Stages of different depth characterize the temporal organization of sleep. Each stage exerts an effect on blood pressure (BP) regulation and contributes to its 24-h variation. The main determinant of the circadian influences of sleep and wakefulness on BP is the daytime sympathetic and nighttime parasympathetic prevalence, but many other physiologic mechanisms known either to induce sleep or determine arousal may play an important role in the mediation of sleep influences on BP. Alteration of one or more of such mechanisms may be reflected in altered circadian BP rhythms. Sleep- and arousal-related mechanisms and phenomena that affect circadian BP rhythms include neurohumoral sleep factors (arginine vasopressin, vasoactive intestinal peptide, somatotropin, insulin, steroid hormones and metabolites, and serotonin among others) and waking factors (corticotropin-releasing factor, adrenocorticotropin, thyrotropin-releasing hormone, endogenous opioids, and prostaglandin (E(2))). Pathologic respiratory variations (sleep-disordered breathing) and insomnia are major causes of the sleep-related alteration of the circadian BP profile, including loss of the expected normal decline in BP by 10-20% from the daytime level. A great number of medical disorders can cause insomnia, but objective sleep studies have been performed only in a minority of them. Overall, the sleep-related pathophysiological mechanisms actually involved in causing altered circadian BP rhythms in different normotensive and hypertensive conditions are not completely understood. In any case, changes in the circadian BP rhythm are known to be strongly related to one's risk of cardiovascular morbidity and mortality, thus representing strong prognostic indicators worthy of further investigation.