Rabbit aorta and pulmonary artery were incubated in the presence and absence of added arachidonic acid, and the synthesis of prostaglandin I2 (PGI2) and thromboxane A2 (TXA2) was studied by radioimmunoassay of the stable hydrolysis products 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) and thromboxane B2 (TXB2). Aorta and pulmonary artery synthesized 6-keto-PGF1 alpha and TXB2 in ratios of 10-60:1. The pulmonary artery appeared to synthesize relatively more thromboxane. This may be because of a thinner muscular layer, since smooth muscle cells have previously been shown to produce only 6-keto-PGF1 alpha, while endothelial cells synthesize both compounds. Pretreatment of animals with aspirin (ASA) in a dose of 1 mg/kg strongly inhibited synthesis of both products by aorta and pulmonary artery. A dose of 0.1 mg/kg was without effect. After a single intravenous dose of ASA, the inhibitory effect was maximal between 4 and 12 hours and was still marked at 24 hours, increasing to normal at approximately 48 hours. Selective suppression of platelet cyclooxygenase activity with sparing of the vascular enzyme appears to be difficult to achieve.