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The present study demonstrates the neuroprotective effect of nebivolol against cerebral ischemia/reperfusion insult. Neuroprotection observed with nebivolol may possibly be explained by regulating eNOS and iNOS expressions and by inhibition of oxidative stress-induced injury. Thus, nebivolol may be considered as a potential candidate for treatment in patients who are prone to stroke.
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The present study aimed to develop and validate the simultaneous estimation of amlodipine and nebivolol in tablet dosage forms.
The aim of the present study is to compare the antihypertensive effects of carvedilol and nebivolol in mild-to-moderate hypertensive patients.
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This prospective case-controlled study included 30 patients having CSF and 30 subjects having normal coronary arteries in coronary angiography. The patients were evaluated with 12-leads electrocardiography and echocardiography before and three months after treatment with nebivolol. The difference between maximum and minimum P wave durations was defined as P-wave dispersion (PWD). Early diastolic flow (E), atrial contraction wave (A) and E deceleration time (DT) and isovolumetric relaxation time (IVRT) were measured. Unpaired and paired t-tests, Chi-square test, Mann-Whitney's U-test and Pearson correlation analysis were used in statistical analysis.
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Nebivolol (Nomexor) is a third generation, vasodilating beta-blocker with a high beta(1)-adrenoceptor selectivity. Nebivolol acts as an agonist at the beta(3) adrenoceptor as well as the estrogen receptor thereby releasing nitric oxide in blood vessels via eNOS. Pleiotropic effects of nebivolol furthermore include a positive influence on cholesterol and triglycerides and a decrease in thrombocyte activity. Nebivolol is recommended in the guidelines of the European cardiac society (ESC) for patients with metabolic syndrome. Nebivolol's main properties in combination with its broad range of beneficial pleiotropic effects allow it to be clearly distinguished from other second and third generation beta-blockers.
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Beta blockers have been used in the treatment of cardiovascular conditions for decades. Despite a long history and status as a guideline-recommended treatment option for hypertension, recent meta-analyses have brought into question whether β blockers are still an appropriate therapy given outcomes data from other antihypertensive drug classes. However, β blockers are a heterogenous class of agents with diverse pharmacologic and physiologic properties. Much of the unfavorable data revealed in the recent meta-analyses were gleaned from studies involving nonvasodilating, traditional β blockers, such as atenolol. However, findings with traditional β blockers may not be extrapolated to other members of the class, particularly those agents with vasodilatory activity. Vasodilatory β blockers (i.e., carvedilol and nebivolol) reduce blood pressure in large part through reducing systemic vascular resistance rather than by decreasing cardiac output, as is observed with traditional β blockers. Vasodilating ability may also ameliorate some of the concerns associated with traditional β blockade, such as the adverse effects on metabolic and lipid parameters, including an increased risk for new-onset diabetes. Furthermore, vasodilating ability is physiologically relevant and important in treating a condition with common co-morbidities involving metabolic and lipid abnormalities such as hypertension. In patients with hypertension and diabetes or coronary artery disease, vasodilating β blockers provide effective blood pressure control with neutral or beneficial effects on important parameters for the co-morbid disease. In conclusion, it is time for a reexamination of the clinical evidence for the use of β blockers in hypertension, recognizing that there are patients for whom β blockers, particularly those with vasodilatory actions, are an appropriate treatment option.
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Beta-blockers play a pivotal role in the treatment of chronic systolic heart failure. However, the pharmacological family of beta-blockers is inhomogeneous regarding their pharmacological properties and their clinical effects can differ substantially according to different pharmacological properties. Because of vasodilator effects, the third generation of beta-blockers has additional potential across the cardiovascular diseases, from hypertension to heart failure. Nebivololol has both high selectivity for beta1-adrenergic receptors, no intrinsic sympathetic activity and ability to stimulate endothelial nitric oxide production. Such properties result in specific hemodynamic effects compared with others beta-blockers. Such properties also result in both high tolerability and positive metabolic effects which are crucial in high-risk groups. In the SENIORS trial, nebivolol demonstrated its efficacy and high tolerability in elderly patients with chronic heart failure irrespective of the left ventricular ejection fraction. More clinical trials would be useful to exhibit specific benefits of nebivolol in other high-risk groups of patients.
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Demographic characteristics and risk factors were similar between groups. We observed the highest NO activity in group N in both endothelial and vasa vasorum samples of LIMA and saphenous veins. NO activity of metoprolol group was similar to controls.
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Anesthetized rats and mice were randomized to receive vehicle or nebivolol (1.25 or 2.5 mg/kg) IV before hemodilution to a hemoglobin concentration near 60 g/L. Drug levels, heart rate (HR), cardiac output (CO), regional cerebral blood flow (rCBF, laser Doppler), and microvascular brain Po(2) (P(Br)O(2), G2 Oxyphor) were measured before and after hemodilution. Endothelial nitric oxide synthase (NOS), neuronal NOS (nNOS), inducible NOS, and hypoxia inducible factor (HIF)-1α were assessed by Western blot. HIF-α expression was also assessed using an HIF-(ODD)-luciferase mouse model. Data were analyzed using analysis of variance with significance assigned at P < 0.05, and corrected P values are reported for all post hoc analyses.
