The physiology of blood pressure is characterized by continuous fluctuations, both in response to daily life stimuli and as a result of the complex interplay between cardiovascular control mechanisms [1]. The first clear description of the occurrence of blood pressure variations over time was provided in 1733 by Stephen Hales, in his pioneering studies performed by inserting a glass pipe into the crural artery of a mare, with the declared aim of ‘seeing the arterial pulse'. Hales was so impressed by the continuous changes of blood levels within the pipe, as to conclude that blood pressure was likely ‘never to be exactly the same, any two minutes, throughout the whole life of an animal’[2]. During the XVIII and XIX Centuries, a number of scientists, including von Haller, Marey, Herisson, Dudgeon, Ludwig and Mayer, to mention just the most famous ones, further clarified the features of blood pressure oscillations in the experimental animal, and provided experimental evidence that blood pressure is also highly variable in humans. In humans, however, only anecdotal observations could be obtained, using instruments that were devised to reproduce the arterial pulse non-invasively, but which were unable to provide quantitative information on blood pressure variability (BPV). Among the first non-invasive, but at the same time quantitative descriptions of BPV in humans obtained in a clinical setting, we should acknowledge the contribution provided at the end of the XIX century by the Italian scientist Scipione Riva-Rocci, who described the occurence of blood pressure changes associated with different behavioural conditions in a paper where he reported the results of his first experiences with the sphygmomanometer [3]. However, a major step-forward in the assessment of BPV in humans over 24 h was only possible in the 1960s, thanks to the technique for ambulatory intra-arterial blood pressure monitoring known as the ‘Oxford System’[4, 5]. Additional, although less precise, information on 24-h BPV has subsequently been obtained through use of the techniques for non-invasive discontinuous ambulatory blood pressure monitoring, now commonly employed in clinical practice [6].

The results obtained by applying these techniques over the last 30 years have stimulated studies aimed at obtaining a deeper insight into the physiology and the pathophysiology of BPV and, in particular, at investigating the possible role of an enhanced BPV in producing cardiovascular complications. These studies have focussed on the following research issues:(i) the possible consequences of an increased BPV on cardiovascular structural changes;(ii) the relationship between BPV and cardiovascular risk;(iii) the mechanisms involved in determining an increase in BPV (including the possible role of arterial baroreflex dysfunction); and (iv) the mechanisms underlying the cardiovascular alterations associated with an enhanced BPV.