedule. Lisinopril 221-231 renin Homo sapiens 74-79 2442559-2 1987 In this trial, we compared the new ACE inhibitor, lisinopril, to captopril during a 12-week randomized double-blind study. Lisinopril 50-60 angiotensin I converting enzyme Homo sapiens 35-38 3016431-1 1986 The angiotensin converting enzyme inhibitor, lisinopril, was studied in a cryo-injury model of chronic heart failure. Lisinopril 45-55 angiotensin I converting enzyme Homo sapiens 4-33 3033998-0 1986 Antihypertensive and hormonal effects of lisinopril, a new angiotensin converting enzyme (ACE) inhibitor in patients with renovascular hypertension. Lisinopril 41-51 angiotensin I converting enzyme Homo sapiens 59-88 3033998-0 1986 Antihypertensive and hormonal effects of lisinopril, a new angiotensin converting enzyme (ACE) inhibitor in patients with renovascular hypertension. Lisinopril 41-51 angiotensin I converting enzyme Homo sapiens 90-93 3033998-1 1986 The antihypertensive and hormonal effects of a new ACE-inhibitor, lisinopril (MK-521), was studied in 11 patients with renal arterial stenosis (bilateral in 1). Lisinopril 66-76 angiotensin I converting enzyme Homo sapiens 51-54 3032561-9 1986 Very long-acting ones, such as lisinopril, a potent ACE inhibitor already shown to be clinically effective, may add value to this group of therapeutic agents. Lisinopril 31-41 angiotensin I converting enzyme Homo sapiens 52-55 3032561-10 1986 Drug compliance may be easily tested by measuring ACE activity in serum from patients treated with stable ACE inhibitors, such as enalapril and lisinopril, which is an obvious advantage compared with other antihypertensive compounds. Lisinopril 144-154 angiotensin I converting enzyme Homo sapiens 50-53 3032561-10 1986 Drug compliance may be easily tested by measuring ACE activity in serum from patients treated with stable ACE inhibitors, such as enalapril and lisinopril, which is an obvious advantage compared with other antihypertensive compounds. Lisinopril 144-154 angiotensin I converting enzyme Homo sapiens 106-109 2999099-2 1985 Angiotensin-converting enzyme was purified from human lung, kidney, testis, blood plasma, and seminal plasma using a facile two-step protocol which included affinity chromatography on Sepharose-bound lisinopril followed by either gel filtration or hydroxylapatite chromatography. Lisinopril 200-210 angiotensin I converting enzyme Homo sapiens 0-29 2438488-3 1986 A derivative of the specific ACE inhibitor, lysinopril, called 125I-351A, was used to label ACE in tissues. Lisinopril 44-54 angiotensin I converting enzyme Homo sapiens 29-32 2438488-3 1986 A derivative of the specific ACE inhibitor, lysinopril, called 125I-351A, was used to label ACE in tissues. Lisinopril 44-54 angiotensin I converting enzyme Homo sapiens 92-95 3009165-4 1985 The reaction was stopped by adding EDTA and MK-521, inhibitors of angiotensin I converting enzyme. Lisinopril 44-50 angiotensin I converting enzyme Homo sapiens 66-97 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. Lisinopril 74-84 angiotensin I converting enzyme Homo sapiens 110-139 2982846-1 1985 Lisinopril (N alpha-[(S)-1-carboxy-3-phenylpropyl]L-lysyl-L-proline), a potent angiotensin-converting enzyme inhibitor, is an exceptionally selective affinity chromatography ligand for this enzyme. Lisinopril 0-10 angiotensin-converting enzyme Oryctolagus cuniculus 79-108 2982846-3 1985 The affinity of angiotensin-converting enzyme for the Sepharose-spacer-lisinopril matrix (Ki matrix = 1 X 10(-5) M) is weak compared to its affinity for free lisinopril (Ki = 1 X 10(-10) M). Lisinopril 71-81 angiotensin-converting enzyme Oryctolagus cuniculus 16-45 2982846-3 1985 The affinity of angiotensin-converting enzyme for the Sepharose-spacer-lisinopril matrix (Ki matrix = 1 X 10(-5) M) is weak compared to its affinity for free lisinopril (Ki = 1 X 10(-10) M). Lisinopril 158-168 angiotensin-converting enzyme Oryctolagus cuniculus 16-45 2982846-8 1985 The exceptional selectivity of lisinopril as an affinity chromatography ligand for angiotensin-converting enzyme suggests it is among the most specific inhibitors designed for any enzyme. Lisinopril 31-41 angiotensin-converting enzyme Oryctolagus cuniculus 83-112 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. Lisinopril 74-84 angiotensin I converting enzyme Homo sapiens 141-144 32693432-0 2021 Physiologically based pharmacokinetic modeling of lisinopril in children: a case story of angiotensin converting enzyme inhibitors. Lisinopril 50-60 angiotensin I converting enzyme Homo sapiens 90-119 27785997-1 1984 The acute hemodynamic and hormonal effects of the oral angiotensin converting enzyme (ACE) inhibitor MK-521 were assessed over a period of 96 hours in 6 patients with heart failure. Lisinopril 101-107 angiotensin I converting enzyme Homo sapiens 55-84 27785997-1 1984 The acute hemodynamic and hormonal effects of the oral angiotensin converting enzyme (ACE) inhibitor MK-521 were assessed over a period of 96 hours in 6 patients with heart failure. Lisinopril 101-107 angiotensin I converting enzyme Homo sapiens 86-89 33694311-11 2021 In a model adjusted for systolic blood pressure, MMP-1/TIMP-1 (p = .02) and Ac-SDKP (p < .001) levels were associated with lisinopril. Lisinopril 123-133 matrix metallopeptidase 1 Homo sapiens 49-54 33694311-11 2021 In a model adjusted for systolic blood pressure, MMP-1/TIMP-1 (p = .02) and Ac-SDKP (p < .001) levels were associated with lisinopril. Lisinopril 123-133 TIMP metallopeptidase inhibitor 1 Homo sapiens 55-61 33986677-5 2021 The goal of the current study is to compare the pharmacokinetics (PK) of a lead angiotensin converting enzyme (ACE) inhibitor, lisinopril, in irradiated vs. nonirradiated rats, as a step toward licensure by the FDA. Lisinopril 127-137 angiotensin I converting enzyme Rattus norvegicus 