Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.15.1 (ACE)
 18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Quinapril, a nonsulfhydryl ACE inhibitor, was evaluated in ten New York Heart Association (NYHA) functional class (FC) II-III CHF patients to determine its effects on regional blood flow [effective renal plasma flow (ERPF), renal blood flow (RBF), renal vascular resistance (RVR), hepatic blood flow (HBF), hepatic vascular resistance (HVR), segmental limb pressure (SLP), creatinine clearance (CRCL)] and cardiac function [left ventricular ejection fraction (LVEF)]. Previous vasodilator therapy was withdrawn 2 weeks before baseline measurements. Stable regimens of digoxin and diuretics were continued throughout the study. ERPF was assessed using p-aminohippurate (PAH), HBF by indocyanine green (ICG) clearance, and LVEF by radionuclide scintography. Segmental limb pressures were measured by Doppler flow detection. Measurements were performed at baseline (B) and after 4 weeks of quinapril therapy (10 mg BID). Quinapril increased renal (P less than 0.05) and hepatic blood flow (P = 0.06) and significantly reduced renal and hepatic vascular resistance. Glomerular filtration rate and left ventricular ejection fraction were unchanged. Mean arterial pressure and brachial segmental pressures decreased without change in heart rate. Noninvasive cardiovascular assessments indicate that quinapril improves regional blood flow while exhibiting no change in left ventricular ejection fraction, in patients with NYHA FC II-III CHF.
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PMID:Evaluation of quinapril on regional blood flow and cardiac function in patients with congestive heart failure. 174 May 40

We assessed the blockade of the renin-angiotensin system (RAS) achieved with 2 angiotensin (Ang) antagonists given either alone at different doses or with an ACE inhibitor. First, 20 normotensive subjects were randomly assigned to 100 mg OD losartan (LOS) or 80 mg OD telmisartan (TEL) for 1 week; during another week, the same doses of LOS and TEL were combined with 20 mg OD lisinopril. Then, 10 subjects were randomly assigned to 200 mg OD LOS and 160 mg OD TEL for 1 week and 100 mg BID LOS and 80 mg BID TEL during the second week. Blockade of the RAS was evaluated with the inhibition of the pressor effect of exogenous Ang I, an ex vivo receptor assay, and the changes in plasma Ang II. Trough blood pressure response to Ang I was blocked by 35+/-16% (mean+/-SD) with 100 mg OD LOS and by 36+/-13% with 80 mg OD TEL. When combined with lisinopril, blockade was 76+/-7% with LOS and 79+/-9% with TEL. With 200 mg OD LOS, trough blockade was 54+/-14%, but with 100 mg BID it increased to 77+/-8% (P<0.01). Telmisartan (160 mg OD and 80 mg BID) produced a comparable effect. Thus, at their maximal recommended doses, neither LOS nor TEL blocks the RAS for 24 hours; hence, the addition of an ACE inhibitor provides an additional blockade. A 24-hour blockade can be achieved with an angiotensin antagonist alone, provided higher doses or a BID regimen is used.
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PMID:Angiotensin II receptor blockade: is there truly a benefit of adding an ACE inhibitor? 1251 26

The objective of this paper was to evaluate potential beneficial effects of combined treatment with slow-release nitrates and angiotensin converting enzyme inhibitors (ACE) on left ventricular remodeling and exercise capacity in patients after acute myocardial infarction. In this study, 141 patients (aged 34 to 74, mean 56.6 years) with sufficient circulation received combined treatment with 24 hour nitroglycerin infusion followed by oral nitrates (isosorbide mononitrate 50 mg OD) from day 2 day 42 after myocardial infarction and ACE inhibitor (captopril 25 mg BID or enalapril 5 mg BID versus placebo) from day 10 to day 42. On days 10 and 42, echocardiographic examination was carried out and recorded on an optical disc. Simultaneously, on the same days, the treadmill exercise test (modified Bruce protocol) was performed. In the echocardiographic study the left ventricular endodiastolic and endosystolic volumes (biplane Simpson formula), ejection fraction, left ventricular wall motion score and left ventricular mass index were analyzed. Treadmill test criteria, used in the study, included exercise duration time and workload (METS). For each patient the data obtained examination II and I were measured and the differences in their values were classified. The obtained results were analyzed with one-way and three-way ANOVA test. A Kruskal-Wallis test was also used in one variable analysis. Results were analyzed after repartition of patients into groups according type of treatment (angiotensin converting ing enzyme inhibitor or placebo), infarct location (anterior or inferior wall) and enzyme level (CPK < 2000 IU/L or CPK > 2000 IU/L). A p value < 0.1 was considered statistically significant. In a single factor analysis ANOVA proved that the patients treated with nitrates and captopril showed greater improvement in exercise capacity (in METS) than patients treated with enalapril or placebo (+1.26 captopril, +0.2 enalapril and +0.29 placebo, p = 0.043). In addition, a decrease in left ventricular mass index was evident only in patients treated with angiotensin converting enzyme inhibitor (placebo +7.37 gm/m2, captopril -12.17 gm/m2, enalapril -10.14 gm/m2, p = 0.0032). The triple factor analysis ANOVA test revealed that the change in endodiastolic left ventricular volume depends on combination of three factors: infarct location, type of treatment and level of cardiac enzymes (p = 0.009). A decrease in left ventricular endodiastolic volume between day 42 and 10 was observed only in patients with inferior wall infarct and CPK level < 2000 IU/L, irrespective of treatment type and in patients with inferior wall infarct and CPK level > 2000 IU/L treated with angiotensin enzyme inhibitor. We noticed also that heart failure, considered as contraindication to randomization, was in addition the most frequent (up to day 10) cause for study termination and initiation of treatment with angiotensin enzyme inhibitor.
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PMID:[The impact of nitrates and mono-therapy and nitrates combined with angiotensin converting enzyme inhibitors on left ventricular remodeling and exercise capacity in patients after acute myocardial infarction]. 1293 52

The aim of the study was to evaluate effectiveness and safety of angiotensin II receptor blockers and inhibitors of angiotensin-converting enzyme (ECE) for protective therapy following medicamentous cardioversion with propafen at a loading dose of 600 mg in patients with paroxysmal atrial fibrillation and arterial hypertension. 101 patients were divided in 2 groups. Group 1 included 75 patients who received ACE inhibitor lisinopril (10 mg BID) after recovery of sinus rhythm by propanorm. 26 patients of group 2 were treated with angiotensin II receptor blocker candesartan (8 mg daily). Combined treatment with angiotensin II receptor blocker and propafenone leads to cardioversion faster than therapy with ACR inhibitor. It is concluded that alternative approach to the maintenance of sinus rhythm using angiotensin II receptor blockers has advantages over traditional anti-arrhythmic therapy; it is well tolerated by the patients and produced no serious side effects.
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PMID:[Preventive strategy for atrial fibrillation in arterial hypertension]. 2001 44