Cardiovascular effects of dl-nebivolol and its enantiomers — a comparison with those of atenolol

Water, A. Van De; Xhonneux, R.; Reneman, Robert S.; Janßen, Paul

doi:10.1016/0014-2999(88)90151-3

Cited by 53 publications

(19 citation statements)

References 4 publications

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“…d-Nebivolol provides selective β 1 -adrenergic receptor blockade whereas both isomers cause endothelial-dependent vasodilation. 19,20 Nebivolol has been shown to increase NO production through β 2 -receptor activation and an adenosine triphosphate-dependent autocrine pathway involving activation of P2Y-purinoceptors. 21,22 Nebivolol has also been reported to inhibit NO synthase uncoupling and interfere with oxidative stress mechanisms.…”

mentioning

confidence: 99%

Loss of Arterial and Renal Nitric Oxide Bioavailability in Hypertensive Rats With Diabetes: Effect of -Blockers

Mason¹,

Kubant²,

Jacob³

et al. 2009

American Journal of Hypertension

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mentioning

confidence: 99%

Loss of Arterial and Renal Nitric Oxide Bioavailability in Hypertensive Rats With Diabetes: Effect of -Blockers

Mason¹,

Kubant²,

Jacob³

et al. 2009

American Journal of Hypertension

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“…When the D-isomer of nebivolol, which is the beta-blocking isomer, is given alone, this atypical hemodynamic profile is not observed. The D-isomer is a potent highly selective beta 1 adrenoceptor antagonist whose hemodynamic profile resembles that of atenolol [77]. Apparently, the presence of the non-beta-blocking L-isomer is responsible for the modification of the hemodynamic response [78].…”

Section: Central and Peripheral Hemodynamicsmentioning

confidence: 97%

The applied pharmacology of beta-adrenoceptor antagonists (beta blockers) in relation to clinical outcomes

Jd¹

1991

Cardiovasc Drug Ther

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Despite the fact that beta blockers were introduced into clinical practice 25 years ago, new beta blockers with differing kinetic and dynamic profiles continue to be developed and marketed. This overview assesses some of the more extensively studied agents from the point of view of proof of utility and the validity of claims for therapeutic advances. The clinical data suggests that despite the expectations of improvements based on kinetic and dynamic consideration, none of the newer agents have been shown unequivocally, either in terms of efficiency or tolerability, to be an advance over the reference agents, the beta 1 antagonists atenolol and metoprolol. This may be either because such improvements will not occur or because of shortcomings in the design and duration of comparative studies. There are trends to suggest that celiprolol has lesser effects on bronchial function and that it has a lesser impact on lipoprotein profiles. Approaches are suggested that might enable clinicians to appraise for themselves the validity of claims for the improved efficiency of new beta blockers.

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“…Nebivolol is a racemic mixture of its D-and L-enantiomers, of which only D-nebivolol functions as a highly selective β 1 -adrenoreceptor antagonist [32]. Antioxidant properties of nebivolol were observed initially in a small clinical study in which the drug was shown to significantly decrease urinary excretion of 8-iso-PGF 2α , a free radical-induced oxidation product of arachidonic acid [33].…”

Section: β Blockersmentioning

confidence: 98%

Advances in Pharmacologic Modulation of Nitric Oxide in Hypertension

Mizuno

Jacob²,

Mason

2010

Curr Cardiol Rep

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A number of structural and functional mechanisms have been identified in the pathogenesis of hypertensive vascular disease, each of which requires effective therapy to reduce global cardiovascular risk. Hypertension, together with other cardiovascular risk factors, promotes endothelial dysfunction as evidenced by decreased nitric oxide (NO) release and reduced vascular responsiveness to normal vasodilatory stimuli. In addition, the mechanical forces inherent in hypertension activate neurohormonal mechanisms, including the renin-angiotensin system, which modulate vessel wall structure and function. Antihypertensive drugs may have class-specific hemodynamic and physiologic effects that attenuate these vascular disease processes. Pharmacologic approaches that enhance endothelial NO bioavailability have been shown to restore vasodilation while reducing clinical events. These agents improve NO bioavailability by increasing endogenous production through enzymatic mechanisms or by promoting the direct release of NO by its redox congeners in a spontaneous fashion. In this article, we review the basic mechanisms of endothelial dysfunction along with the use and comparative therapeutic benefits of various pharmacologic interventions, with particular emphasis on antihypertensive agents.

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Cardiovascular effects of dl-nebivolol and its enantiomers — a comparison with those of atenolol

Cited by 53 publications

References 4 publications

Loss of Arterial and Renal Nitric Oxide Bioavailability in Hypertensive Rats With Diabetes: Effect of -Blockers

Loss of Arterial and Renal Nitric Oxide Bioavailability in Hypertensive Rats With Diabetes: Effect of -Blockers

The applied pharmacology of beta-adrenoceptor antagonists (beta blockers) in relation to clinical outcomes

Advances in Pharmacologic Modulation of Nitric Oxide in Hypertension

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