Epidemiologic and experimental studies disclosed that the sympathetic nervous system might play a pivotal role in the pathogenesis of essential hypertension. Although systolic pressure exhibits a weak endogenous rhythm, diurnal fluctuations of arterial pressure are provoked primarily by physical or emotional stress factors. The magnitude of the cardiovascular response, however, varies widely from individual to individual. Subjects at high risk of future hypertension,--such as those with a positive history of familial hypertension, high resting heart rate, or transient increase in arterial hypertension--revealed blood pressure hyperresponsiveness to stress stimuli mediated by an overreactivity of the sympathetic nervous system. Furthermore, cardiovascular reactivity to mental arithmetic tasks and to traffic noise put a patient at high risk of developing arterial hypertension. In women, exaggerated cardiovascular response to stress stimuli appeared to be mitigated by estrogens, whereas oral contraceptives overrode this 'protective' effect of estrogens. At a certain point, repeated episodes of high stress blood pressure could produce structural vascular changes finally inducing sustained hypertension.