Interaction between furosemide-induced renal vasodilation and the prostaglandin system.

The effect of intravenous furosemide, 5 mg/kg, on renal hemodynamics as it relates to the prostaglandin cascade was examined in dogs. In 11 dogs the vasculature to the kidney was isolated and a femoral to renal arterial and a renal to femoral venous shunt was performed. With the use of a protein-free salt solution to perfuse the kidney for 3 minutes, the renal cortex was enriched with tritiated arachidonic acid. After blood perfusion to the kidney was re-established, the renal effluent radioactivity was followed before and after furosemide administration. Furosemide produced two types of response. In six dogs there was renal vasodilation, diuresis, and a three and one-half fold increase in renal venous radioactivity. In five dogs that were in renal failure, furosemide administration caused no change in renal effluent radioactivity. On thin-layer chromatography most of the released radioactivity by the kidney after furosemide administration traveled as arachidonic acid. In a separate seven dogs, we measured the total unesterified arachidonic acid concentration in the plasma before and after furosemide by the use of gas chromatography-flame ionization. Even though in these dogs furosemide caused a significant increase in renal blood flow and diuresis, renal venous plasma levels of arachidonic acid were unaltered. Our data suggest that furosemide causes a release of arachidonic acid from the kidney from a small pool at fast turnover lipid stores and that the stimulus for arachidonic acid release after furosemide depends on a intra-renal mechanism whereby the diuresis is coupled to the increase in renal blood flow.