Isolated perfused kidneys removed from a rabbit 24-48 hours after renal vein constriction exhibited a markedly enhanced release of renal prostaglandins (PG's) induced by vasoactive peptides. Stimulation of the perfused renal vein-constricted kidney with 300 ng of bradykinin (BK) caused the release of 5980 ± 1409 ng of PGE2compared to a release of 290 ± 45 ng from the contralateral control kidney. Infusion of indomethacin abolished the PGE2formation (confirmed by radiochromatography) in both the renal vein-constricted and contralateral kidneys. Bradykinin and angiotensin II stimulation of the renal vein-constricted kidney (but not the contralateral kidney) also revealed the presence in the renal venous effluent of a rabbit aorta-contracting substance (RCS). Identification of the RCS as thromboxane A2(TxA2) was confirmed by determining the biological half life (38 ± 6 sec) in comparison with standard TxA2(30 ± 3 sec) and PG endoperoxide (135 ± 13 sec). Incubation with [l4C]arachidonate of the renal vein-constricted cortical or medullary microsomes resulted in the formation of [14C]-thromboxane B2. The renal thromboxane synthetase was inhibited by preincubation with imidazole. This study demonstrates exaggerated prostaglandin and thromboxane production by the kidney with renal vein constriction. These in vitro experiments suggest that relative changes in cortical synthesis of vasodilating PGE2and vasoconstricting TxA2xs may function to modulate renal vascular resistance in states of increased renal venous pressure.Circ Res 47: 231-237, 1980