80-109 33986677-5 2021 The goal of the current study is to compare the pharmacokinetics (PK) of a lead angiotensin converting enzyme (ACE) inhibitor, lisinopril, in irradiated vs. nonirradiated rats, as a step toward licensure by the FDA. Lisinopril 127-137 angiotensin I converting enzyme Rattus norvegicus 111-114 33915312-8 2021 We conclude that activating GPER with G1 augments components of the cardiac RAS and improves diastolic function without lowering blood pressure, and that lisinopril-induced blood pressure control and cardiac alterations in OVX SHR are permissive in facilitating G1 to augment Ang-(1-7) in serum, thereby strengthening its cardioprotective benefits. Lisinopril 154-164 angiogenin Rattus norvegicus 276-284 34046276-1 2021 Lisinopril is an angiotensin-converting enzyme (ACE) inhibitor that is used as one of the first-line antihypertensive medications. Lisinopril 0-10 angiotensin I converting enzyme Homo sapiens 17-46 34046276-1 2021 Lisinopril is an angiotensin-converting enzyme (ACE) inhibitor that is used as one of the first-line antihypertensive medications. Lisinopril 0-10 angiotensin I converting enzyme Homo sapiens 48-51 6323225-1 1984 MK-521 is a new orally active, nonsulfhydryl angiotensin-converting enzyme (ACE) inhibitor. Lisinopril 0-6 angiotensin I converting enzyme Homo sapiens 45-74 6323225-1 1984 MK-521 is a new orally active, nonsulfhydryl angiotensin-converting enzyme (ACE) inhibitor. Lisinopril 0-6 angiotensin I converting enzyme Homo sapiens 76-79 6323225-3 1984 All doses of MK-521 caused profound suppression of ACE activity for more than 24 h and decreased standing diastolic blood pressure for more than 12 h without changes in pulse rate. Lisinopril 13-19 angiotensin I converting enzyme Homo sapiens 51-54 6089311-1 1984 The acute hemodynamic and hormonal effects of the oral angiotensin converting enzyme (ACE) inhibitor MK-521 were assessed over a period of 96 hours in 6 patients with heart failure. Lisinopril 101-107 angiotensin I converting enzyme Homo sapiens 55-84 6089311-1 1984 The acute hemodynamic and hormonal effects of the oral angiotensin converting enzyme (ACE) inhibitor MK-521 were assessed over a period of 96 hours in 6 patients with heart failure. Lisinopril 101-107 angiotensin I converting enzyme Homo sapiens 86-89 32693432-1 2021 AIMS: Lisinopril is an angiotensin converting enzyme inhibitor to treat hypertension. Lisinopril 6-16 angiotensin I converting enzyme Homo sapiens 23-52 32665926-1 2020 Lisinopril is an angiotensin converting enzyme inhibitor (ACE-I) that has been on market for more than 25 years. Lisinopril 0-10 angiotensin I converting enzyme Homo sapiens 17-46 33048477-1 2021 Lisinopril, a highly hydrophilic long-acting ACE inhibitor, is frequently prescribed for the treatment of hypertension and congestive heart failure. Lisinopril 0-10 angiotensin I converting enzyme Homo sapiens 45-48 33506137-9 2021 Oral treatment with Lis (20 mg/kg) and Enal (40 mg/kg) for 15 consecutive days reversed DOX effects as they reduced the serum creatinine and BUN, kidney levels of MPO and MDA, whereas the drugs increased tissue TAC. Lisinopril 20-23 myeloperoxidase Rattus norvegicus 163-166 33506137-10 2021 The administration of Lis and Enal with DOX also reduced KIM-1and HO-1 RNA expression. Lisinopril 22-25 hepatitis A virus cellular receptor 1 Rattus norvegicus 57-62 33506137-10 2021 The administration of Lis and Enal with DOX also reduced KIM-1and HO-1 RNA expression. Lisinopril 22-25 heme oxygenase 1 Rattus norvegicus 66-70 33305304-6 2020 A binding model is used to confirm the interactions between lisinopril and ACE on the surface of cells, as well as remdesivir and its intracellular targeting protein (RNA-dependent RNA polymerase (RdRp)). Lisinopril 60-70 angiotensin I converting enzyme Homo sapiens 75-78 32422184-11 2020 However, co-treatment with either Naringenin or Lisinopril mitigated both renal and neuronal oxidative stress, normalized blood pressure and lowered the expressions of kidney injury molecule 1, mineralocorticoid receptor and angiotensin converting enzyme. Lisinopril 48-58 hepatitis A virus cellular receptor 1 Rattus norvegicus 168-192 32422184-11 2020 However, co-treatment with either Naringenin or Lisinopril mitigated both renal and neuronal oxidative stress, normalized blood pressure and lowered the expressions of kidney injury molecule 1, mineralocorticoid receptor and angiotensin converting enzyme. Lisinopril 48-58 nuclear receptor subfamily 3, group C, member 2 Rattus norvegicus 194-220 32422184-11 2020 However, co-treatment with either Naringenin or Lisinopril mitigated both renal and neuronal oxidative stress, normalized blood pressure and lowered the expressions of kidney injury molecule 1, mineralocorticoid receptor and angiotensin converting enzyme. Lisinopril 48-58 angiotensin I converting enzyme Rattus norvegicus 225-254 33013477-8 2020 Moreover, additional blood pressure lowering of about 22 mmHg could be achieved when BTTQ was administered on top of ACE inhibitor lisinopril, a current standard of care in the treatment of hypertension. Lisinopril 131-141 angiotensin I converting enzyme Rattus norvegicus 117-120 32752951-7 2021 The results obtained from this study showed that Ramipril, Delapril and Lisinopril could bind with ACE2 receptor and [SARS-CoV-2/ACE2] complex better than chloroquine and hydroxychloroquine. Lisinopril 72-82 angiotensin converting enzyme 2 Homo sapiens 99-103 32605800-7 2020 In a parallel study, rats given N-omega-nitro-L-arginine and the angiotensin converting enzyme inhibitor lisinopril at a relatively low dose in their food were divided into two groups; without and with thiosulfate in the drinking water. Lisinopril 105-115 angiotensin I converting enzyme Rattus norvegicus 65-94 32665926-14 2020 LEARNING POINTS: Angiotensin