There is a lot of evidence showing that sympathetic activity is increased in a large proportion of patients with hypertension. However, the clinical impact of this state is frequently underestimated. Several factors seem to be misunderstood, such as whether sympathetic overactivity is reproducibly present, whether it lasts throughout 24 h, and what is the significance of its association with tachycardia. In this review, we present data to indicate that several haemodynamic changes in hypertension such as elevated cardiac output and heart rate and alteration in vascular resistance are neurogenic. The relationship between the increased sympathetic tone and decreased parasympathetic tone in hypertension is reciprocal, which strongly suggests that the abnormality emanates from the brain. The increase in sympathetic drive in hypertension is widespread across many organs. Beside the heart it is seen in the kidney and skeletal muscle, and even in platelets. We also discuss the possible mechanisms of the haemodynamic transition from this hyperkinetic state to established hypertension. We propose a hypothesis where down-regulation of beta-adrenergic responsiveness plays a major role in explaining the haemodynamic changes as well as metabolic alterations, such as hyperinsulinaemia and even the gain of weight in hypertension. Thus, the increased sympathetic tone may be involved in the genesis of multiple, pressure-independent coronary risk factors in hypertension.