Beta-blockers in the treatment of hypertension: are there clinically relevant differences?

Are all beta-blockers alike? This is an important question with the recent controversy surrounding their role as a first-line treatment of hypertension. This class of drugs is heterogeneous. The sympathetic nervous system (SNS)--the presumed main target of beta-blocker activity--is one of the central pathways in the pathophysiology of hypertension, both through its own effects on the heart and vasculature and through its interactions with the renin-angiotensin-aldosterone system. The beta-blockers are defined by, and exert their influence through, blocking catecholamine binding to the beta1-, beta2-, and alpha1-adrenergic receptors. Traditional beta-blockers (eg, atenolol, metoprolol, propranolol) affect only the beta-adrenergic receptors, whereas carvedilol and labetalol mediate vasodilation through blockade of the alpha1-adrenergic receptor. Other drugs like nebivolol may exert vasodilation via stimulation of nitric oxide. Vasodilation may be important not only for blood pressure reduction, but also for tolerability. The importance of SNS activation in the pathogenesis of hypertension and the utility of beta-blockers in certain compelling indications for cardiovascular disease indicate that these drugs still have an important role for many patients in the management of hypertension.