Acetylsalicyclic acid (aspirin) inhibits prostanoid synthesis^1,2 by irreversible acetylation of fatty acid cyclooxygenase (EC 1.14.99.1)³. It thereby inhibits synthesis of pro-aggregatory thromboxane A₂ (TXA₂) by platelets^2,4 and is widely used in the treatment and prophylaxis of vascular disease. Its efficacy, however, may be reduced since it also inhibits formation of prostacyclin (PGI₂)^5,6 which is a vasodilator and anti-aggregatory agent^7,8. There is uncertainty over the optimum dose regimen for aspirin since although it inhibits platelet thromboxane production for many days⁴, the magnitude and duration of its effect on PGI₂ production by vascular endothelium in vivo is unknown. Resting plasma concentrations of PGI₂ (measured as the stable hydrolysis product 6-oxo-PGF_1α) are at or below the limit of sensitivity of the most sensitive assays⁹ and cannot therefore be used to demonstrate a reduction in production. Bradykinin stimulates PGI₂ synthesis by cultured human vascular endothelial cells¹⁰ and we have shown that it stimulates PGI₂ production by man in vivo¹¹. We report here that an oral dose of aspirin (600 mg) causes rapid and substantial inhibition of bradykinin-stimulated PGI₂ production, but recovery occurs within 6 hours; this implies that endothelial PGI₂ synthesis would be spared most of the time during dosing once daily with even this relatively large dose of aspirin.