In a given hypertensive patient, clinically overt cardiovascular disease is often preceded by a number of signs of target organ damage at the cardiac, arterial and renal levels. These changes have been collectively defined "pre-clinical cardiovascular disease", and carry a substantially increased risk for future cardiovascular complications. The present article examines the relationship between blood pressure components and target organ damage in essential hypertension. Arterial pressure can be split into a steady component (represented by the mean arterial pressure), which is a measure of the average level of pressure in a given artery, and a pulsatile component (represented by the pulse pressure), which estimates the cyclic oscillations around the mean. All blood pressure components show a positive, linear correlation with left ventricular mass, both in the general population and in patients with essential hypertension. However, the association is significantly stronger for the steady blood pressure components (systolic and mean arterial pressure) than for the pulse pressure. Available data regarding arterial changes suggest that the association is partly different. The majority of available studies show that large-artery intima-media thickening and discrete atherosclerotic plaques are better predicted by pulse pressure than by other blood pressure components, particularly in the elderly. After the age of 60, there is clear-cut evidence for a J-shaped relationship between diastolic blood pressure and arterial thickening or plaques, while for younger age groups the relationship appears to be linear. These data might offer an explanation for the observed superior prognostic value of pulse pressure in the elderly. The relationship between the different blood pressure components and renal damage is more controversial. In summary, pulsatile, cyclic stress (as represented by pulse pressure) appears to be more important in determining arterial changes in hypertensive patients, while steady blood pressure components play a dominant role in the development of hypertensive left ventricular hypertrophy.