Nebivolol decreases oxidative stress in essential hypertensive patients and increases nitric oxide by reducing its oxidative inactivation

Pasini, Anna Fratta; Garbin, Ulisse; Nava, Maria Cristina; Stranieri, Chiara; Davoli, A.; Sawamura, Tatsuya; Cascio, Vincenzo Lo; Cominacini, Luciano

doi:10.1097/01.hjh.0000160216.86597.ff

Cited by 110 publications

(69 citation statements)

References 39 publications

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“…This is consistent with earlier studies that indicated an antioxidant benefit for nebivolol through inhibition of NAD(P)H oxidase activity, 12,13 as well with a very recent study that demonstrated that nebivolol decreases oxidative stress in patients with essential hypertension. 21 However, it has been demonstrated that an acute infusion of antioxidant (ascorbic acid) improved vasodilation equally in black and white subjects. 22 This suggests that the difference in oxidative stress alone may not be sufficient to explain the differences in endothelial function of blacks and whites.…”

Section: Discussionmentioning

confidence: 99%

Nebivolol Reduces Nitroxidative Stress and Restores Nitric Oxide Bioavailability in Endothelium of Black Americans

et al. 2005

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Background-Alterations in endothelial function may contribute to increased susceptibility of black Americans to cardiovascular disease. The ability to pharmacologically reverse endothelial dysfunction in blacks was tested with nebivolol, a ␤ 1 -selective agent with vasodilating and antioxidant properties. Methods and Results-The effects of nebivolol on endothelial nitric oxide (NO), superoxide (O 2 Ϫ ), and peroxynitrite concentration (ONOO Ϫ ) release were studied in human umbilical vein endothelial cells and iliac artery endothelial cells isolated from age-matched black and white donors. Kinetics and concentrations of NO/O 2 Ϫ /ONOO Ϫ were measured simultaneously with nanosensors from single cells and shown to have significant interracial differences. The rate of NO release was Ϸ5 times slower in blacks than in whites (94 versus 505 nmol · L Ϫ1 · s

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Section: Discussionmentioning

confidence: 99%

Nebivolol Reduces Nitroxidative Stress and Restores Nitric Oxide Bioavailability in Endothelium of Black Americans

et al. 2005

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“…Third-generation β-blockers also have neutral or favorable effects on lipid parameters [106,109,111]. Representative older and third-generation β-blockers have demonstrated antioxidant properties, including the ability to scavenge ROS, but thirdgeneration agents have shown these effects more consistently [111,[113][114][115][116].…”

Section: Mechanismsmentioning

confidence: 99%

Treating hypertension while protecting the vulnerable islet in the cardiometabolic syndrome

Hayden

Sowers

2008

Journal of the American Society of Hypertension

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Hypertension, a multifactorial-polygenic disease, interacts with multiple environmental stressors and results in functional and structural changes in numerous end organs, including the cardiovascular system. This can result in coronary heart disease, stroke, peripheral vascular disease, congestive heart failure, end-stage renal disease, insulin resistance, and damage to the pancreatic islet. Hypertension is the most important modifiable risk factor for major health problems encountered in clinical practice. Whereas hypertension was once thought to be a medical condition based on discrete blood pressure readings, a new concept has emerged defining hypertension as part of a complex and progressive metabolic and cardiovascular disease, an important part of a cardiometabolic syndrome. The central role of insulin resistance, oxidative stress, endothelial dysfunction, metabolic signaling defects within tissues, and the role of enhanced tissue renin-angiotensin-aldosterone system activity as it relates to hypertension and type 2 diabetes mellitus is emphasized. Additionally, this review focuses on the effect of hypertension on functional and structural changes associated with the vulnerable pancreatic islet. Various classes of antihypertensive drugs are reviewed, especially their roles in delaying or preventing damage to the vulnerable pancreatic islet, and thus delaying the development of type 2 diabetes mellitus.

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“…Indeed, treatment strategies to increase bioavailable NO have been shown to protect against renal damage in several rodent models of RAAS and SNS-mediated renal sclerosis [9,10,11,12,13]. In this context, beta-blockers are known to suppress both the SNS and RAAS [14,15,16,17,18,19]. Nebivolol is a third-generation β 1 -adrenergic blocker with distinct pharmacologic and pharmacodynamic properties compared with other agents in its class [16].…”

Section: Introductionmentioning

confidence: 99%

Nebivolol Reduces Proteinuria and Renal NADPH Oxidase-Generated Reactive Oxygen Species in the Transgenic Ren2 Rat

Whaley‐Connell

Habibi²,

Johnson³

et al. 2009

Am J Nephrol

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Background/Aims: Renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system activation are crucial in the pathogenesis of hypertension, cardiovascular and renal disease. NADPH oxidase-mediated increases in reactive oxygen species (ROS) are an important mediator for RAAS-induced cardiovascular and renal injury. Increased levels of ROS can diminish the bioactivity of nitric oxide (NO), a critical modulator of RAAS effects on the kidney. Thereby, we hypothesized that in vivo nebivolol therapy in a rodent model of activated RAAS would attenuate glomerular damage and proteinuria through its actions to reduce NADPH oxidase activity/ROS and increase bioavailable NO. Methods: We utilized the transgenic Ren2 rat which displays heightened tissue RAAS, hypertension, and proteinuria. Ren2 rats (6–9 weeks of age) and age-matched Sprague-Dawley littermates were treated with nebivolol 10 mg/kg/day (osmotic mini-pump) for 21 days. Results: Ren2 rats exhibited increases in systolic blood pressure, proteinuria, kidney cortical tissue total NADPH oxidase activity and subunits (Rac1, p67^phox, and p47^phox), ROS and 3-nitrotyrosine, as well as reductions in podocyte protein markers; each of these parameters improved with nebivolol treatment along with increases in renal endothelial NO synthase expression. Conclusions: Our data suggest that nebivolol improves proteinuria through reductions in renal RAAS-mediated increases in NADPH oxidase/ROS and increases in bioavailable NO.

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Nebivolol decreases oxidative stress in essential hypertensive patients and increases nitric oxide by reducing its oxidative inactivation

Abstract: The findings of the present study indicate that nebivolol, through its antioxidant properties, increases NO also by decreasing its oxidative inactivation.

Cited by 110 publications

References 39 publications

Nebivolol Reduces Nitroxidative Stress and Restores Nitric Oxide Bioavailability in Endothelium of Black Americans

Nebivolol Reduces Nitroxidative Stress and Restores Nitric Oxide Bioavailability in Endothelium of Black Americans

Treating hypertension while protecting the vulnerable islet in the cardiometabolic syndrome

Nebivolol Reduces Proteinuria and Renal NADPH Oxidase-Generated Reactive Oxygen Species in the Transgenic Ren2 Rat

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