The effects of beta-blocking propranolol, metoprolol, atenolol and labetalol on the production of the proaggregatory and vasoconstrictive thromboxane A2 (TxA2) by fetal platelets were studied. To this end, umbilical blood samples were allowed to clot in the absence or presence of various concentrations of these agents, and the release of TxB2 (a metabolite of TxA2) was measured. Propranolol and labetalol inhibited TxA2 production in 0.1-mmol concentrations and metoprolol and atenolol in 1-mmol concentrations. The required concentration was always higher than could be achieved by peroral treatment. Beta blockers may have this effect through phospholipase A2 because the conversion of exogenous arachidonic acid to TxB2 was not affected except in the case of propranolol, which inhibited slightly TxB2 formation from exogenous arachidonic acid.