Effects of nebivolol and atenolol on small arteries and microcirculatory endothelium-dependent dilation in hypertensive patients undergoing isometric stress

Arosio, Enrico; Marchi, Sergio De; Prior, Manlio; Zannoni, M; Lechi, Alessandro

doi:10.1097/00004872-200209000-00024

Cited by 37 publications

(30 citation statements)

References 18 publications

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“…16 Nebivolol improved the small artery distensibility index in hypertensive subjects and, in contrast to the effect of atenolol, increased endothelium-dependent cutaneous vasodilation. 17 In a comparative study in uncomplicated hypertension, the BP-lowering effect of atenolol was strongly related to reduced cardiac output through more significant heart rate reduction, whereas, for nebivolol, the BP-lowering effect was achieved by the reduction in peripheral resistance (which increased with atenolol) and increase in stroke volume. 10 Our study extends earlier observations showing that, in essential hypertension, nebivolol reduces not only aortic stiffness but also arterial wave reflection and central aortic PP.…”

Section: Discussionmentioning

confidence: 99%

-Blockers Reduce Aortic Stiffness in Hypertension but Nebivolol, Not Atenolol, Reduces Wave Reflection

Mahmud

Feely

2008

American Journal of Hypertension

124

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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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Section: Discussionmentioning

confidence: 99%

-Blockers Reduce Aortic Stiffness in Hypertension but Nebivolol, Not Atenolol, Reduces Wave Reflection

Mahmud

Feely

2008

American Journal of Hypertension

124

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“…It has been demonstrated that nebivolol vasodilates the human forearm vasculature through the L-arginine pathway, 14 improves small artery distensibility index, and increases endothelium-dependent cutaneous vasodilation. 15 At the same time, cardioselective BB do not reduce total peripheral resistance or sympathetic activity, 16 which may lead to small artery vasoconstriction and increased media:lumen ratio. 17 The AIx and pulse pressure amplification are related to wave reflection depending on the amplitude and site of wave reflection and on the speed at which pressure waves travel along the arterial tree.…”

Section: Bb and Reduction In Central Aortic Pressurementioning

confidence: 99%

Differential Effects of Nebivolol and Metoprolol on Central Aortic Pressure and Left Ventricular Wall Thickness

et al. 2011

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Abstract-The aim of this study was to investigate the effects of the vasodilating ␤-blocker nebivolol and the cardioselective ␤-blocker metoprolol succinate on aortic blood pressure and left ventricular wall thickness. We conducted a randomized, double-blind study on 80 hypertensive patients. The patients received either 5 mg of nebivolol or 50 to 100 mg of metoprolol succinate daily for 1 year. Their heart rate, central and brachial blood pressures, mean arterial pressure, augmentation index, carotid-femoral pulse wave velocity, and left ventricular wall thickness were measured at baseline and at the end of the study. Nebivolol and metoprolol significantly reduced heart rate, brachial blood pressure, and mean arterial pressure to the same degree. However, reductions in central systolic and diastolic blood pressures, central pulse pressure, and left ventricular wall thickness were significant only in the nebivolol group. The change in left ventricular septal wall thickness was significantly correlated with central systolic blood pressure change (rϭ0.41; Pϭ0.001) and with central pulse pressure change (rϭ0.32; Pϭ0.01). No significant changes in augmentation index or carotid-femoral pulse wave velocity were detected in either treatment group. This proof-ofprinciple study provides evidence to suggest that ␤-blockers with vasodilating properties may offer advantages over conventional ␤-blockers in antihypertensive therapy; however, this remains to be tested in a larger trial. lood pressure (BP) varies throughout the arterial tree because of pulse wave amplification, a phenomenon of wave reflection and arterial stiffness. 1 Because of pulse wave amplification, reduction in brachial BP does not reflect changes in central BP, which may become a more important target in the treatment of hypertension. Recent data from the Strong Heart Study 2 confirm earlier results from smaller studies on high-risk patients 3,4 that central pulse pressure is superior to brachial pulse pressure in the prediction of further cardiovascular events. Moreover, several studies have demonstrated that brachial BP is not a good surrogate for the hemodynamic effects of drug therapies on central circulation. The recently published EX-PLOR Study 5 and the Conduit Artery Function Evaluation Study 6 clearly demonstrated that angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and calcium channel blockers have a more pronounced effect on reducing central BP compared with the cardioselective ␤-blocker (BB) atenolol. Different effects of BB on central BP can explain the findings of a recent meta-analysis published by Law et al, 7 which demonstrates a slight inferiority of BB in preventing stroke. The detrimental effect of BB on central BP has generated criticism regarding its use as first line therapy for essential hypertension. Dhakam et al 8 questioned the hypothesis that the inferiority of atenolol in reducing central BP is a class effect of BB. They demonstrated that the novel vasodilating BB nebivolol (NEB) reduces central BP si...

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“…Given the changes in diameter in the microcirculation can be orders of magnitude greater than observed in central elastic or muscular arteries, significant changes in the compliance characteristics would be expected to accompany changes in resistance to flow. Therefore, flow resistance and the compliance characteristics of the microvasculature will change in a dynamic fashion to both acute and chronic stimuli [20]. The ability of a vessel or network to distend in response to a pressure load might be more sensitive than a caliber change in identifying abnormal structure or tone in microcirculation [7•].…”

Section: Microcirculation In Hypertensionmentioning

confidence: 99%

Vascular abnormalities in hypertension: Cause, effect, or therapeutic target?

McVeigh¹,

Plumb²,

Hughes³

2004

Current Science Inc

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Alteration in the physical properties of arterial blood vessels act as the substrate for end-organ damage and the occurrence of vascular events in hypertension. Structural and functional alteration in the microcirculation represents a prevalent and characteristic abnormality described in the earliest stages of hypertension. In addition to lowering arterial pressure, the importance of reversing structural abnormalities and restoring endothelial function has recently been emphasized. The normalization of microvascular function does not always correlate with blood pressure reduction and might depend on the class of antihypertensive agent employed. Because altered resistance vessel structure and function is a recognized hallmark of hypertension, institution of drug therapy that corrects the associated pathogenic vascular abnormalities is a rational, if unproven, clinical goal.

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Effects of nebivolol and atenolol on small arteries and microcirculatory endothelium-dependent dilation in hypertensive patients undergoing isometric stress

Cited by 37 publications

References 18 publications

-Blockers Reduce Aortic Stiffness in Hypertension but Nebivolol, Not Atenolol, Reduces Wave Reflection

-Blockers Reduce Aortic Stiffness in Hypertension but Nebivolol, Not Atenolol, Reduces Wave Reflection

Differential Effects of Nebivolol and Metoprolol on Central Aortic Pressure and Left Ventricular Wall Thickness

Vascular abnormalities in hypertension: Cause, effect, or therapeutic target?

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