converting enzyme inhibitors (ACE-I) rarely have serious or life-threatening side effects.Lisinopril-induced liver injury can present as hepatocellular or cholestatic injury.Severe hepatotoxicity secondary to lisinopril can be life threatening irrespective of the liver injury pattern. Lisinopril 119-129 angiotensin I converting enzyme Homo sapiens 17-46 32665926-14 2020 LEARNING POINTS: Angiotensin converting enzyme inhibitors (ACE-I) rarely have serious or life-threatening side effects.Lisinopril-induced liver injury can present as hepatocellular or cholestatic injury.Severe hepatotoxicity secondary to lisinopril can be life threatening irrespective of the liver injury pattern. Lisinopril 238-248 angiotensin I converting enzyme Homo sapiens 17-46 32006628-2 2020 Previous studies revealed that sEH activity is inhibited by specific binding of electrophiles to a redox-sensitive thiol (Cys521) adjacent to the catalytic center of the hydrolase. Lisinopril 122-128 epoxide hydrolase 2, cytoplasmic Mus musculus 31-34 31953678-0 2020 Silibinin enhances anti-renal fibrosis effect of MK-521 via downregulation of TGF-beta signaling pathway. Lisinopril 49-55 transforming growth factor alpha Mus musculus 78-86 31953678-8 2020 The expressions of collagen I, alpha-SMA, Smad2 and Smad3 in TGF-beta-treated HK-2 cells were notably decreased by MK-521, which was further inhibited in the presence of silibinin. Lisinopril 115-121 SMAD family member 2 Mus musculus 42-47 31953678-8 2020 The expressions of collagen I, alpha-SMA, Smad2 and Smad3 in TGF-beta-treated HK-2 cells were notably decreased by MK-521, which was further inhibited in the presence of silibinin. Lisinopril 115-121 SMAD family member 3 Mus musculus 52-57 31953678-8 2020 The expressions of collagen I, alpha-SMA, Smad2 and Smad3 in TGF-beta-treated HK-2 cells were notably decreased by MK-521, which was further inhibited in the presence of silibinin. Lisinopril 115-121 transforming growth factor alpha Mus musculus 61-69 31953678-8 2020 The expressions of collagen I, alpha-SMA, Smad2 and Smad3 in TGF-beta-treated HK-2 cells were notably decreased by MK-521, which was further inhibited in the presence of silibinin. Lisinopril 115-121 hexokinase 2 Mus musculus 78-82 31926091-9 2020 Drug interactions may occur in patients who use premixed insulin with glimepiride, lisinopril, fenofibrate, candesartan, irbesartan, and gemfibrozil. Lisinopril 83-93 insulin Homo sapiens 57-64 32013233-7 2020 Furthermore, peptides IIAE and LVYPFP interacted with the amino acid residues Gln 259 and His 331, respectively, also in common with other ACE-inhibitory drugs such as Captopril, Lisinopril and Elanapril. Lisinopril 179-189 angiotensin I converting enzyme Homo sapiens 139-142 31794021-10 2020 Beneficial ACE10 phenotype was reversed by the angiotensin-converting enzyme inhibitor (lisinopril) and thus was dependent on angiotensin-converting enzyme catalytic activity. Lisinopril 88-98 angiotensin I converting enzyme (peptidyl-dipeptidase A) 1 Mus musculus 47-76 31794021-10 2020 Beneficial ACE10 phenotype was reversed by the angiotensin-converting enzyme inhibitor (lisinopril) and thus was dependent on angiotensin-converting enzyme catalytic activity. Lisinopril 88-98 angiotensin I converting enzyme (peptidyl-dipeptidase A) 1 Mus musculus 126-155 31926628-5 2020 LLc1 cells were engineered to stably overexpress wild-type or C521S sEH, with the latter exhibiting resistance to nitro-oleate-dependent hydrolase inhibition and the associated stimulation of tumor growth in vitro or in vivo. Lisinopril 62-67 epoxide hydrolase 2, cytoplasmic Mus musculus 68-71 32727672-0 2020 C1 esterase inhibitor use in the management of lisinopril-induced angioedema: A case series. Lisinopril 47-57 serpin family G member 1 Homo sapiens 0-21 32727672-1 2020 OBJECTIVE: Review 4 patients who presented with presumed lisinopril-induced angioedema and received C1 esterase inhibitor (C1-INH). Lisinopril 57-67 serpin family G member 1 Homo sapiens 100-121 32727672-1 2020 OBJECTIVE: Review 4 patients who presented with presumed lisinopril-induced angioedema and received C1 esterase inhibitor (C1-INH). Lisinopril 57-67 serpin family G member 1 Homo sapiens 123-129 32727672-2 2020 CASE SUMMARY: Four patients received C1-INH for presumed lisinopril-induced angioedema. Lisinopril 57-67 serpin family G member 1 Homo sapiens 37-43 31550726-3 2020 OBJECTIVES: We assessed whether treatment with an orally available inhibitor of autotaxin (ATXi), the main LPA-producing enzyme, could slow the progression of chronic allograft injury in a fully major histocompatibility complex-mismatched rat kidney transplant model and compared its effects with those of the angiotensin-converting enzyme inhibitor lisinopril. Lisinopril 350-360 ectonucleotide pyrophosphatase/phosphodiesterase 2 Rattus norvegicus 91-95 31550726-3 2020 OBJECTIVES: We assessed whether treatment with an orally available inhibitor of autotaxin (ATXi), the main LPA-producing enzyme, could slow the progression of chronic allograft injury in a fully major histocompatibility complex-mismatched rat kidney transplant model and compared its effects with those of the angiotensin-converting enzyme inhibitor lisinopril. Lisinopril 350-360 ectonucleotide pyrophosphatase/phosphodiesterase 2 Rattus norvegicus 80-89 31926628-1 2020 Nitro-oleate (10-nitro-octadec-9-enoic acid), which inhibits soluble epoxide hydrolase (sEH) by covalently adducting to C521, increases the abundance of epoxyeicosatrienoic acids (EETs) that can be health promoting, for example by lowering blood pressure or their anti-inflammatory actions. Lisinopril 120-124 epoxide hydrolase 2, cytoplasmic Mus musculus 61-86 31489273-5 2019 This report describes a patient without diabetes experiencing recurrent severe hypoglycemia induced by the ACE inhibitor