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nebivolol prevented salt-induced kidney injury and associated proteinuria in SHR through a blood pressure-independent mechanism. Its protective effects may be related to reduction in oxidative stress, increases in neuronal NOS and restoration of angiotensin II type 1/mas receptor balance.
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Pentobarbital-anesthetized dogs were administered either dl-propranolol, atenolol or dl-nebivolol at cumulative doses of 0 (vehicle), 0.0025, 0.01, 0.04, 0.16 and 0.64 mg/kg i.v. After each dose, heart rate and diastolic blood pressure responses to isoproterenol (0.125 micrograms/kg/min i.v. for 5 min), as well as plasma glucose, insulin, lactate and free fatty acid responses, were measured. Heart rate and free fatty acid changes were taken as beta-1 adrenergic indices, with the other parameters taken as beta-2 adrenergic indices. The antagonist dose estimated to cause 50% inhibition of each isoproterenol response (ID50) was calculated. Nebivolol and atenolol had nearly identical cardiovascular profiles, which were much more beta-1 selective than that of propranolol [heart rate and blood pressure ID50 values, mg/kg: 0.034, 0.036 (propranolol); 0.058, 0.713 (nebivolol); 0.047, 0.506 (atenolol)]. Propranolol also potently inhibited isoproterenol-stimulated glucose, insulin and lactate increases (ID50S: 0.020, 0.078 and 0.007 mg/kg, respectively). Nebivolol and atenolol were much weaker inhibitors of these metabolic responses than propranolol (5-fold-35-fold and 8-fold-greater than 90-fold, respectively). Insulin responses were equivalently inhibited by both nebivolol and atenolol (ID50S greater than 0.4 mg/kg), whereas glucose and lactate ID50S for nebivolol were 0.183 and 0.243 mg/kg, respectively, with atenolol ID50S greater than 0.64 mg/kg. Free fatty acid responses were attenuated by all three antagonists with ID50 values of 0.103, 0.100 and 0.028 mg/kg for propranolol, nebivolol and atenolol, respectively. These in vivo studies demonstrate that dl-nebivolol significantly inhibited the beta-1 cardiac response at doses which did not produce either beta-2 cardiovascular or metabolic effects.
A 48-year-old man was brought to the emergency department after ingesting nebivolol and ethanol, along with possibly diazepam and cocaine. He had a heart rate of 71/min and a blood pressure of 98/61 mmHg. The initial ECG showed sinus rhythm with a QTc of 483 ms and a QRS of 112 ms. Over the subsequent 4 h, he became bradycardic and hypotensive and developed bradyasystolic cardiac arrest. Standard resuscitation including epinephrine had no effect. Spontaneous circulation returned 30 s after a 100 mL bolus of 20% IFE, and the patient then became briefly hypertensive and tachycardic with heart rate and blood pressure measured as high as 123/min and 251/162 mmHg, respectively. His care included IFE infusion along with HDI bolus and infusion with doses as high as 21.8 units/kg/h. With subsequent hypotension, vasopressors were withheld in favor of HDI and supportive care. He was discharged with baseline neurologic function.
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The effect of beta-blockade with nebivolol in elderly patients with HF in this study was similar in those with preserved and impaired EF.
Factors affecting liver regeneration are still relevant. The purpose of this study is to investigate the effect of nebivolol treatment on liver regeneration in rats in which 70% partial hepatectomy was performed.
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Nebivolol hydrochloride (R067555), is a new antihypertensive drug. Aromatic and alicyclic hydroxylation at the benzopyran ring systems of nebivolol are important metabolic pathways. Generally, NMR is used to unambiguously assign the sites of hydroxylation. Because of the low dose rates and the extensive metabolism of nebivolol in the different species, NMR identification is not always possible, and therefore another spectroscopic technique was searched for to address this problem. UV-chromophore absorption is affected by the kind and arrangement of adjacent atoms and groups (auxochromes). The effect of these auxochromes (e.g. -NH2, -NR2, -SH, -OH, -OR and halogens) can be strongly influenced by the pH. This paper proves that HPLC at high pH combined with on-line diode-array detection is an excellent technique for the location of the hydroxyl functions in hydroxylated metabolites of nebivolol. With this technique it is possible to differentiate between glucuronidation at the automatic and aliphatic or alicyclic hydroxyl functions.
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ISR results from excessive neointimal proliferation. Nebivolol inhibits proliferation of human coronary endothelial and smooth muscle cells in vitro. Its efficacy has not been studied in clinical trials.
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Forty six CHD patients with postinfarction cardiac dysfunction in MS were randomized into two groups. Group 1 consisted of 22 patients with impaired glucose tolerance, group 2--of 24 type 2 diabetics. Treatment included combination of losartan (50 mg/day) with indapamide (1.5 mg/day), on demand nitrates, nebivolol. Basic therapy in diabetes included sugar-reducing drugs. Clinical condition, findings of echocardiography, parameters of lipid and carbohydrate metabolisms, immunoglobulins, circulating immune complexes, autoantibodies to cardiolipin (AB to CL), spectrum of proinflammatory cytokines were studied before and 3 months after course treatment.
