The blood pressure (BP) waveform varies substantially between the peripheral conduit (brachial) and the central elastic (aorta) arteries mainly do a gradual increase of systolic BP, as the wave propagates distally. This phenomenon is called BP amplification and is principally generated by the presence of arterial stiffness gradient and wave reflections along the arterial bed. More and more clinical studies suggest that central BP may provide additional information regarding cardiovascular risk beyond peripheral BP. Arterial properties and thus pressure amplification, are modulated by age, cardiovascular risk factors, vasoactive substances and drugs. Recent evidence suggests, beyond any doubt, that antihypertensive drugs affect peripheral and central BP differentially and alter pressure amplification. The aim of the present review (Part II) is to summarize the available evidence regarding: (i) the specific class-effect of antihypertensive drugs on central BP beyond peripheral BP, as well as the potential underlying hemodynamic mechanisms, (ii) head to head comparison of the effect of different classes of antihypertensive drugs on central BP, (iii) the effect of combination drug treatment on central BP. Finally to attempt an interpretation of the clinical trials in hypertension, which classically record brachial BP, based on the results of studies which assessed central BP. Several conclusions were drawn. First, it is clear that there are important differences between the classes of antihypertensive drugs regarding their effects on BP amplification. Second, it seems that the newer antihypertensive drugs [angiotensin converting enzyme inhibitors (ACEIs), angiotensin receptor blockers and dihydropyridine calcium blockers], as well as nitrates, have a more beneficial effect on BP amplification than the older drugs (diuretics and BBs). Third, there is compelling evidence regarding the detrimental effect of BBs (mainly atenolol) on central BBs and convincing evidence that ACEIs increase BP amplification.