lisinopril. Lisinopril 121-131 angiotensin I converting enzyme Homo sapiens 107-110 31926628-1 2020 Nitro-oleate (10-nitro-octadec-9-enoic acid), which inhibits soluble epoxide hydrolase (sEH) by covalently adducting to C521, increases the abundance of epoxyeicosatrienoic acids (EETs) that can be health promoting, for example by lowering blood pressure or their anti-inflammatory actions. Lisinopril 120-124 epoxide hydrolase 2, cytoplasmic Mus musculus 88-91 31583478-7 2019 RESULTS: BMI (p = 0.009), GFR (p = 0.015) and 2-oxoglutarate were included in a logistic regression model to predict response to lisinopril. Lisinopril 129-139 Rap guanine nucleotide exchange factor 5 Homo sapiens 26-29 31295065-4 2019 Lisinopril (Lis) protects skeletal muscle and improves cardiac function in dystrophin-deficient mice, therefore it was included in this study to evaluate the effects of lisinopril used with quercetin and NR. Lisinopril 0-10 dystrophin, muscular dystrophy Mus musculus 75-85 31197356-4 2019 Here, we tested the effects of the ACE-inhibitor Lisinopril on life span, and age-specific speed, endurance, and strength using three genotypes of the D. melanogaster Genetic Reference Panel. Lisinopril 49-59 angiotensin I converting enzyme Homo sapiens 35-38 31197356-8 2019 Knockdown of skeletal muscle-specific Ance, the Drosophila ortholog of ACE, abolished the effects of Lisinopril on lifespan, implying a role for skeletal muscle Ance in survivorship. Lisinopril 101-111 Angiotensin converting enzyme Drosophila melanogaster 38-42 31197356-8 2019 Knockdown of skeletal muscle-specific Ance, the Drosophila ortholog of ACE, abolished the effects of Lisinopril on lifespan, implying a role for skeletal muscle Ance in survivorship. Lisinopril 101-111 angiotensin I converting enzyme Homo sapiens 71-74 31307778-5 2019 BTBR ob/ob mice received vehicle, cAng-(1-7), or the ACE inhibitor lisinopril. Lisinopril 67-77 angiotensin I converting enzyme (peptidyl-dipeptidase A) 1 Mus musculus 53-56 30788074-4 2019 We present a case of a patient on lisinopril therapy for one year who experienced severe airway compromise without the classic symptoms of ACE inhibitor induced angioedema. Lisinopril 34-44 angiotensin I converting enzyme Homo sapiens 139-142 31171092-10 2019 CONCLUSIONS: In patients with HER2-positive breast cancer treated with trastuzumab, both lisinopril and carvedilol prevented cardiotoxicity in patients receiving anthracyclines. Lisinopril 89-99 erb-b2 receptor tyrosine kinase 2 Homo sapiens 30-34 30975293-10 2019 When the mean daily post-operative lisinopril-equivalent ACE inhibitor/ARB dose was >5 mg, the risk of major GIB decreased in a dose-threshold manner (aHR: 0.28; 95% CI: 0.09 to 0.85; p = 0.025). Lisinopril 35-45 angiotensin I converting enzyme Homo sapiens 57-60 29890165-8 2018 The hepatic areas stained with Sirius red and thenumber of cells marked by alpha-SMA in animals treated with aliskiren, bradykinin, lisinopril and losartan were diminished when compared to control group, demonstrating reduced hepatic fibrosis after RAS blockade. Lisinopril 132-142 actin alpha 2, smooth muscle, aorta Mus musculus 75-84 29971804-6 2018 RESULTS: Included studies demonstrated significant positive effects of lisinopril on proteinuric kidney disease; however, lisinopril caused a slight reduction of glomerular filtration rate (GFR) especially for patients with GFR < 90 ml min-1 . Lisinopril 122-132 CD59 molecule (CD59 blood group) Homo sapiens 239-244 30243070-6 2018 Our results revealed that down-regulation of NFkBp65 mRNA expression and inhibition of phosphorylation of NFkBp65 (at Ser536) and NFkBia were implicated in the anti-fibrotic effect of both LIS and SIL. Lisinopril 189-192 NFKB inhibitor alpha Rattus norvegicus 130-136 30243070-9 2018 In addition, LIS augmented the inhibitory effect of SIL on NFkB pathway at lower dose level. Lisinopril 13-16 RELA proto-oncogene, NF-kB subunit Rattus norvegicus 59-63 30243070-10 2018 We concluded that LIS, via targeting NFkB pathway, increases anti-oxidant capacity of liver tissue and exhibits anti-inflammatory, anti-fibrotic and anti-angiogenic activity and augments sensitivity to SIL. Lisinopril 18-21 RELA proto-oncogene, NF-kB subunit Rattus norvegicus 37-41 30373167-0 2018 Age- and Genotype-Specific Effects of the Angiotensin-Converting Enzyme Inhibitor Lisinopril on Mitochondrial and Metabolic Parameters in Drosophila melanogaster. Lisinopril 82-92 Angiotensin converting enzyme Drosophila melanogaster 42-71 29687225-15 2018 Overall, the results from our analysis highlights that lisinopril (DB00722) is predicted to bind better with NA than currently approved drug. Lisinopril 55-65 neuraminidase 1 Homo sapiens 109-111 29061652-8 2018 In this model, separate treatment of hyperglycemia with rosiglitazone or hypertension with lisinopril partially reduced ACR, consistent with independent contributions of these disorders to renal disease. Lisinopril 91-101 acrosin prepropeptide Mus musculus 120-123 29276932-2 2017 The fixed combination of rosuvastatin with ACE inhibitor lisinopril and calcium antagonist amlodipine allows to control effectively two main cardiovascular risk factors: hypercholesterolemia and arterial hypertension. Lisinopril 57-67 angiotensin I converting enzyme Homo sapiens 43-46 28695320-11 2018 Pretreatment with ACE inhibitor lisinopril (0.5 nmol/100 nL) reduced the pressor response, but did not affect ARS-evoked tachycardia. Lisinopril 32-42 angiotensin I converting enzyme Rattus norvegicus 18-21 30564469-12 2018 Tom"s medical history includes hypertension that is adequately controlled with lisinopril (20 mg/day), coronary artery disease (on daily aspirin 81 mg) with left ventricular ejection fraction (LVEF) of > 50%, which is within the normal range (50%-75%), benign prostatic hyperplasia for which