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About: Lisinopril is a(n) research topic. Over the lifetime, 2172 publication(s) have been published within this topic receiving 71191 citation(s). The topic is also known as: Prinivil® & Zestril®. more


Open accessJournal ArticleDOI: 10.1161/01.RES.87.5.E1
Mary Donoghue1, Frank Y. Hsieh1, Elizabeth Baronas1, Kevin Godbout1  +8 moreInstitutions (1)
Abstract: ACE2, the first known human homologue of angiotensin-converting enzyme (ACE), was identified from 5' sequencing of a human heart failure ventricle cDNA library. ACE2 has an apparent signal peptide, a single metalloprotease active site, and a transmembrane domain. The metalloprotease catalytic domains of ACE2 and ACE are 42% identical, and comparison of the genomic structures indicates that the two genes arose through duplication. In contrast to the more ubiquitous ACE, ACE2 transcripts are found only in heart, kidney, and testis of 23 human tissues examined. Immunohistochemistry shows ACE2 protein predominantly in the endothelium of coronary and intrarenal vessels and in renal tubular epithelium. Active ACE2 enzyme is secreted from transfected cells by cleavage N-terminal to the transmembrane domain. Recombinant ACE2 hydrolyzes the carboxy terminal leucine from angiotensin I to generate angiotensin 1-9, which is converted to smaller angiotensin peptides by ACE in vitro and by cardiomyocytes in culture. ACE2 can also cleave des-Arg bradykinin and neurotensin but not bradykinin or 15 other vasoactive and hormonal peptides tested. ACE2 is not inhibited by lisinopril or captopril. The organ- and cell-specific expression of ACE2 and its unique cleavage of key vasoactive peptides suggest an essential role for ACE2 in the local renin-angiotensin system of the heart and kidney. The full text of this article is available at http://www. more

2,337 Citations

Journal ArticleDOI: 10.1016/S0140-6736(99)10327-1
Lennart Hansson1, Lars H Lindholm2, Tord Ekbom3, Björn Dahlöf4  +5 moreInstitutions (6)
20 Nov 1999-The Lancet
Abstract: Summary Background The efficacy of new antihypertensive drugs has been questioned. We compared the effects of conventional and newer antihypertensive drugs on cardiovascular mortality and morbidity in elderly patients. Methods We did a prospective, randomised trial in 6614 patients aged 70–84 years with hypertension (blood pressure ≥180 mm Hg systolic, ≥105 mm Hg diastolic, or both). Patients were randomly assigned conventional antihypertensive drugs (atenolol 50 mg, metoprolol 100 mg, pindolol 5 mg, or hydrochlorothiazide 25 mg plus amiloride 2·5 mg daily) or newer drugs (enalapril 10 mg or lisinopril 10 mg, or felodipine 2·5 mg or isradipine 2–5 mg daily). We assessed fatal stroke, fatal myocardial infarction, and other fatal cardiovascular disease. Analysis was by intention to treat. Findings Blood pressure was decreased similarly in all treatment groups. The primary combined endpoint of fatal stroke, fatal myocardial infarction, and other fatal cardiovascular disease occurred in 221 of 2213 patients in the conventional drugs group (19·8 events per 1000 patientyears) and in 438 of 4401 in the newer drugs group (19·8 per 1000; relative risk 0·99 [95% Cl 0·84–1·16], p=0·89). The combined endpoint of fatal and non-fatal stroke, fatal and non-fatal myocardial infarction, and other cardiovascular mortality occurred in 460 patients taking conventional drugs and in 887 taking newer drugs (0·96 [0·86–1·08], p=0·49). Interpretation Old and new antihypertensive drugs were similar in prevention of cardiovascular mortality or major events. Decrease in blood pressure was of major importance for the prevention of cardiovascular events. more

Topics: Blood pressure (52%), Stroke (52%), Atenolol (51%) more

1,407 Citations

Open accessJournal ArticleDOI: 10.1161/CIRCULATIONAHA.104.510461
24 May 2005-Circulation
Abstract: Background— Angiotensin-converting enzyme 2 (ACE2) has emerged as a novel regulator of cardiac function and arterial pressure by converting angiotensin II (Ang II) into the vasodilator and antitrop... more

