The vasodilatory beta-blockers

Abstract

Although well established in treating hypertension and cardiovascular (CV) disease, clinical trial data suggest that beta-blockers (eg, atenolol) may be less effective than other antihypertensive classes in reducing stroke and CV mortality despite similar blood pressure (BP) reductions. One possible explanation is that atenolol is less effective in reducing central aortic pressure. Newer vasodilating beta-blockers may prove more effective in reducing central pressure and cardiovascular events. Carvedilol and labetalol appear to cause vasodilation through alpha(1)-receptor blockade; nebivolol induces endothelium-dependent vasodilation by stimulating nitric oxide bioactivity. Their favorable hemodynamic profile includes reduction of peripheral vascular resistance (PVR) while maintaining or improving cardiac output (CO), stroke volume, and left ventricular function, whereas nonvasodilating beta-blockers tend to raise PVR and reduce CO and left ventricular function. Compared with conventional beta-blockers, vasodilating beta-blockers have beneficial hemodynamic effects including decreased pressure wave reflection from the periphery, leading to decreases in central aortic blood pressure. Larger trials are needed to determine whether reduced central pressure will translate into improved CV outcomes compared with nonvasodilating beta-blockers.

Recruitment ofβ-Arrestin 1 and 2 to theβ2-Adrenoceptor: Analysis of 65 Ligands

“…First, experiments by Wisler et al (2007) were performed with b 2 AR/ vasopressin V2 receptor chimeras, which may have altered receptor characteristics. Second, CAR effects may also result from antagonizing a 1 ARs and not only bARs (Pedersen and Cockcroft, 2007). Third, the high concentrations of antagonists used may have caused off-target effects (Hagelüken et al, 1994).…”

Effects of Combination of Carvedilol and Melatonin on Induced Metabolic Syndrome in Rats

“…This may be explained by the effects of the 2 β-blockers on clinical outcomes need to be compared in long-term clinical trials. Carvedilol prevents norepinephrine binding to α1-adrenegric receptors, which decreases peripheral vascular resistance and increases peripheral blood flow and glucose uptake [49].…”

Therapeutic Role of Beta-blockers in Hypertension: A Pragmatic Reappraisal

“…Thus, they reduce blood pressure by reducing systemic vascular resistance while maintaining cardiac output. 38,39 Vasodilatory beta-blockers are also devoid of any adverse effect on lipid and glucose metabolism and they can HTNJ reverse arterial remodeling. Remodeled (Stiff) arteries increase distal wave reflection of blood back to the aorta, which augment central systolic pulse wave emanating from the heart to increase central aortic pressure.…”

“…Labetalol and carvedilol are non-selective beta-blockers with alpha 1 receptor-blocking activity and minimal (labetalol) or no (carvedilol) intrinsic sympathomimetic activity. 38,39 Nebivolol is a high beta 1 -selective blocker that does not have alpha 1 -blocking activity or intrinsic sympathomimetic activity. 38,39 Nebivolol mediates endothelium-dependent vasodilatation via the L-arginine-nitric oxide (NO)-dependent pathway.…”