Results from many studies suggest that the central nervous system may play an important role in enhancing and maintaining sympathetic, metabolic and haemodynamic effects in patients with hypertension. Likewise, emotional and mental stresses may provoke phasic and sustained adrenergic responses in normotensive and untreated hypertensive patients. Because the various antihypertensive medications have different mechanisms of action, and elicit different neurovegetative responses, it is useful to distinguish between the effects of different treatments on sympathetic activity. To identify the effect of stress on sympathetic reactivity, we evaluated the extracardiovascular and haemodynamic responses to various stressor agents using noninvasive techniques. This psychophysiological approach allowed us to standardise stress, to identify individual cardioneurovegetative responses both before and during treatment, and to establish the effects of various treatments on the cardioneurovegetative response. The extracardiovascular psychophysiological response of patients with a family history of hypertension and of normotensive patients who later became hypertensive was characterised by an inability to recover after mental challenge. Therefore, prolonged sympathetic activity resulting from mental stimulation may contribute to the development of hypertension. Antihypertensive medications affected sympathetic reactivity differently. For example, nifedipine worsened sympathetic reactivity, while verapamil was able to correct abnormal neuroadrenergic responses. Furthermore, verapamil was successfully combined with enalapril in patients whose hypertension was resistant to monotherapy with the angiotensin converting enzyme (ACE) inhibitor. Therefore, the functional and structural consequences of sympathetic stimulation resulting from daily activation and pharmacological blood pressure adjustments are important in hypertensive patients, because they may have abnormal sympathetic reactivity to various stimuli.