It is important to know which patients with hypertension will benefit from beta-blocker therapy and which beta-blockers should be used in the treatment of hypertension to reduce cardiovascular events and mortality.
The beta-blockers, atenolol and nebivolol, have a similar effect in reducing arterial stiffness in the large elastic aorta, largely secondary to BP reduction. Nebivolol, in contrast to atenolol, has an effect on small muscular arteries, increasing PP amplification and reducing wave reflection, possibly because of increased levels of nitric oxide (NO). Such ancillary properties may impart important distinct hemodynamic effects, and therefore beta-blockers cannot be regarded as a homogeneous group.
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Intolerance of antihypertensive medications is a major cause of non-adherence to pharmacotherapy leading to poor blood pressure control in the hypertensive population. We investigated the role of a central iliac arteriovenous (AV) anastomosis in a woman with uncontrolled hypertension due to multidrug intolerances.
Nebivolol (nebilet) is an effective hypotensive drug with mild side effects. Further studies on nebivolol effects on myocardial mass are needed.
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It has been shown that beta-glucan (BG), which has antioxidant and immunomodulatory effects, attenuats renal ischemia-reperfusion injury. We aimed to investigate whether BG might have a preventive role against the development of contrast-induced nephropathy and to compare its effect with nebivolol (Nb) and N-acetylcysteine (NAC).
Following a single administration into a conjunctival sac, all drugs decreased intraocular pressure. Iris blood flow was decreased following administration of propranol, but increased by nebivolol and carvedilol. After single and repeated oral administration of nebivolol and carvedilol an IOP decrease was demonstrated, but with no effect of all applied doses on iris or retina/choroid blood flow.
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Mean age at baseline (ITT) was 50.7 years, and the mean SBP/DBP values were 167/101 mm Hg; 202 (47.3%) participants were women, 276 (63.9%) had body mass index ≥30 kg/m(2), 152 (35.2%) were black, and 161 (37.3%) were Hispanic. Completion rates were 79.7% (PBO) and 90.3% (NEB). After 2 weeks of treatment, 92% and 95% participants in the NEB and PBO groups, respectively, had SBP in the range of 130 to 180 mm Hg and were titrated to the 20-mg/d NEB dose or its matching PBO tablet. After 6 weeks of treatment, the NEB group experienced significant mean reductions compared with the PBO group for both SBP (-18.2 vs -12.3 mm Hg; P < 0.001) and DBP (-12.3 vs -5.7 mm Hg; P < 0.001), down to mean SBP/DBP values of 149/89 mm Hg and 155/95 mm Hg, respectively, and had a significantly higher percentage of individuals who achieved BP control (SBP/DBP <140/90 mm Hg, 30.6% vs 17.3%; P = 0.004). Post hoc analyses suggest that NEB was not efficacious in reducing SBP in black participants. Mean changes in pulse rate were -12.8 beats/min for the NEB group and -1.6 beats/min for the PBO group (P < 0.001). Rates of discontinuations due to an AE (NEB vs PBO) were 1.4% in both groups, rates of any treatment-emergent AEs were 19.7% versus 19.0%, and rates of serious AEs were 0.3% versus 2.1%. The most common AEs (NEB vs PBO) were headache (2.1% vs 2.8%) and hypertension (0.7% vs 2.1%).
dl-Nebivolol, a selective β1-adrenergic receptor antagonist, besides its hypotensive activity exerts vasodilatory and platelet inhibitory effects in vitro by a mechanism involving nitric oxide (NO). Our aim was to evaluate whether nebivolol exerts in vivo antithrombotic effects, to unravel the mechanism of this action and to clarify the relative roles of its 2 enantiomers: d- and l-nebivolol.
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Bacterial translocation is a frequent event in cirrhosis leading to an increased inflammatory response. Splanchnic adrenergic system hyperactivation has been related with increased bacterial translocation. We aim at evaluating the interacting mechanism between hepatic norepinephrine and inflammation during liver damage in the presence of bacterial-DNA.
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The decrease of creatinine clearance was 0.180 +/- 0.11 mg/dl in CM, and 0.030 +/- 0.10 mg/dl in NCM (P = 0.01). Microproteinuria was ameliorated using nebivolol (P = 0.001). Serum protein carbonyl content, malonyldialdehyde and kidney thiobarbituric acid-reacting substances levels were higher in CM than in C (P = 0.003, P < 0.001 and P = 0.034, respectively) and serum thiol was lower in CM than in C (P = 0.001). However, oxidative stress markers were similar in NCM and C. Diatrizoate decreased kidney nitrite levels, but nebivolol increased them (P = 0.027). Nebivolol attenuated the tubular necrosis, proteinaceous casts and medullary congestion, although significant protective effects, were observed in tubular necrosis (P = 0.001) and proteinaceous cast (P < 0.001).
