Platelet function can be assessed by various techniques in vitro or in vivo, but methodological problems in the field are considerable. By use of the conventional in vitro technique (Born aggregometry), it has been shown that sympathoadrenal activation in vivo (e.g., mental stress, epinephrine infusions, exercise, and surgical stress) may result in either enhanced or reduced platelet aggregability in vitro. In vivo measures of platelet function (platelet counts, size distribution, and aggregability, as reflected by filtragometry ex vivo) more consistently indicate platelet activation during stress. Platelet-specific proteins in plasma are less readily affected by stress. Elevations of circulating epinephrine do not seem to explain proaggregatory effects of stress. Aggregatory responses to epinephrine may be enhanced by propranolol in vitro, because of unopposed alpha 2-stimulation (beta 2-stimulation attenuates aggregation). Other in vitro effects of beta-blockade seem to be related to nonspecific effects at very high concentrations. Studies of the effects of beta-blockade in vivo have yielded conflicting data. Some studies suggest that beta 2-blockade may reduce platelet cAMP and enhance aggregability in vitro; other studies show that propranolol attenuates platelet aggregability, particularly in patients with ischemic heart disease. There is, however, a need for well-conducted studies assessing platelet function in vivo during beta-blockade to evaluate whether platelet responses contribute to favorable effects of beta-blockade in unstable angina, for example, or after myocardial infarction. Methodological developments are needed to better understand platelet function in vivo in humans. Available data suggest that stress enhances and beta-blockade reduces platelet function. This may influence thrombus formation in the short term and atherosclerosis in the long term.