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A total of 60 patients (13 males, 47 females; mean age: 54.3 ± 10.7 years) were enrolled in the present study. The patients were randomly selected to receive either nebivolol 5 mg/day (n = 30) or metoprolol 50 mg/day (n = 30) for 8 weeks. At the end of the 8th week, each of the patients received exercise stress test according to Bruce protocol and their blood pressures were remeasured after rest, exercise, and recovery.
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Although increased eNOS immunoreactivity was observed with nebivolol and nebivolol-flutamide in endothelial cells laying cavernous tissue, a lower score was observed after ICI-182.780 application, when compared with control cases. AR immunoreactivity in cavernosal endothelium was clearly higher with nebivolol. Higher H score and ER immunoreactivity were observed in the cavernous endothelium and smooth muscles in the nebivolol, carvedilol, and metoprolol groups when compared with control cases.
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This study assessed blood pressure (BP) reductions and response rates following addition of nebivolol to ongoing antihypertensive therapy in patients with uncontrolled stage I-II hypertension despite antihypertensive treatment. Patients with an average sitting diastolic BP (SiDBP) > or =90 and < or =109 mm Hg while taking an antihypertensive regimen were included in this double-blind, placebo-controlled, parallel-group study. The primary efficacy end point was reduction from baseline to week 12 in mean trough SiDBP. In total, 669 patients were randomized to once-daily nebivolol 5, 10 or 20 mg or placebo. Addition of nebivolol 5, 10 and 20 mg significantly reduced BP; placebo-subtracted least squares mean reductions in trough SiDBP were -3.3, -3.5 and -4.6 mm Hg, respectively (P<0.001) and -5.7, -3.7 and -6.2 mm Hg in trough sitting systolic BP (SiSBP), respectively (P< or =0.015). Adding nebivolol 5-20 mg resulted in significantly more responders (SiDBP <90 or > or =10 mm Hg reduction; range: 53.0-65.1 vs 41.3% with placebo; P< or =0.028) and significantly better control rates (SiSBP/SiDBP <140/90 mm Hg; range: 41.3-52.7 vs 29.3% with placebo; P< or =0.029). Nebivolol was well tolerated; the incidence of adverse events with nebivolol was similar to that with placebo (40.2 vs 38.9%, respectively; P=0.763). Addition of once-daily nebivolol to ongoing antihypertensive therapy provided significant additional BP reductions and better response rates in patients with uncontrolled hypertension and was well tolerated.
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Diabetes mellitus as comorbidity is present in 20-25% of patients suffering from high blood pressure. Because simultaneous presence of these two diseases results in a significant increase of cardiovascular risk, various guidelines chiefly focus on the antihypertensive treatment of patients with diabetes. Combined drug therapy is usually required to achieve the blood pressure target value of <140/85 mmHg defined for patients with diabetes, which must be based on angiotensin converting enzyme-inhibitors or angiotensin receptor blockers. These can be/must be combined with low dose, primarily thiazide-like diuretics, calcium channel blockers with neutral metabolic effect, and further options include the addition of beta blockers, imidazoline-l-receptor antagonists, or alpha-1-adrenoreceptor blockers. Evidence-based guidelines are obviously present in local practice. Although most of the patients receive angiotensin converting enzyme-inhibitor+indapamide or angiotensin converting enzyme-inhibitor+calcium channel blocker combined therapy with favorable metabolic effects, yet the use of angiotensin converting enzyme-inhibitors containing hydrochlorothiazide having diabetogenic potential, and angiotensin receptor blocker fixed combinations is still widespread. Similarly, interesting therapeutic practice can be observed with the use of less differentiated beta blockers, where the 3rd generation carvedilol and nebivolol are still in minority.
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Rats were divided into four groups: sham operated (sham-control), MI-induced (MI-control), immediate nebivolol loaded (MI-neb1), orally nebivolol treated (MI-neb2). MI was induced by the ligation of the LAD. Loading dose of nebivolol (0.1 mg/kg) was administrated i.v. during reperfusion and continuation dose was administrated orally (2 mg/kg) by gastric gavages once daily. NOS related mechanisms were assessed either in acute (2nd day) and sub-acute (28th day) period of MI by histologic, hemodynamic and biologic studies.
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All 20 rats (nebivolol group, n = 10; control group, n = 10) survived throughout the study period. Mean (SD) MDA concentration was significantly lower in the nebivolol group than in the control group (69.25 [5.82] vs 77.67 [6.87] nmol/g tissue; P = 0.009). GSH concentration was significantly higher in the nebivolol group than in the control group (2.14 [0.15] vs 1.88 [0.22] nmol/mg tissue; P = 0.004). SOD activity was significantly greater in the nebivolol group than in the control group (49.28 [5.49] vs 42.09 [4.95] U/g tissue; P = 0.007). The percentage of the flap that was necrotic was significantly lower in the nebivolol group than in the control group (40.27 [4.08] vs 48.87 [6.35]; P = 0.007).
