Animal studies have shown conclusively that sympathetic neural factors are involved in the development and/or maintenance of high blood pressure. Whether this is also the case for human hypertension has been documented less conclusively, owing to technical difficulties in assessing human adrenergic function. Recent studies have used sophisticated and sensitive techniques to evaluate sympathetic activity in humans, e.g. the norepinephrine spillover method and the microneurographic quantification of sympathetic nerve traffic, allowing documentation of the participation of adrenergic mechanisms in the early and late phases of the hypertensive process. Evidence has been also provided that the activation of the sympathetic nervous system (1) is peculiar to the essential hypertensive state, (2) parallels the degree of the blood pressure elevation, (3) is triggered by reflex and humoral mechanisms and (4) may exert deleterious metabolic and cardiovascular effects, accelerating the progression of the end organ damage accompanying hypertension. These findings explain why non-pharmacological and pharmacological approaches to the treatment of hypertension should be aimed not only at lowering elevated blood pressure values but also at exerting sympathoinhibitory effects.