Interaction of the kinin and prostaglandin systems in mediating renal function and intrarenal hemodynamics.

The roles of the renal kinin and prostaglandin (PG) systems were indirectly assessed in conscious rats by inhibition of PG synthesis with indomethacin (INDO) and of kinin synthesis with aprotinin (APRO). In control animals APRO and INDO had no effect on urine flow, Na and K excretion, GFR, RPF or arterial pressure. Both inhibitors, however, significantly depressed renal PG synthesis and deep cortical and medullary plasma flow. Acute saline loading was achieved by i.v. 0.9% NaCl to increase body weight by 10%. APRO and INDO decreased urine flow and Na and K excretion to a similar degree which was highly significant as compared to saline loading in the absence of APRO or INDO. The decrease in RPF following APRO and INDO during saline loading was completely due to a decrease in outer cortical perfusion. APRO suppressed the early rise in PGE2 excretion during saline loading. The similar effects of inhibition of kinin- and PG-synthesis on renal function support the concept that both systems are closely interrelated. The present results also suggest that the integrity of the kinin and PG systems represents an important prerequisite for appropriate vascular and natriuretic responses of the kidney to an acute isotonic saline load.