Exaggerated prostaglandin and thromboxane synthesis in the rabbit with renal vein constriction.

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Abstract
Isolated perfused kidneys removed from a rabbit 24-48 h after renal vein constriction exhibited a markedly enhanced release of renal prostaglandins (PG) 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 PGE2 compared to a release of 290 .+-. 45 ng from the contralateral control kidney. Infusion of indomethacin abolished the PGE2 formation (confirmed by radiochromatography) in the renal vein-constricted and contralateral kidneys. Bradykinin and angiotensin II stimulation of the renal vein-constricted kidney (but not the contralateral kidney) 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 s) compared with standard TxA2 (30 .+-. 3 s) and PG endoperoxide (135 .+-. 13 s). Incubation with [14C]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. Exaggerated prostaglandin and thromboxane production by the kidney with renal vein constriction is demonstrated. These in vitro experiments suggest that relative changes in cortical synthesis of vasodilating PGE2 and vasoconstricting TxA2 may function to modulate renal vascular resistance in states of increased renal venous pressure.