he is treated with finasteride, and hyperlipidemia that is treated with atorvastatin. Lisinopril 79-89 pre-mRNA processing factor 6 Homo sapiens 0-3 28364692-10 2017 RESULTS: All examined ACE-Is: lisinopril, perindopril and ramipril decreased KYNA production in rat kidney in vitro. Lisinopril 30-40 angiotensin I converting enzyme Rattus norvegicus 22-25 28364692-11 2017 KAT I activity was decreased by lisinopril and ramipril whereas the activity of KAT II was lowered by ramipril. Lisinopril 32-42 kynurenine aminotransferase 1 Rattus norvegicus 0-5 31994092-10 2017 RESULTS: All examined ACE-Is: lisinopril, perindopril and ramipril decreased KYNA production in rat kidney in vitro. Lisinopril 30-40 angiotensin I converting enzyme Rattus norvegicus 22-25 31994092-11 2017 KAT I activity was decreased by lisinopril and ramipril whereas the activity of KAT II was lowered by ramipril. Lisinopril 32-42 kynurenine aminotransferase 1 Rattus norvegicus 0-5 27728854-2 2017 Some commercially available ACE inhibitors are captopril, lisinopril and enalapril; due to their side effects, naturally occurring inhibitors have been prospected. Lisinopril 58-68 angiotensin I converting enzyme Bos taurus 28-31 28445490-2 2017 It has also been shown that the ACE inhibitor lisinopril, and the natural product curcumin are also beneficial in different models of CKD in rats. Lisinopril 46-56 angiotensin I converting enzyme Rattus norvegicus 32-35 27615269-11 2017 CONCLUSION: The present study suggested a cardio-protective effect of lisinopril on acute EAM in rats, probably through a mechanism related to its suppressive effect on angiotensin II formation. Lisinopril 70-80 angiotensinogen Rattus norvegicus 169-183 28416926-2 2017 We aim to investigate the role of COX enzymes in the effects of losartan, an angiotensin II (Ang II) receptor antagonist or lisinopril, an ACE inhibitor, on the contractions of rat thoracic aorta in isolated tissue bath. Lisinopril 124-134 angiotensin I converting enzyme Rattus norvegicus 139-142 28416926-4 2017 RESULTS: When used alone, dipyrone and losartan inhibited Phe, KCl, and Ang II-induced contractions, whereas lisinopril inhibited only Phe and Ang II-induced contractions. Lisinopril 109-119 angiotensinogen Rattus norvegicus 143-149 27728854-6 2017 Moreover, as proof of concept, the ACE-MBs was inhibited by lisinopril with a half maximal inhibitory concentration (IC50) of 10nM. Lisinopril 60-70 angiotensin I converting enzyme Bos taurus 35-38 28101033-4 2016 The patient was treated with the cardioprotective agent dexrazoxane, and changes in cardiac markers [e.g. decreases in ejection fraction (EF)] were immediately addressed by therapeutic intervention with the ACE inhibitor lisinopril and beta-blocker metoprolol. Lisinopril 221-231 angiotensin I converting enzyme Homo sapiens 207-210 27992423-8 2016 Further studies in melanoma cells (TM-5) showed that Ang-II induced cell proliferation through ACE activation, an event that could be inhibited either by ACE inhibitor (Lisinopril) or by the silencing of ACE. Lisinopril 169-179 angiotensin I converting enzyme (peptidyl-dipeptidase A) 1 Mus musculus 154-157 28808443-6 2017 In contrast, although 1 week of lisinopril significantly decreased SBP and increased PRA among participants without P-HPT, there were no changes in PTH or calcium. Lisinopril 32-42 S100 calcium binding protein A6 Homo sapiens 85-88 27992423-8 2016 Further studies in melanoma cells (TM-5) showed that Ang-II induced cell proliferation through ACE activation, an event that could be inhibited either by ACE inhibitor (Lisinopril) or by the silencing of ACE. Lisinopril 169-179 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 53-59 27992423-8 2016 Further studies in melanoma cells (TM-5) showed that Ang-II induced cell proliferation through ACE activation, an event that could be inhibited either by ACE inhibitor (Lisinopril) or by the silencing of ACE. Lisinopril 169-179 angiotensin I converting enzyme (peptidyl-dipeptidase A) 1 Mus musculus 95-98 27992423-8 2016 Further studies in melanoma cells (TM-5) showed that Ang-II induced cell proliferation through ACE activation, an event that could be inhibited either by ACE inhibitor (Lisinopril) or by the silencing of ACE. Lisinopril 169-179 angiotensin I converting enzyme (peptidyl-dipeptidase A) 1 Mus musculus 154-157 27829805-6 2016 RESULTS: Rats pre-treated with amlodipine, lisinopril or allopurinol showed significantly lower serum transaminases, significantly lower hepatic malondialdehyde, myeloperoxidase and nitrate/nitrite, as well as significantly higher hepatic glutathione and catalase levels, compared with acetaminophen control rats. Lisinopril 43-53 catalase Rattus norvegicus 255-263 27829805-6 2016 RESULTS: Rats pre-treated with amlodipine, lisinopril or allopurinol showed significantly lower serum transaminases, significantly lower hepatic malondialdehyde, myeloperoxidase and nitrate/nitrite, as well as significantly higher hepatic glutathione and catalase levels, compared with acetaminophen control rats. Lisinopril 43-53 myeloperoxidase Rattus norvegicus 162-177 27682899-6 2016 In this model, the ACE inhibitor lisinopril (at ~24 mg m d started orally in the drinking water at 7 d after irradiation and continued to >=150 d) mitigated late effects in the lungs and kidneys after 12.5-Gy leg-out PBI. Lisinopril 33-43 angiotensin I converting enzyme Rattus norvegicus 19-22 27976638-3 2016 The present study has been conducted to evaluate the potential effect of an ACE inhibitor, lisinopril, on the morphological and biochemical aspects of fibrotic liver regeneration. Lisinopril 91-101 angiotensin I converting enzyme Rattus norvegicus 76-79 27976638-11 2016 CONCLUSION: ACE inhibitor lisinopril did not produce major histomorphological alterations in regenerating fibrotic