Our library of drug research abstracts drawn from the medical literature is updated on a regular schedule, and you can be assured that new enalapril research articles will be listed here shortly after becoming available to us.
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Medical research on enalapril
Cardiovasc Res. 2008 Jun 19;
de Miguel LS, Neysari S, Jakob S, Petrimpol M, Butz N, Banfi A, Zaugg CE, Humar R, Battegay EJ
AIMS: Angiotensin converting enzyme (ACE) inhibition reduces heart disease and vascular stiffness in hypertension and leads to kinin accumulation. In this study, we analyzed the role and importance of two kinin receptor subtypes in angiogenesis during ACE inhibition in an in vitro model of angiogenesis of the mouse heart. Methods and Results First, we analyzed the angiogenic properties of bradykinin and enalapril on wild-type C57Bl/6 and B2 receptor-/- mouse heart under normoxia (21% O2) and hypoxia (1% O2) in vitro and the contribution of B1 and B2 kinin receptors to this effect. Bradykinin induced dose-dependent endothelial sprout formation in vitro in adult mouse heart only under hypoxia (1.7 fold, n = 6, p < 0.05). The B2 receptor mediated sprouting that was induced by bradykinin and vascular endothelial growth factor (VEGF164; n = 6, p < 0.05) but did not mediate sprouting that was induced by growth factors bFGF or PDGF-BB. Enalapril induced sprouting through both the B1 and B2 kinin receptors, but it required the presence of the B2 receptor in both scenarios and was dependent on BK synthesis. B1-receptor agonists induced sprout formation via the B1 receptor (2.5 fold, n = 6, p < 0.05), but it required the presence of the B2 receptor for them to do so. Both B2-receptor and B1-receptor agonist-induced angiogenesis required nitric oxide biosynthesis. CONCLUSION: The kinin B2 receptor plays a crucial role in angiogenesis that is induced by different vasoactive molecules, namely bradykinin, ACE inhibitors, B1-stimulating kinin metabolites, and VEGF164 in an in vitro model of angiogenesis of mouse heart under hypoxia. Therapeutic treatment of hypertensive patients by using ACE inhibitors may potentially benefit the ischemic heart through inducing B2-dependent heart neovascularization.
Med J Malaysia. 2007 Oct; 62(4): 294-8
Dinesh KU, Subish P, Pranaya M, Shankar PR, Anil SK, Durga B
A prospective study was conducted at Manipal Teaching Hospital, Pokhara, Nepal to identify and analyze the pattern of the potential DDIs (drug-drug interaction) in diabetes patients. A total of 182 patients who were prescribed 685 drugs (average, 3.76 drugs per prescription) were enrolled. Patients 51 to 60 years of age had a higher risk [43 patients, or (23.6%)] of developing DDIs. It was found that 174 (92.1%) of the potential DDIs were of "moderate" severity. Cardiovascular drugs carried a risk of DDIs (187 drugs, or 49.5%). The most common potential DDI observed was between metformin and enalapril (n = 64).
Kardiologiia. 2008; 48(5): 10-5
Ageev FT, Drobizhev MB, Smirnova MD, Fofanova TV, Plisiuk AG, Kadushina EB
Fixed-dose lercanidipine/enalapril for hypertension.
Drugs Today (Barc). 2008 Apr; 44(4): 261-70
Menne J, Haller H
The dihydropyridine calcium channel blocker lercanidipine and the ACE inhibitor enalapril are frequently used in the treatment of hypertensive patients. In April 2007, a fixed-dose combination of the two drugs was approved in Germany for the treatment of patients not responding to monotherapy. It is expected that the drug will soon be available in the other European Union markets. In this review the present literature is summarized. Two doses will be available with 10 mg lercanidipine each and 10 or 20 mg enalapril. The medication should be taken once daily, optimally =15 minutes before a meal and the consumption of grapefruit juice should be avoided. The fixed-dose combination of the two drugs has a stronger blood pressure-lowering effect than monotherapy with 20 mg enalapril or 10 mg lercanidipine. The combination is well tolerated and few patients stopped the treatment because of side effects. As expected, the most common side effects reported are cough, peripheral edema, flushing, dizziness and vertigo, occurring in 1-5% of patients. This new fixed-dose combination is a useful adjunct to the present treatment and should increase compliance and help reduce hypertension-related costs. Copyright 2008 Prous Science, S.A.U. or its licensors. All rights reserved.
Cardiovasc Drugs Ther. 2008 Jun 5;
Dobre D, van Veldhuisen DJ, Goulder MA, Krum H, Willenheimer R
PURPOSE: To assess the clinical effects and safety profile of initial monotherapy with either bisoprolol or enalapril in elderly patients with heart failure (HF). METHODS: In CIBIS III, 1010 patients with mild to moderate HF and age >/=65 years were randomized to monotherapy with either bisoprolol or enalapril for 6 months. RESULTS: Bisoprolol had a similar effect as enalapril on the combined end-point of all-cause mortality or hospitalization (HR 1.02; p = 0.90), as well as on each of the individual end-points. A trend towards fewer sudden deaths was observed with bisoprolol (NS). On the other hand, more cases of worsening HF requiring hospitalization or occurring while in hospital were observed in the bisoprolol group (HR 1.67; p = 0.03). The two groups were similar with regard to treatment cessations and early introduction of the second drug. CONCLUSIONS: Bisoprolol and enalapril had a similar effect on the combined end-point of mortality or hospitalization during 6 months monotherapy. However, more worsening HF events were observed in the bisoprolol group.
