with consequent reduction in angiotensin II concentrations.A sympatholytic effect also occurs by blocking 2-receptor–mediated increases in norepinephrine release from sympathetic nerve terminals. These mechanisms of action have implications for the effectiveness of -blockers in AfricanAmericans and in the elderly. Because African Americanstend to have low-renin and salt-sensitive hypertension, it is not surprising that -blockers reduce blood pressure much less in this ethnic group than in Caucasian hypertensive patients.25 African Americans with heart failure, however, experience the same reduction in mortality and morbidity with-blockers as do Caucasian patients.26 The elderly tend not only to have a higher incidence of low-renin hypertension than younger individuals but also to exhibit blunted-receptor–mediated responses to -agonists.27 These differences may explain why the elderly derive less survival benefit from -blockersthan do their younger counterparts.28 A concern has been expressed in the literature about using-blockers in patients with cardiovascular disease who have concomitant reactive airway disease. -blockers, especially those with a high affinity for the 2 receptor, are relatively contraindicated in patients with asthma and chronic lung disease with a significant bronchospastic component. 29 The results of a recent meta-analysis of studies that have explored the use of cardioselective-blockers in these patients suggest that cardioselective -blockers not only are safe but actually may enhance sensitivity to inhaled -agonists because of receptor activation.30,31 Although-blockers have been used extensively in hypertension and related disorders for a number of years, a recent extensive re-analysis of various trials suggested that atenolol exerts no therapeutic benefits whatsoever.32 The investigators surveyed the major trials in hypertension that used atenolol and concluded that it was no better than a placebo and significantly inferior to other antihypertensive drugs. Whether these findings are applicable to other -blockers is unclear. Nevertheless, this provocative re-appraisal of atenolol casts doubt on the relative use of -blocker therapy in patients with hypertension. Much debate can be expected as a result of this observation from atenolol-based studies. Some credence to these observations is gained by the demonstration of reduced benefits from atenolol therapy compared with losartan in the Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) study.33 In this trial, losartan-based treatment compared with an atenolol-based regimen at equivalent blood pressure levels decreased the risk for fatal and nonfatal strokes in a high-risk population. Thus, one could argue for angiotensin-receptor blockade over -blockade for superior target organ protection in patients with hypertension, at least in those older patients with left ventricular hypertrophy.