liver following partial hepatectomy, however, it may improve its functional capability. Lisinopril 26-36 angiotensin I converting enzyme Rattus norvegicus 12-15 27404504-8 2016 Dextrose induced ER stress was reduced with pharmacologic blockers of AT1 (losartan and candesartan) and mineralocorticoid receptor blocker (spironolactone) but not with angiotensin converting enzyme inhibitors (captopril and lisinopril). Lisinopril 226-236 angiotensin II receptor type 1 Homo sapiens 70-73 27423316-9 2016 Lisinopril increased KAT I activity and perindopril did not affect it. Lisinopril 0-10 kynurenine aminotransferase 1 Rattus norvegicus 21-26 26407530-3 2016 We hypothesized that transcript expression of pro-angiogenic factors (VEGF, tenascin-C, Angpt1, Angpt1R) and oxygen metabolism (COX4I1, COX4I2, HIF-1alpha) in human muscle after an endurance stimulus depends on vasoconstriction, and would be modulated through angiotensin-converting enzyme inhibition by intake of lisinopril. Lisinopril 314-324 tenascin C Homo sapiens 76-86 26407530-3 2016 We hypothesized that transcript expression of pro-angiogenic factors (VEGF, tenascin-C, Angpt1, Angpt1R) and oxygen metabolism (COX4I1, COX4I2, HIF-1alpha) in human muscle after an endurance stimulus depends on vasoconstriction, and would be modulated through angiotensin-converting enzyme inhibition by intake of lisinopril. Lisinopril 314-324 cytochrome c oxidase subunit 4I1 Homo sapiens 128-134 26407530-8 2016 Conversely, there was a specific exercise-induced increase in VEGF transcript (P = 0.04) and protein levels (P = 0.03) and a trend for increased tenascin-c transcript levels (P = 0.09) for subjects consuming lisinopril. Lisinopril 208-218 tenascin C Homo sapiens 145-155 27928554-7 2016 Further, Bleo inducetion of both AGT protein and of caspase-9 were prevented by the ACE inhibitor lisinopril. Lisinopril 98-108 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 33-36 27928554-7 2016 Further, Bleo inducetion of both AGT protein and of caspase-9 were prevented by the ACE inhibitor lisinopril. Lisinopril 98-108 caspase 9 Mus musculus 52-61 27928554-7 2016 Further, Bleo inducetion of both AGT protein and of caspase-9 were prevented by the ACE inhibitor lisinopril. Lisinopril 98-108 angiotensin I converting enzyme (peptidyl-dipeptidase A) 1 Mus musculus 84-87 29879347-8 2016 Dopamine, glutamine, piperine, berberine, nuciferine, lisinopril and fosinopril could inhibit ergothioneine or mildronate uptake by MDCK- hOCTN1/2. Lisinopril 54-64 solute carrier family 22 member 4 Homo sapiens 138-146 27288733-4 2016 Treatment with either B1 receptor antagonist (BI113823) or an ACE inhibitor (lisinopril) alone or in combination significantly reduced the heart weight-to-body weight and lung weight-to-body weight ratios, and improved postinfarction cardiac function as evidenced by greater cardiac output, the maximum rate of left ventricular pressure rise (+-dP/dtmax), left ventricle ejection fraction, fractional shorting, better wall motion, and attenuation of elevated left ventricular end diastolic pressure (LVEDP). Lisinopril 77-87 angiotensin I converting enzyme Rattus norvegicus 62-65 26300521-0 2016 Combined spectroscopies and molecular docking approach to characterizing the binding interaction between lisinopril and bovine serum albumin. Lisinopril 105-115 albumin Homo sapiens 127-140 26943616-0 2016 Garlic capsule and selenium-vitamins ACE combination therapy modulate key antioxidant proteins and cellular adenosine triphosphate in lisinopril-induced lung damage in rats. Lisinopril 134-144 angiotensin I converting enzyme Rattus norvegicus 37-40 26943616-8 2016 RESULTS: Administration of therapeutic dose of LIS to male rats depleted enzymatic antioxidants (superoxide dismutase and catalase) and cellular adenosine triphosphate content with concomitant increase in lipid peroxidation. Lisinopril 47-50 catalase Rattus norvegicus 122-130 26948539-6 2016 In anesthetized rats, unilateral PVN microinjection of BDNF increased MAP by 31+-4mmHg (P<0.001 vs vehicle), which was prevented by PVN microinjection pretreatments with the high-affinity BDNF receptor TrkB antagonist ANA-12, losartan, the angiotensin converting enzyme inhibitor lisinopril, or by intravenous hexamethonium. Lisinopril 283-293 brain-derived neurotrophic factor Rattus norvegicus 55-59 27222603-1 2016 Lisinopril is a drug of the angiotensin-converting enzyme (ACE) inhibitor class that is primarily used in the treatment of hypertension. Lisinopril 0-10 angiotensin I converting enzyme Homo sapiens 28-57 27222603-1 2016 Lisinopril is a drug of the angiotensin-converting enzyme (ACE) inhibitor class that is primarily used in the treatment of hypertension. Lisinopril 0-10 angiotensin I converting enzyme Homo sapiens 59-62 26300521-1 2016 To further understand the mode of action and pharmacokinetics of lisinopril, the binding interaction of lisinopril with bovine serum albumin (BSA) under imitated physiological conditions (pH 7.4) was investigated using fluorescence emission spectroscopy, synchronous fluorescence spectroscopy, Fourier transform infrared spectroscopy (FTIR), circular dichroism (CD) and molecular docking methods. Lisinopril 104-114 albumin Homo sapiens 127-140 26725563-2 2015 Treatment with lisinopril as an angiotensin converting enzyme (ACE) inhibitor, can be a reason of angioedema. Lisinopril 15-25 angiotensin I converting enzyme Homo sapiens 32-61 26225637-10 2015 Using liquid chromatography time-of-flight mass spectrometry, the presence of lisinopril was confirmed in a subset of specimens with low ACE activity. Lisinopril 78-88 angiotensin I converting enzyme Homo sapiens 137-140 26866372-5 2016 Both lisinopril (ACEi) and MSC treatment prevented monocyte infiltration, reduced tubular cell apoptosis, renal fibrosis and TGFbeta expression. Lisinopril 