Treatment of hypertensive patients with dl-propranolol (640 mg/day) significantly inhibited thromboxane synthesis by their platelets and platelet aggregation induced by thrombin or arachidonic acid. The effects were dose-related and were also caused by the stereoisomer, d-propranolol (640 mg/day), which has very little beta-blocking activity. These findings suggest that the cardioprotective effects of propranolol may be due partly to this anti-platelet activity, to a reduction in thromboxane-induced coronary-artery vasoconstriction, or to both. d-Propranolol treatment may be particularly useful, since this isomer provides similar benefits without causing pronounced beta-adrenergic blockade.