Leptin has received extensive attention as an endogenously produced satiety factor. Although once considered to be solely derived from adipose tissue, it is now apparent that leptin can be produced by various tissues including those comprising the cardiovascular system such as blood vessels and cardiomyocytes. Moreover, leptin receptors (OBR) have been identified in cardiovascular tissues. The increased cardiovascular risk associated with obesity is well known and many of the effects of leptin appear to be compatible with its potential role as a contributing factor to increased cardiovascular morbidity associated with obesity. Evidence from both animal and human studies implicated leptin as a potential contributor to the increased incidence of cardiovascular morbidity associated with hyperleptinemic conditions. This review focuses on some of the complex vascular actions of leptin and the emerging role of leptin as a cardiovascular regulator in terms of normal homeostatic function, but particularly in cardiovascular pathology.