5-15 transforming growth factor, beta 1 Rattus norvegicus 125-132 26866372-7 2016 Lisinopril alone caused a rebound activation of Renin-Angiotensin System (RAS), while MSC suppressed RENmRNA and Renin synthesis and induced a decrease of AII and aldosterone serum levels. Lisinopril 0-10 renin Rattus norvegicus 48-53 26792980-5 2016 In a docking analysis with testicular ACE (tACE), the most promising inhibitor (4j) was efficiently accommodated in the deep cleft of the protein cavity, making close interatomic contacts with Glu162, His353, and Ala356, comparable with lisinopril. Lisinopril 237-247 angiotensin I converting enzyme Rattus norvegicus 38-41 26391272-6 2016 Kidneys from Agt-ASO-treated mice were not as enlarged and showed reduced cystic volume compared with lisinopril or control treatments. Lisinopril 102-112 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 13-16 26725563-2 2015 Treatment with lisinopril as an angiotensin converting enzyme (ACE) inhibitor, can be a reason of angioedema. Lisinopril 15-25 angiotensin I converting enzyme Homo sapiens 63-66 25757657-5 2015 RESULTS: Administration of lisinopril or LisW-S caused a significant decrease in Ang 1-8/Ang 1-10 ratios as determined by circulating and equilibrium peptide level analysis. Lisinopril 27-37 angiopoietin 1 Rattus norvegicus 81-86 25757657-5 2015 RESULTS: Administration of lisinopril or LisW-S caused a significant decrease in Ang 1-8/Ang 1-10 ratios as determined by circulating and equilibrium peptide level analysis. Lisinopril 27-37 angiopoietin 1 Rattus norvegicus 89-94 24464858-2 2015 Candesartan (AT1 antagonist) and lisinopril (ACE inhibitor) has been reported to possess antioxidant and neuroprotective effects. Lisinopril 33-43 angiotensin I converting enzyme Rattus norvegicus 45-48 25757657-6 2015 Furthermore, Ang 1-7 levels were elevated by both ACE inhibitors, but only lisinopril decreased the Ang 1-5/Ang 1-7 ratio. Lisinopril 75-85 angiopoietin 1 Rattus norvegicus 100-105 25757657-6 2015 Furthermore, Ang 1-7 levels were elevated by both ACE inhibitors, but only lisinopril decreased the Ang 1-5/Ang 1-7 ratio. Lisinopril 75-85 angiopoietin 1 Rattus norvegicus 100-105 25757657-8 2015 Further corroboration of LisW-S C-domain specificity is that only lisinopril increased the circulating levels of the N-domain ACE substrate Ac-SDKP. Lisinopril 66-76 angiotensin I converting enzyme Rattus norvegicus 126-129 26234277-1 2015 We have previously shown that cough potentiation induced by intravenous administration of the AT1 receptor antagonist losartan is lower than that induced by the ACE inhibitor lisinopril in anesthetized and awake rabbits. Lisinopril 175-185 angiotensin-converting enzyme Oryctolagus cuniculus 161-164 25002132-2 2015 The present study sought to determine the association of the I/D gene polymorphism among Malay male essential hypertensive subjects in response to ACE inhibitors (enalapril and lisinopril). Lisinopril 177-187 angiotensin I converting enzyme Homo sapiens 147-150 26147666-8 2015 The increased Ang II was suppressed using lisinopril (an ACE inhibitor) treatment. Lisinopril 42-52 angiotensinogen Homo sapiens 14-20 25837018-1 2015 BACKGROUND: Angiotensin converting enzyme (ACE) inhibitors such as lisinopril, represent the front line pharmacological treatment for heart failure, which is characterised by marked left ventricular (LV) dilatation and hypertrophy. Lisinopril 67-77 angiotensin I converting enzyme Rattus norvegicus 12-41 25837018-1 2015 BACKGROUND: Angiotensin converting enzyme (ACE) inhibitors such as lisinopril, represent the front line pharmacological treatment for heart failure, which is characterised by marked left ventricular (LV) dilatation and hypertrophy. Lisinopril 67-77 angiotensin I converting enzyme Rattus norvegicus 43-46 26147666-8 2015 The increased Ang II was suppressed using lisinopril (an ACE inhibitor) treatment. Lisinopril 42-52 angiotensin I converting enzyme Homo sapiens 57-60 25680080-5 2015 ACE inhibitors such as ramipril, captopril, perindopril, quinapril, lisinopril, enalapril, and trandolapril have been documented to ameliorate the above neurodegenerative disorders. Lisinopril 68-78 angiotensin I converting enzyme Homo sapiens 0-3 25924878-3 2015 Treatment of Cyp4a12tg mice with DOX increased systolic blood pressure (SBP; 136 +- 2 vs. 102 +- 1 mmHg; P < 0.05), and this increase was prevented by administration of 20-HEDGE, lisinopril, or losartan. Lisinopril 182-192 cytochrome P450, family 4, subfamily a, polypeptide 12a Mus musculus 13-20 25701466-4 2015 METHODOLOGY: ACE activity of 86 SCZ patients and 100 HCs paired by age, gender and educational level was measured, using the FRET peptide substrate and the specific inhibitor lisinopril. Lisinopril 175-185 angiotensin I converting enzyme Homo sapiens 13-16 28294850-1 2015 OBJECTIVE: to review the available results of clinical trials on the efficacy and safety of a fixed combination of an angiotensin-converting enzyme (ACE) inhibitor lisinopril and the calcium antagonist amlodipine, including an analysis of the actual antihypertensive effect and organoprotective action in the russian population of patients. Lisinopril 164-174 angiotensin I converting enzyme Homo sapiens 118-147 25544039-6 2015 The enzyme was strongly inhibited by the specific ACE inhibitor lisinopril (Ki of 1.26 nM). Lisinopril 64-74 angiotensin I converting enzyme Homo sapiens 50-53 28294850-1 2015 OBJECTIVE: to review the available results of clinical trials on the efficacy and safety of a fixed combination of an angiotensin-converting enzyme (ACE) inhibitor lisinopril and the calcium antagonist amlodipine, including an analysis of the actual antihypertensive effect and organoprotective action in the russian population of patients. Lisinopril 164-174 angiotensin I converting enzyme