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Beta-blockers refer to a mixed group of drugs with diverse pharmacodynamic and pharmacokinetic properties. They have shown long-term beneficial effects on mortality and cardiovascular disease (CVD) when used in people with heart failure or acute myocardial infarction. Beta-blockers were thought to have similar beneficial effects when used as first-line therapy for hypertension. However, the benefit of beta-blockers as first-line therapy for hypertension without compelling indications is controversial. This review is an update of a Cochrane Review initially published in 2007 and updated in 2012.
A total of 50 patients who had been diagnosed with stage 1 hypertension according to the Joint National Committee (JNC) VII criteria and who had not received any anti-hypertensive treatment were enrolled in this study. Patients were randomized to receive either 25 mg/day carvedilol (n=25) or 5 mg/day nebivolol (n=25) for 3 months at the beginning of the study. Three patients (1 in the carvedilol group, 2 in the nebivolol group) who did not attend 3 month follow-up measurements were excluded from the study. The study was completed with 47 patients (25 women; mean age: 49 ± 9 years). The aortic elastic parameters such as aortic strain (AS), aortic distensibility (AD), and aortic stiffness index (ASI) were measured by echocardiography.
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We studied eight patients with uncomplicated essential hypertension and serum cholesterol less than 6.9 mmol l-1. Antihypertensive medication was discontinued 2 weeks before the study in previously treated patients. Following cannulation of the left brachial artery, saline was infused to establish baseline blood flow, followed by increasing doses of nebivolol (88.5, 177 and 354 microg min-1, each dose for 6 min), followed by saline for 12 min, followed by a 30 min infusion of L-NMMA (2 mg min-1 ). During the final 18 min of the L-NMMA infusion, nebivolol was coinfused using the same doses as before. Forearm blood flow was measured in both arms using venous occlusion plethysmography.
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CINAHL(1982-2011), Cochrane Collaboration Central Register of Controlled Trials (-2011), Embase (1980-2011), Medline/PubMed (1966-2011), and Web of Science (1965-2011).
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To assess the effects of nebivolol on CFR in patients with IDC.
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Data were extracted by one author (DAL) and checked by the other (GYHL). Potentially eligible studies were excluded when the results presentation prevented adequate extraction of data and enquiries to authors did not yield raw data.
Nebivolol is a highly selective beta(1)-adrenoceptor antagonist with beta(3)-adrenoceptor agonist properties and is a racemate mixture of D- and L-enantiomers. However, the cellular mechanisms of the effects of each enantiomer are not yet clear and are a matter for debate. The aim of the present experiments was to determine the adrenoceptors involved in the vascular effects of D- and L-enantiomers of nebivolol in rat thoracic aorta.
Inappropriate patients' concerns about adverse effects of cardiovascular drugs on erectile function might limit the use of important medications in cardiovascular high-risk patients. Knowledge about the effects of drug-treatments on erectile function and about the major role of the endothelium in penile function might improve patients' adherence to evidence based treatment of cardiovascular diseases.
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This study sought to test the hypothesis that nebivolol, a β1-antagonist and β2,3-agonist, may improve PAH and reverse the PAH-related phenotype of pulmonary ECs (P-EC).
Nebivolol and its 4-keto derivative prevented in a dose-dependent manner the increase of ROS (p < 0.001) and O(2)(*-) (p < 0.001) in bovine aortic endothelial cells (BAECs), human umbilical vein endothelial cells (HUVECs), and BLOX-1-CHO cells stimulated with ox-LDL. Atenolol had no effect. The incubation of HUVECs and BAECs with ox-LDL reduced basal and bradykinin-induced NO and nitrite concentration (p from <0.001 to <0.01). Nebivolol and its 4-keto derivative prevented the reduction of basal and stimulated NO and nitrite concentration (p from <0.001 to <0.01) while atenolol had no effect. The preincubation of BAECs with blocking anti-LOX-1 monoclonal antibody (LOX-1 mAb) significantly counteracted the effect of ox-LDL on stimulated generation of NO (p < 0.001), but the effect was significantly lower than that of nebivolol and its 4-keto derivative alone (p < 0.01).
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Nebivolol (Nebilet) has been shown to promote increase in the content of inducible and total NO-synthase, which fact can have a positive effect on the functional condition of the endothelium and its antioxidant properties in patients with type II diabetes mellitus concurrent with arterial hypertension. It is recommended that nebivolol be taken in by the above patients to normalize arterial pressure.
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During continuous standard therapy comprising dihydropyridine calcium antagonists, warfarin, and diuretics, 12 patients with IPH and functional class (FC) II-III received nebivolol in a dose of 5 mg/day for 24 weeks. According to the data of right heart catheterization, all the patients had a positive acute pharmacological test with a vasodilator (NO). Six-minute walk test (6'WT), estimation of the Borg dyspnea index (BDI) and FC, transthoracic echocardiography (EchoCG), and measurements of the levels of NO metabolites, endothelin-1, (ET-1), thromboxane B2 (TxB2), and 6-keto-prostaglandin F1alpha (6-ketoPG F1alpha) were done at baseline and after 12 and 24 weeks of the therapy.