1. Human platelet-rich plasma incubated at 37°C generates an antiaggregatory prostaglandin which is spasmogenic on gastrointestinal smooth muscle. 2. Platelet-rich plasma from female donors generated more biological activity and was more sensitive to the anti-aggregatory activity of added prostaglandin I 2 (PGI 2 ) compared with that from age-matched male controls. 3. After thin-layer chromatography of extracted platelet-rich plasma, biological activity was detected in a zone which co-chromatographed with 6-oxoprostaglandin E 1 . 4. Neither extracted platelet-rich plasma nor authentic 6-oxoprostaglandin E 1 were inactivated following incubation with purified 15-hydroxyprostaglandin dehydrogenase. 5. The relevance of these findings for regulating platelet reactivity is discussed.

1. Microsomal prostaglandin synthesis and tissue prostaglandin concentrations in the kidneys of rats made diabetic by pretreatment with alloxan or streptozotocin were significantly decreased but were unchanged in lungs. 2. Prostaglandin inactivation was increased in kidneys of alloxan-diabetic rats but not changed in streptozotocin-diabetic kidneys or in the lungs of either group. 3. These changes in prostaglandin metabolism may cause a renal prostaglandin deficit and could contribute to certain pathological sequelae observed in diabetes mellitus.