Homo sapiens 149-152 26320298-1 2015 OBJECTIVE: to review the available results of clinical trials on the efficacy and safety of a fixed combination of an angiotensin-converting enzyme (ACE) inhibitor lisinopril and the calcium antagonist amlodipine, including an analysis of the actual antihypertensive effect and organoprotective action in the russian population of patients. Lisinopril 164-174 angiotensin I converting enzyme Homo sapiens 118-147 25300038-1 2015 This work describes a RP-HPLC method for the determination and interaction studies of cefpirome with ACE-inhibitors (captopril, enalapril and lisinopril) in various buffers. Lisinopril 142-152 angiotensin I converting enzyme Homo sapiens 101-104 25874328-3 2015 To render support to the experimental results, a series of quinazolinone derivatives were docked into active site of ACE and identified the probable binding modes compared to Lisinopril. Lisinopril 175-185 angiotensin I converting enzyme Homo sapiens 117-120 26320298-1 2015 OBJECTIVE: to review the available results of clinical trials on the efficacy and safety of a fixed combination of an angiotensin-converting enzyme (ACE) inhibitor lisinopril and the calcium antagonist amlodipine, including an analysis of the actual antihypertensive effect and organoprotective action in the russian population of patients. Lisinopril 164-174 angiotensin I converting enzyme Homo sapiens 149-152 25745598-3 2014 We report a case of angioedema caused by ACE inhibitors confined to the upper airway after four years on treatment with Lisinopril which persisted for three weeks and required endotracheal intubation and subsequent tracheostomy due to delayed resolution. Lisinopril 120-130 angiotensin I converting enzyme Homo sapiens 41-44 25845252-5 2015 RESULTS: ACE inhibitors protein binding data varied from negligible (lisinopril) to 99% (fosinopril). Lisinopril 69-79 angiotensin I converting enzyme Homo sapiens 9-12 25402658-6 2014 In addition, the binding mechanism of IVR has been rationalized through docking simulations using the testicular ACE (tACE)-lisinopril complex at 2 A resolution (PDB 108A ). Lisinopril 124-134 angiotensin-converting enzyme Pelodiscus sinensis 113-116 25131919-1 2014 BACKGROUND: Perindopril and lisinopril are two common ACE inhibitors prescribed for management of hypertension. Lisinopril 28-38 angiotensin I converting enzyme Homo sapiens 54-57 24881253-2 2014 The clinical working diagnosis of angioedema as a result of the use of ACE-inhibitors (lisinopril) was made. Lisinopril 87-97 angiotensin I converting enzyme Homo sapiens 71-74 24937322-5 2014 Renovascular hypertensive rats received bilateral PVN infusion with ACE inhibitor lisinopril (LSP, 10mug/h) or vehicle via osmotic minipump for 4weeks. Lisinopril 82-92 angiotensin I converting enzyme Rattus norvegicus 68-71 24561703-4 2014 Lisinopril-tryptophan (LisW-S), an analogue of the ACE inhibitor lisinopril, is highly selective for the C-domain. Lisinopril 65-75 angiotensin I converting enzyme Rattus norvegicus 51-54 24448204-8 2014 For example, our results suggest that the interaction of Lisinopril, an ACE inhibitor commonly prescribed for hypertension, and the antidepressant sertraline can potentially increase the likelihood and possibly the severity of psoriasis. Lisinopril 57-67 angiotensin I converting enzyme Homo sapiens 72-75 25325125-23 2014 When a diuretic cannot be used, it is better to choose an ACE inhibitor: captopril, lisinopril or ramipril. Lisinopril 84-94 angiotensin I converting enzyme Homo sapiens 58-61 24506807-6 2014 Treatment with the non-selective ACEI lisinopril (1 mg/kg of body weight per day via an osmotic mini-pump for 2 weeks) reduced SBP (127+-3 compared with. Lisinopril 38-48 spermine binding protein Mus musculus 127-130 24506807-9 2014 Treatment with lisinopril or lisW-S significantly reduced levels of AngII in kidneys (~4-fold; P<0.001). Lisinopril 15-25 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 68-73 24853572-2 2014 A case is described of Angiotensin converting enzyme inhibitor (ACEi) and sitagliptin induced angioedema, where AO attacks decreased after the withdrawal of lisinopril but resolved only after the withdrawal of sitagliptin, an inhibitor of dipeptylpeptidase IV. Lisinopril 157-167 angiotensin I converting enzyme Homo sapiens 23-52 24959410-1 2014 Lisinopril is an angiotensin-converting enzyme (ACE) inhibitor, primarily used for the treatment of hypertension, congestive heart failure, and heart attack. Lisinopril 0-10 angiotensin I converting enzyme Homo sapiens 17-46 24959410-1 2014 Lisinopril is an angiotensin-converting enzyme (ACE) inhibitor, primarily used for the treatment of hypertension, congestive heart failure, and heart attack. Lisinopril 0-10 angiotensin I converting enzyme Homo sapiens 48-51 25767848-0 2014 Captopril and lisinopril only inhibit matrix metalloproteinase-2 (MMP-2) activity at millimolar concentrations. Lisinopril 14-24 matrix metallopeptidase 2 Homo sapiens 38-64 25767848-0 2014 Captopril and lisinopril only inhibit matrix metalloproteinase-2 (MMP-2) activity at millimolar concentrations. Lisinopril 14-24 matrix metallopeptidase 2 Homo sapiens 66-71 25767848-3 2014 This study aimed to investigate the inhibitory potential of captopril and lisinopril regarding MMP-2 activity. Lisinopril 74-84 matrix metallopeptidase 2 Homo sapiens 95-100 25767848-5 2014 The second objective was to test the direct inhibitory effect of captopril and lisinopril on plasma MMP-2 and on recombinant human MMP-2 (rhMMP-2). Lisinopril 79-89 matrix metallopeptidase 2 Homo sapiens 100-105 25767848-11 2014 The captopril and lisinopril concentrations found to inhibit MMP-2 are 3 orders of magnitude higher than those present in vivo after drug administration. Lisinopril 18-28 matrix metallopeptidase 2 Homo sapiens 61-66