ROLE OF PROSTAGLANDINS AND NITRIC-OXIDE IN MEDIATING RENAL RESPONSE TO VOLUME EXPANSION

The objective of the present study was to examine, in anesthetized dog s, the possible interaction between prostaglandins (PG) and nitric oxi de (NO) in mediating the renal response to an extracellular volume exp ansion (ECVE). The renal response to ECVE was examined during 1) intra renal infusion of a PG synthesis inhibitor, 2) intrarenal administrati on of a NO synthesis inhibitor, and 3) simultaneous inhibition of PG a nd NO synthesis in the right kidney. Compared with the control group, the ECVE-induced increments in sodium excretion and fractional excreti on of lithium were not affected by the PG synthesis inhibition. The NO synthesis inhibition did not induce changes in renal hemodynamics but reduced (P < 0.05) the ECVE-induced increments in sodium excretion an d fractional excretion of lithium. When PG and NO synthesis were simul taneously inhibited in the right kidney during ECVE, there were no sig nificant differences between the renal hemodynamics of both kidneys. H owever, compared with the left kidney, the ECVE-induced changes in sod ium excretion and fractional excretion of lithium were reduced in the right kidney. The reduction of the natriuretic response to ECVE was gr eater (P < 0.05) than in the dogs where only NO synthesis was inhibite d. Our results suggest a major interaction between NO and PG in mediat ing the renal hemodynamic and excretory responses to an increase in ex tracellular volume.