The aim of the study was to determine whether aspirin influences sympathoadrenal output in normal human subjects. Plasma and platelet adrenaline and noradrenaline levels were measured before and after chronic administration of oral aspirin (300 mg per day for 7 days). Catecholamine concentrations measured immediately following aspirin did not differ from control (pre-treatment) values. Platelet noradrenaline and plasma adrenaline levels were, however, significantly increased 2 weeks after cessation of treatment. Platelet TxB2 generation was significantly reduced following aspirin treatment indicating that platelet cyclooxygenase had been inhibited. Catecholamine concentrations did not correlate with TxB2 generation. In vitro platelet aggregation induced by ADP, adrenaline and collagen was reduced after aspirin providing additional confirmation of cyclooxygenase inhibition. However, the in vivo markers of platelet function, beta-TG and PF4 were unaffected. These data do not provide convincing evidence for an action of aspirin on sympathoadrenal outflow, either directly or via a prostaglandin (thromboxane) mediated effect, although this does not exclude a later, delayed effect. There was no evidence for interactions between thromboxane, catecholamine levels in plasma and platelets, and platelet function.