Autonomic control of blood pressure appears to decline with age giving rise to an increased risk of orthostatic hypotension and major hypotensive reactions to antihypertensive drugs. In the past few years, many workers have assessed autonomic function in the elderly and sometimes found controversial results. Baroreflex sensitivity, as measured by the steepness of the heart rate/mean pressure curve, decreases with age. However, this phenomenon does not correlate well with orthostatic impairment. Sympathetic dysfunction might be more responsible for syncopal symptoms in the elderly, a finding supported by the fact that elderly with orthostatic symptoms never collapse within a few seconds, but do so after 1 or more minutes of standing. However, the results of sympathetic function testing in the elderly indicate that sympathetic function in most elderly is not impaired and that sympathetic activity, as measured by circulating levels of catecholamines, is usually increased rather than decreased. In various populations with increased sympathetic activity, but not in the elderly, β-adrenoceptor antagonists (β-blockers) have been demonstrated to cause pressor effects, presumably due to α-adrenoceptor-mediated vasoconstriction unopposed by β-receptor-mediated vasodilation. In the past year, large studies have been completed indicating that the same is true for the elderly, and that the depressor effect on pulse pressure upon standing in this category of patients can be offset and turned into a pressor effect by long-term β-blocker treatment. This phenomenon could not be demonstrated with non-β-blocker antihypertensive drugs, including ACE inhibitors, calcium channel antagonists, diuretics and angiotensin II receptor antagonists. In elderly patients β-blockers may, therefore, be the most appropriate antihypertensive agents as they protect the elderly from orthostatic impairment.