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Nebivolol is a vasodilating β-blocker, which can be distinguished from other β-blockers by its haemodynamic profile. It combines β-adrenergic blocking activity with a vasodilating effect mediated by the endothelial Larginine 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. Clinical trials have demonstrated that nebivolol reduces blood pressure similarly to atenolol, bisoprolol, amlodipine, nifedipine, lisinopril, and hydrochlorothiazide. The tolerability of nebivolol is similar to or better than that of these 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.Key words: Vasodilating β-blocker; nitric oxide (NO); peripheral resistance; arterial stiffness DOI: 10.3329/uhj.v6i2.7254University Heart Journal Vol. 6, No. 2, July 2010 pp.93-96

Distensibility of human cerebral arteries was compared quantitatively with extracranial arteries using a parameter which was obtained from the pressure-radius data. It was found that cerebral arteries were much stiffer than the extracranial arteries of comparative sizes. The stifiness of cerebral arteries reached nearly maximum at the middle age and did not progress thereafter. Effect of arterial stiffness on blood flow was also examined using pulsatile flow in polymer tubes with different distensibility under the influence of sinusoidally oscillating pressure. The stiffer the tube was, the higher was pulsatile pressure. It is concluded that much larger fluctuation of pressure may occur in the cerebral arteries compared with extracranial arteries and induce the degenerative change or structural weakness in the wall, especially at the apex of bifurcation, which may play important roles in the pathogenesis of cerebral aneurysms and the mechanism of their growth and rupture.

The visco-elastic properties of arterial walls vary with the structural alterations which occur secondary to aging. An ultrasonic echo-tracking device developed in this laboratory was used for noninvasive estimation of these properties. Femoral artery compliance (% Δ V/V) and pressure strain elastic modulus (Ep) were estimated in 36 normal subjects (68 vessels). The subjects were divided into three groups according to age: 60. The femoral arterial diameter and changes in diameter with each pulse beat were measured transcutaneously with the echo-tracking device. Brachial arterial blood pressure was obtained by means of a cuff and stethoscope. The results showed a progressive increase in Ep and a complementary decrease in % Δ V/V with increasing age. Ep varied from 2.64 dynes/cm2 ± 0.26 SEM in the young group to 6.28 dynes/cm2 ± 1.03 SEM in the old group. % Δ V/V varied from 6.0% ± 0.5 SEM in the young group to 3.3% ± 10.5 SEM in the old group. Statistical comparisons of Ep showed significant differences between the groups, indicating that arterial stiffness increases with age. % Δ V/V was significantly lower in the old group than in the young. Variation within groups increased markedly with advancing age, and values for Ep and % Δ V/V overlapped in all groups.