The autocrin-paracrin prostanoid system plays a major role in the enhancement or inhibition of renal tissue damage. Our hypothesis was that there might be circulating factors in the plasma with a capability to modify renal (glomerular) prostanoid synthesis. We measured the synthesis of prostacyclin 1-2 (PGI2) and thromboxan A-2 (TxA2) of isolated glomeruli, incubated in plasma samples obtained from hypertensive and diabetic (NIDDM) patients. It was found that these plasma samples decreased the renal PGI2/TxA2 ratio, mostly by decreasing glomerular PGI2 synthesis and, to a lesser extent, increasing the synthesis of TxA2. Our results demonstrate that circulating factors in hypertension and diabetes might play a role in renal damage seen in these conditions.