Vital organs are exposed to the central rather than the brachial blood pressure. To date, central blood pressure can be assessed noninvasively through the use of several devices. In this review, we critically discuss the clinical relevance of central blood pressure assessment. Considerable evidence suggests that central blood pressure is a better predictor of end-organ damage than brachial blood pressure. However, there is still uncertainty concerning the value of central pressure for predicting cardiovascular outcomes, as the existing studies are underpowered to address this issue. A full synthesis of the available data is needed in this regard. Among the different antihypertensive drug classes, beta-blockers appear to lower central blood pressure less than brachial blood pressure. This difference may, at least in part, explain the reduced efficacy of beta-blockers in the prevention of cardiovascular outcomes compared with the other antihypertensive drug classes, which may lower central and brachial blood pressure to a similar extent. Nevertheless, this differential effect might not be relevant to the newer beta-blockers with vasodilating properties, including nebivolol, celliprolol and carvedilol. However, whether a preferential reduction of central blood pressure results in better outcomes should be further assessed by appropriately powered clinical trials. Other emerging challenges include the assessment of the potential predictive value of central blood pressure variability and the development of new antihypertensive medications based on central blood pressure rather than brachial blood pressure.
To evaluate the effect of nebivolol and nitrate administration on the arterial compliance--an essential factor for left ventricular hypertrophy regression.
Nebivolol, a third generation β-adrenoceptor (β-AR) antagonist (β-blocker), causes vasodilation by inducing nitric oxide (NO) production. The mechanism via which nebivolol induces NO production remains unknown, resulting in the genesis of much of the controversy regarding the pharmacological action of nebivolol. Carvedilol is another β-blocker that induces NO production. A prominent pharmacological mechanism of carvedilol is biased agonism that is independent of Gαs and involves G protein-coupled receptor kinase (GRK)/β-arrestin signaling with downstream activation of the epidermal growth factor receptor (EGFR) and extracellular signal-regulated kinase (ERK). Due to the pharmacological similarities between nebivolol and carvedilol, we hypothesized that nebivolol is also a GRK/β-arrestin biased agonist. We tested this hypothesis utilizing mouse embryonic fibroblasts (MEFs) that solely express β2-ARs, and HL-1 cardiac myocytes that express β1- and β2-ARs and no detectable β3-ARs. We confirmed previous reports that nebivolol does not significantly alter cAMP levels and thus is not a classical agonist. Moreover, in both cell types, nebivolol induced rapid internalization of β-ARs indicating that nebivolol is also not a classical β-blocker. Furthermore, nebivolol treatment resulted in a time-dependent phosphorylation of ERK that was indistinguishable from carvedilol and similar in duration, but not amplitude, to isoproterenol. Nebivolol-mediated phosphorylation of ERK was sensitive to propranolol (non-selective β-AR-blocker), AG1478 (EGFR inhibitor), indicating that the signaling emanates from β-ARs and involves the EGFR. Furthermore, in MEFs, nebivolol-mediated phosphorylation of ERK was sensitive to pharmacological inhibition of GRK2 as well as siRNA knockdown of β-arrestin 1/2. Additionally, nebivolol induced redistribution of β-arrestin 2 from a diffuse staining pattern into more intense punctate spots. We conclude that nebivolol is a β2-AR, and likely β1-AR, GRK/β-arrestin biased agonist, which suggests that some of the unique clinically beneficial effects of nebivolol may be due to biased agonism at β1- and/or β2-ARs.
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Hispanics have lower rates of hypertension control compared with black and white patients. Nebivolol is a vasodilatory β1-selective blocker, with neutral metabolic effects. This phase IV trial evaluated the efficacy and safety of nebivolol in Hispanics with stage I-II hypertension.
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The study included 67 patients with stable Functional Classes (FC) II and II CHF who received the standard therapy and BAB non-included into the guidelines for the management of CHF. The patients were randomized to the groups taking bisoprolol (n = 35) or nebivolol (n = 32) in doses of 1.25 to 10 mg/day. Before and 6 months after therapy, the investigators assessed the patient's clinical status and quality of life (QL), performed a six-minute walk test and echography, and determined the blood level of the N-terminal fragment of brain natriuretic peptide prohormone (NT-proBNP).
