Thrombin induced thromboxane A2 and prostaglandin E2 production were significantly increased in platelets of streptozotocin induced diabetic rats as compared to non-diabetic control rats, while collagen induced thromboxane A2 production was decreased. Using exogenous arachidonic acid, prostaglandin E2 production, but not thromboxane A2 production, was increased in platelets from streptozotocin treated animals. Prostacyclin production in the diabetic aorta was significantly lowered; however, control levels of prostacyclin production resulted after incubation of the tissue with dipyridamole. Diabetic animals demonstrated a fivefold decrease in the endogenous arterial prostacyclin/platelet thromboxane A2 ration when thrombin or ADP was used to induce thromboxane A2 production. This elevated ratio could be a contributing factor to the vascular complications of diabetes. Dipyridamole, due to its ability to partially normalize this ratio, may be useful as a therapeutic agent in this and related vascular diseases.