Iloprost preserves kidney function against anoxia

Tissue protective activity of iloprost against anoxia was studied in the isolated perfused rabbit kidney. Addition of iloprost to the perfusion medium at concentrations between 10(-9)-10(-7) M attenuated the release of noradrenaline due to periarterial stimulation and decreased urine outflow. Iloprost also caused a concentration-dependent decrease in perfusion pressure. The potentiation by angiotensin II of the vasoconstriction due to periarterial stimulation and increase in urine volume were also decreased by further addition of iloprost into the medium. Iloprost at concentrations below 10(-7) M did not alter the vasoconstrictor effect of exogenously applied noradrenaline. UK 38 485, a powerful thromboxane A2 synthetase inhibitor, significantly suppressed the vascular but greatly potentiated the diuretic effects of angiotensin II. In kidneys exposed to anoxia for 24 hours in Krebs medium, the vascular and diuretic effects of angiotensin II and the release of noradrenaline due to periarterial stimulation were significantly diminished. In addition, interation between UK 38 485 and angiotensin II in both perfusion pressure and urine volume was also reduced after anoxia for 24 hours. On the other hand, no significant loss was observed in all investigated parameters measured in this study, in kidneys exposed to anoxia for 48 hours in the presence of iloprost. From these results it was concluded that iloprost preserves kidneys functionally against anoxia and possible mechanisms of this effect are discussed.