Prostacyclin (PGI2) activity in rat kidney-stimulated by angiotensin II.

Prostacyclin (PG X, PG I₂) activity can be found in renal tissue as indicated by platelet aggregation inhibition. The activity of the medullal tissue in terms of wet weight is significantly higher (P < 0.01) than that of the cortex. The activity decreases with time, and disappears within one hour nearly completely. Boiling for 30 sec destroys the inhibitory effect of the prostacyclin on platelet aggregation. Angiotensin II is able to stimulate the prostacyclin availability of the tissue after incubation for 3 min. Addition of angiotensin II to platelet rich plasma (PRP) has no significant effect on the ADP induced platelet aggregation. The spontaneous generation of prostacyclin as well as that stimulated by angiotensin II can be suppressed by previous incubation of the tissue with a prostaglandin synthetase inhibitor such as Ketoprofen. The tissues which have only a small amount of inhibitory activity upon incubation in buffer show an increased platelet aggregation inhibitory effect after adding to PRP. A significant difference between medulla and cortex is found in this assay as well. The different release of prostacyclin can not be related to different endothelial surface area, because the endothelial surface in medulla and cortex is similar. These results suggest that prostacyclin could have an important influence on renal function. The different capacity of renal medulla and cortex in generation of prostacyclin could be a very important point for understanding physiology and pathophysiology of kidney function.