The ability of plasma to support prostacyclin like activity from human umbilical arterial rings was studied in 17 patients with Henoch-Schönlein purpura and 17 controls matched for age and sex. Plasma from 13 of the 17 patients showed a diminished or absent ability to support prostacyclin like activity in vitro. Six patients whose plasma had a low or absent ability to support prostacyclin like activity showed evidence of inhibitory activity. Plasma from three of these patients also failed to preserve the effect of a stable prostacyclin like analogue (ZK36-374). The plasma concentration of prostacyclin metabolite and the serum concentration of thromboxane A2 metabolite, thromboxane B2, were measured simultaneously. The concentration of plasma prostacyclin metabolite in 10 of the 14 patients was decreased, and a positive correlation was found between the plasma prostacyclin metabolite values and the ability of the plasma to support prostacyclin like activity. There was no significant difference in the serum thromboxane A2 metabolite concentrations between the patients and controls. These data suggest that abnormalities of vascular prostaglandin metabolism are involved in the pathophysiology of Henoch-Schönlein purpura.