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To determine the effects of nebivolol on diastolic functions of the left ventricle in the hypertensive patients in the early treatment period.
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Twelve randomized controlled studies were included in which nebivolol 5 mg once daily was compared with the recommended clinical doses of other antihypertensive drugs (n = 9), placebo (n = 2), and both (n = 1). The clinical studies were selected after a MEDLINE search up to 2007 using the key words 'nebivolol' and 'hypertension.'
We compared the antihypertensive activity of DL- and D-nebivolol in patients with essential hypertension on clinic and 24-h ambulatory blood pressure (BP) and during dynamic exercise as well. After a 4-week placebo run-in period, 30 patients (mean age 48 years) were randomly allocated to double-blind treatment with either DL-nebivolol 5 mg or D-nebivolol 2.5 mg once daily for 4 weeks. After an interim single-blind placebo washout of 2-4 weeks, all patients crossed over double-blind to the alternative DL- or D-nebivolol treatment for 4 weeks. The results show that DL- and D-nebivolol produced similar reductions in clinic trough (delta systolic/delta diastolic BP (delta SBP/delta DBP): -10/-8 and -13/-9 mm Hg, respectively, all p < 0.0001 vs. placebo), 24-h ambulatory (-12/-11 and -13/-11 mm Hg, respectively, all p < 0.0001), and peak exercise BP (-13/-6, both p < 0.01; and -13/-7 mm Hg, both p < 0.0001, respectively) as compared with placebo (SBP/DBP clinic 147/99, ambulatory 147/94, exercise 211/103 mm Hg). Our results showing superimposable clinic and ambulatory BP profiles as well as exercise BP responses with DL- and D-nebivolol treatment do not confirm results of animal pharmacologic experiments in which the L-isomer potentiated the antihypertensive effect of the D-isomer.
Nebivolol treatment significantly reduced systolic arterial pressure in 30% and diastolic arterial pressure in 50% patients, heart rate decreased on the treatment day 7-10. On the treatment day 56-60 systolic and diastolic pressure lowered significantly in 53.3% and 66.7% patients, respectively. The analysis of changes in echocardiographic evidence found no significant shifts in volume and linear parameters. Nebivolol was well tolerated by 85% patients. Side effects included head ache, cardialgia, dizziness, weakness and nausea.
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To evaluate the effectiveness and safety of the beta-adrenoblocker nebivolol in patients with mild and moderate essential hypertension.
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40 EMs and 3 PMs were differentiated by using the pharmacokinetic parameters of nebivolol and its active metabolite. The study highlighted the existence of interphenotype differences regarding nebivolol metabolism and bioavailability.
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Identification and management of cardiovascular risk factors, such as hypertension, diabetes mellitus, and dyslipidemia, is essential not only for prevention of cardiovascular disease, but also for slowing the progression of existing cardiovascular disease. A major underlying mechanism that links various cardiovascular risk factors and manifestations of cardiovascular disease is endothelial dysfunction, characterized by impaired nitric oxide bioactivity. Oxidative stress is an important cause of impaired nitric oxide bioactivity, and a major pathogenic mechanism of atherosclerosis. Several pharmacologic therapies, including angiotensin-converting enzyme inhibitors, calcium channel blockers, statins, and the vasodilating beta blocker nebivolol, have been shown to enhance nitric oxide bioactivity and improve endothelial function. This effect may help explain the cardioprotective benefits of these agents and may stimulate further use of nitric oxide modulation for the treatment of cardiovascular risk factors and manifestations of cardiovascular disease.
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To determine the relative beta1-selectivity of three beta-blockers (nebivolol, bisoprolol and atenolol), administered orally at normal therapeutic doses, by assessing their impact on the beta2-mediated, haemodynamic and biochemical responses to a terbutaline infusion, which decreases serum potassium and increases serum glucose and insulin.