The Mechanism and Site of the Enhanced Arachidonate Metabolism in Ureter Obstruction
Several renal diseases and pathological models of renal damage, e.g., Bartter’s syndrome,1 hydronephrosis,2–4 renal venous constriction,5 and glycerol-induced tubular necrosis,6 exhibit markedly enhanced prostaglandin (PG) production by the kidney. Furthermore, the nature of the prostaglandins released by the damaged kidney is dramatically changed. In perfused kidneys isolated from rabbits with unilateral ureteral obstruction (3 days), enhancement of the basal and hormonal [bradykinin (BK), angiotensin II (AII), and norepinephrine] stimulated release of prostaglandins was observed.2 The basal resistance in this rabbit model of hydronephrosis was dependent in part on endogenous vasodepressor prostaglandin biosynthesis, since indomethacin treatment increased basal perfusion pressure.2 We also observed marked enhancement and prolongation of the effect of angiotensin II on perfusion pressure with indomethacin treatment in the perfused hydronephrotic kidney.2 These results suggested that vascular tone was partially under the influence of a dilator prostaglandin and that a dilator prostaglandin was modulating the effect of angiotensin II on vasoconstriction.
KeywordsPerfusion Pressure Unilateral Ureteral Obstruction Ureteral Obstruction Ureter Obstruction Prostaglandin Biosynthesis
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