1,177 Citations

Journal ArticleDOI: 10.1016/S0140-6736(94)90232-1
07 May 1994-The Lancet
Abstract: GISSI-3 is a multicentre randomised clinical trial to assess the efficacy of lisinopril, transdermal glyceryl trinitrate (GTN), and theircombination in improving survival and ventricular function after acute myocardial infarction (AMI). Between June, 1991, and July, 1993, 19 394 patients were randomised from 200 coronary care units in Italy. Eligible patients presented within 24 h of symptom onset and had no clear indications for or against the study treatments. In a factorial design patients were randomly assigned 6 weeks of oral lisinopril (5 mg initial dose and then 10 mg daily) or open control as well as nitrates (intravenous for the first 24 h followed by transdermal GTN 10 mg daily) or open control. Complete clinical data and 6-week follow-up were available for 18895 (97·4%) patients randomised. Two-dimensional echocardiographic data were available for 14 209 patients. Overall 6-week mortality was 6·7%. Lisinopril, started within 24 h from AMI symptoms, produced significant reductions in overall mortality (odds ratio 0·88 [95% CI 0·79-0·99]) and in the combined outcome measure of mortality and severe ventricular dysfunction (0·90 [0·84-0·98]). In the same trial the systematic administration of transdermal GTN did not show any independent effect on the same outcome measures (0·94 [0·84-1·05] and 0·94 [0·87-1·02]). Systematic combined administration of lisinopril and GTN also produced significant reductions in overall mortality (0·83 [0·70-0·97]) and in the combined endpoint (0·85 [0·76-0·94]). The favourable effect of lisinopril alone or with GTN was clear also in the predefined high-risk populations (elderly patients and women) for the combined endpoint. These findings were obtained in a population intensively exposed to recommended treatments (thrombolysis 72%, beta-blockade 31%, and aspirin 84%); non-protocol treatment with angiotensin-converting-enzyme inhibitors and nitrates was allowed for specific clinical indications. No excess of unfavourable clinically relevant events in the treated groups was reported. more

Topics: Lisinopril (53%), Population (51%)

1,130 Citations

Open accessJournal ArticleDOI: 10.1161/01.CIR.100.23.2312
07 Dec 1999-Circulation
Abstract: Background—Angiotensin-converting enzyme (ACE) inhibitors are generally prescribed by physicians in doses lower than the large doses that have been shown to reduce morbidity and mortality in patients with heart failure. It is unclear, however, if low doses and high doses of ACE inhibitors have similar benefits. Methods and Results—We randomly assigned 3164 patients with New York Heart Association class II to IV heart failure and an ejection fraction #30% to double-blind treatment with either low doses (2.5 to 5.0 mg daily, n51596) or high doses (32.5 to 35 mg daily, n51568) of the ACE inhibitor, lisinopril, for 39 to 58 months, while background therapy for heart failure was continued. When compared with the low-dose group, patients in the high-dose group had a nonsignificant 8% lower risk of death (P50.128) but a significant 12% lower risk of death or hospitalization for any reason (P50.002) and 24% fewer hospitalizations for heart failure (P50.002). Dizziness and renal insufficiency was observed more frequently in the high-dose group, but the 2 groups were similar in the number of patients requiring discontinuation of the study medication. Conclusions—These findings indicate that patients with heart failure should not generally be maintained on very low doses of an ACE inhibitor (unless these are the only doses that can be tolerated) and suggest that the difference in efficacy between intermediate and high doses of an ACE inhibitor (if any) is likely to be very small. (Circulation. 1999;100:2312-2318.) more

Topics: Lisinopril (66%), ACE inhibitor (60%), Heart failure (57%) more

1,038 Citations

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Topic's top 5 most impactful authors

Barry R. Davis

34 papers, 3K citations

Carlos M. Ferrario

16 papers, 2.9K citations

Giuseppe Remuzzi

11 papers, 763 citations

William C. Cushman

10 papers, 1.5K citations

Andrea Remuzzi

9 papers, 662 citations

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