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Intimal hyperplasia is a major cause of restenosis after the interventional or surgical treatment of occlusive arterial disease. We investigated the effects of clopidogrel, calcium dobesilate, nebivolol, and atorvastatin on the development of intimal hyperplasia in rabbits after carotid venous bypass surgery. We divided 40 male New Zealand rabbits into 4 study groups and 1 control group. After occluding the carotid arteries of the rabbits, we constructed jugular venous grafts between the proximal and the distal segments of the occluded artery. Thereafter, group 1 (control) received no medication. We administered daily oral doses of clopidogrel to group 2, calcium dobesilate to group 3, nebivolol to group 4, and atorvastatin to group 5. The rabbits were killed 28 days postoperatively. The arterialized jugular venous grafts were extracted for histopathologic examination. Intimal thicknesses were 42.87 +/- 6.95 microm (group 2), 46.5 +/- 9.02 microm (group 3), 34.12 +/- 5.64 microm (group 4), and 48.37 +/- 6.16 microm (group 5), all significantly less than the 95.12 +/- 9.93 microm in group 1 (all P < 0.001). Medial thicknesses were 94 +/- 6 microm (group 2), 101.5 +/- 13.52 microm (group 3), 90.5 +/- 9.69 microm (group 4), and 101.37 +/- 7.99 microm (group 5), all significantly thinner than the 126.62 +/- 13.53 microm in group 1 (all P < 0.001). In our experimental model of carotid venous bypass grafting in rabbits, clopidogrel, calcium dobesilate, nebivolol, and atorvastatin each effectively reduced the development of intimal hyperplasia. Herein, we discuss our findings and review the medical literature.
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Nebivolol in vivo activated the NO/cGMP pathway, enhanced erectile response and reversed ED in diabetic rats. Moreover, nebivolol in vitro potentiated NO/cGMP-mediated relaxation of human erectile tissues. These effects may account for the low incidence of ED in nebivolol-treated hypertensive patients. Nebivolol therefore may have utility in the treatment of ED, particularly ED associated with diabetes.
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Emerging evidence reveals physiological differences within the β-blocker class and in comparison to other antihypertensives. These differences provide insight into the diverse clinical effects β-blockers provide in cardiovascular disease.
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The present study evaluated the pharmacodynamics and pharmacokinetics of nebivolol enantiomers in patients with chronic kidney disease (CKD) and in patients undergoing haemodialysis.
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Nebivolol and carvedilol are third-generation beta-adrenoreceptor antagonists, which unlike classic beta-blockers, have additional endothelium-dependent vasodilating properties specifically related to microcirculation by a molecular mechanism that still remains unclear. We hypothesized that nebivolol and carvedilol stimulate NO release from microvascular endothelial cells by extracellular ATP, which is a well-established potent autocrine and paracrine signaling factor modulating a variety of cellular functions through the activation of P2-purinoceptors.
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Safety, tolerability and antihypertensive efficacy of a cardioselective beta-blocker nebivolol was studied in 30 patients with mild and moderate hypertension and concomitant stage I chronic obstructive bronchitis. Nebivolol (5 mg/day) was given for 1 month; in 5 patients complementary hydrochlorothiazide (12.5 mg/day) was required for sufficient antihypertensive effect. Nebivolol was well tolerated (only 1 patient complained of head ache), did not cause worsening of bronchitis and spirometric parameters, exerted no cardiodepressive action, and did not induce apparent disturbances of metabolism.
* The variability in drug metabolism has been recognized as an important factor in the occurrence of adverse effects or lack of therapeutic efficacy. * The metabolism of the third-generation beta(1)-receptor antagonist nebivolol has been shown to be highly dependent on cytochrome P450 2D6 enzymatic activity in preclinical studies.
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Nebivolol is a vasodilating beta-blocker, which can be distinguished from other beta-blockers by its haemodynamic profile. It combines beta-adrenergic blocking activity with a vasodilating effect mediated by the endothelial L-arginine nitric oxide (NO) pathway. The blood pressure lowering effect of nebivolol is linked to a reduction in peripheral resistance and an increase in stroke volume and preservation of cardiac output. The effects of nebivolol have been compared with other beta-blockers and also with other classes of antihypertensive agents. In general, response rates to treatment are higher and the frequency and severity of adverse events are either comparable or lower with nebivolol. Endothelium-derived NO is important in the regulation of large arterial stiffness, which in turn is a major risk factor for cardiovascular disease. Therefore, antihypertensive drugs, such as nebivolol, that also improve endothelial function and decrease arterial stiffness, may contribute to a reduction in cardiovascular risk.