title: β-blockade: benefits beyond blood pressure reduction?
abstract: Hypertension is a major cardiovascular (CV) risk factor, but several other common conditions, including chronic obstructive pulmonary disease (COPD), osteoporosis, and peripheral arterial disease (PAD), have been shown to independently increase the risk of CV events and death. The physiological basis for an increased CV risk in those conditions probably lies in the augmentations of oxidative stress, endothelial dysfunction, systemic inflammation, and arterial stiffness, which all are also hallmarks of hypertension. β-Blockers have been used for the treatment of hypertension for more than 40 years, but a number of meta-analyses have demonstrated that treatment with these agents may be associated with an increased risk of CV events and mortality. However, the majority of primary prevention β-blocker trials employed atenolol, an earlier-generation β(1) -selective blocker whose mechanism of action is based on a reduction of cardiac output. Available evidence suggests that vasodilatory β-blockers may be free of the deleterious effects of atenolol. The purpose of this review is to summarize pathophysiologic mechanisms thought to be responsible for the increased CV risk associated with COPD, osteoporosis, and PAD, and examine the possible benefits of vasodilatory β-blockade in those conditions. Our examination focused on nebivolol, a β(1) -selective agent with vasodilatory effects most likely mediated via β(3) activation.
authors.affiliation: From the Department of Cardiology, University of Cardiff, University Hospital, Cardiff, UK; 1 and the Royal Brompton Hospital, London, UK2.
authors.forename: John R
authors.initials: JR
authors.lastname: Cockcroft
authors.affiliation: From the Department of Cardiology, University of Cardiff, University Hospital, Cardiff, UK; 1 and the Royal Brompton Hospital, London, UK2.
authors.forename: Michala E
authors.initials: ME
authors.lastname: Pedersen
mesh_terms: D058671:Adrenergic beta-1 Receptor Antagonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology / Q000627:therapeutic use*; D000818:Animals; D001578:Benzopyrans / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects; D002097:C-Reactive Protein / Q000032:analysis; D002318:Cardiovascular Diseases / Q000503:physiopathology; D015897:Comorbidity; D004730:Endothelium, Vascular / Q000503:physiopathology; D004983:Ethanolamines / Q000494:pharmacology; D006801:Humans; D000068577:Nebivolol; D010024:Osteoporosis / Q000453:epidemiology / Q000503:physiopathology; D058729:Peripheral Arterial Disease / Q000453:epidemiology / Q000503:physiopathology; D029424:Pulmonary Disease, Chronic Obstructive / Q000453:epidemiology / Q000503:physiopathology; D059289:Vascular Stiffness / Q000502:physiology; D014665:Vasodilator Agents / Q000494:pharmacology*
chemical_list: D058671:Adrenergic beta-1 Receptor Antagonists; D000319:Adrenergic beta-Antagonists; D001578:Benzopyrans; D004983:Ethanolamines; D014665:Vasodilator Agents; D000068577:Nebivolol; D002097:C-Reactive Protein