Activation of macrophages and release of mediators that activate the coagulation system characterize proliferative glomerulonephritis. To evaluate the possible role of prostanoids in this process, isolated rat glomeruli (G) and peritoneal macrophages (M) or a combination of the two (G + M) were incubated in the presence of thrombin (2 U/ml). In G, thrombin inhibited only the synthesis of thromboxane B2. In M and G + M incubations, the synthesis of prostaglandin I2 and thromboxane A2 was inhibited by thrombin. This effect was abolished by the addition of arachidonic acid. As prostanoids may play a modulatory role in the interaction between macrophages and glomerular cells, inhibition of their synthesis by thrombin might enhance macrophage activity.