Hypertens Res. 2008 Mar; 31(3): 575-84
Imanishi T, Kuroi A, Ikejima H, Kobayashi K, Muragaki Y, Mochizuki S, Goto M, Yoshida K, Akasaka T
We investigated the effects of co-administration of an angiotensin-converting enzyme inhibitor (ACEI) and angiotensin type 1 receptor blocker (ARB) on nitric oxide (NO) bioavailability in genetically hyperlipidemic rabbits with our newly developed NO sensor. Plasma NO was measured using the new NO sensor in the abdominal aorta of anesthetized Watanabe heritable hyperlipidemic (WHHL) rabbits. Acetylcholine (ACh)-stimulated (20 microg in 5 min into the aortic arch) NO production was recorded after an 8 week per os pretreatment with 1) vehicle (control), 2) the ACEI enalapril (E: 3 mg/kg/day), 3) the ARB losartan (L: 30 mg/kg/day) and 4) enalapril (1.5 mg/kg/day)+losartan (15 mg/kg/day) (E+L). Intra-aortic infusion of ACh produced an increase in plasma NO concentration, which was significantly greater with all the drug treatments than with the control. E increased ACh-induced NO significantly more than L (by 6.9 nmol/L, and 4.7 nmol/L, respectively). E+L increased ACh-induced NO by 9.5 nmol/L, significantly more than either E or L. Plasma peroxynitrite concentration was 1.2 pmol/mg protein in the control group and significantly less than in the E- and L-group. The lowest peroxynitrite concentration was observed in the E+L group (0.5 pmol/mg protein), which was significantly lower than in the E-group and the L-group. Optical coherence tomography and histology of the thoracic aorta revealed that the plaque area decreased significantly more with the combination than with the monotherapy (p
[Endothelioprotective properties of L-arginine on a nitric oxide deficiency model]
Eksp Klin Farmakol. 2008 Mar-Apr; 71(2): 29-31
In laboratory animals with endothelial dysfunction (nitric oxide deficiency) modeled by the introduction of NO-synthase inhibitor L-NAME, the activation of endothelioprotective effects of enalapril, lozartan, amlodipine, indapamide and nebivolol is revealed for their introduction in combination with L-arginine. This result was confirmed by the behavior of a generalizing parameter, the coefficient of endothelial dysfunction (CED) calculated using the results of tests on endothelium-dependent and -independent vasodilation.
Ther Clin Risk Manag. 2007 Aug; 3(4): 569-78
Metra M, Nodari S, Bordonali T, Milani P, Lombardi C, Bugatti S, Fontanella B, Verzura G, Danesi R, Dei Cas L
Clinical trials have consistently shown the benefits of beta-blocker treatment in patients with chronic heart failure (HF). As a result, bisoprolol, carvedilol, and metoprolol succinate are now indicated for the treatment of all patients with chronic HF who do not have major contraindications. Bisoprolol is the first beta-blocker shown to improve survival in an outcome trial. In the Cardiac Insufficiency Bisoprolol Study II (CIBIS-II), all-cause mortality and sudden death were reduced in patients treated with bisoprolol compared with those on placebo (11.8% vs 17.3%; p < 0.0001 and 3.6% vs 6.3%, p < 0.002; respectively) regardless of age, NYHA functional class, and co-morbidities. Further studies have shown both the efficacy of bisoprolol on secondary endpoints and patients subgroups as well its high cost effectiveness. More recently, CIBIS-III has shown similar efficacy and safety of the initiation of HF treatment with either bisoprolol or enalapril, with a tendency to a survival advantage with bisoprolol. Nowadays, the role of bisoprolol, as well as that of carvedilol and metoprolol succinate, in HF treatment is firmly established and research is mainly focused on implementation of treatment and better dosing. This article will summarize evidence for the efficacy of bisoprolol in the treatment of HF.
Enalaprilat induced acute parotitis.
J Assoc Physicians India. 2008 Feb; 56: 128-9
Chauhan V, Negi RC, Sharma A, Gupta S, Mokta J, Verma B, Thakur S
Drug induced acute parotitis is a very uncommon complication reported with a few drugs only. There is no case of acute bilateral parotitis reported previously with i.v. enalaprilat. We present here a female patient who developed acute bilateral parotitis within minutes of i.v. enalaprilat injection and recovered within 24 hours of stopping the drug and with symptomatic treatment.
J Pharm Biomed Anal. 2008 Aug 5; 47(4-5): 934-7
Lima DM, Dos Santos LD, Lima EM
Stability of enalapril maleate formulations can be affected when the product is exposed to higher temperature and humidity, with the formation of two main degradation products: enalaprilat and a diketopiperazine derivative. In this work, stability and drug release profiles of 20mg enalapril maleate tablets (reference, generic and similar products) were evaluated. After 180 days of the accelerated stability testing, most products did not exhibit the specified amount of drug. Additionally, drug release profiles were markedly different from that of the reference product, mainly due to drug degradation. Changes in drug concentration and drug release profile of enalapril formulations are strong indicators of a compromised bioavailability, with possible interferences on the therapeutic response for this drug.