The gut-brain peptide cholecystokinin (CCK) has been implicated in a wide range of physiological processes including digestion, satiety, anxiety, nociception and lordosis. In addition, it is becoming clear that CCK is involved in regulating certain aspects of cardiovascular function. This article reviews the cardiovascular effects elicited by CCK via its actions at both central and peripheral sites and considers the physiological role of the peptide with respect to the cardiovascular function in different physiological and pathophysiological states. In the periphery CCK released from entoeroendocrine cells in the gut wall in response to a meal triggers a local postprandial hyperaemia in the gut that could promote digestion by facilitating intestinal motility and secretory processes. In addition, activation of CCK receptors on abdominal vagal afferents elicits a reflexly evoked hyperaemia that potentiates these effects and is also gasroprotective. In the brain CCK appears to act as a neuromodulator rather than a direct mediator within cardiovascular control circuits. In particular, it facilitates activity in amygdalar, hypothalamic and midbrain circuits that are involved in mediating acute cardiovascular and behavioural responses to an extreme physical or psychologically stressful challenge. Whilst in the short term activation of the CCK system appears to be beneficial to the organism, chronic stimulation of the system may be maladaptive, laying the foundation for the development of pathophysiological conditions such as panic disorder and chronic pain, both of which are states characterised by significant autonomic activation.