The mechanism for the renal hemodynamic and tubular action of furosemide.
The mechanism for the renal hemodynamic and tubular action of furosemide (F) was investigated in nine anesthetized dogs. F was administered intrarenally at 50 micrograms/ml/min in isotonic saline with and without the addition of indomethacin (I) at 36 micrograms/ml/min and PGE1 at 2 micrograms/ml/min in isotonic saline. F increased the ERPF, RBF, UV, Cosm, CH20, UNaV and UKV from the experimental kidney and UV, Cosm, CH20, UNaV and UKV from the control kidney. It decreased the RVR of the experimental kidney and had no effect on GFR and MAP. I administration alone produced effects opposite to those of F. The addition of F to I reversed the renal hemodynamic effects of I but partly its tubular effects. The addition of PGE1 to I + F infusion further increased the fractional excretion of free water by both kidneys but had not other effects. The results of the present investigation suggest that the renal hemodynamic effects of F ar not mediated through the action of prostaglandins but rather due to a direct vascular effect of the drug. On the other hand, its tubular actions are mediated through prostaglandins.
D000818:Animals; D004285:Dogs; D005260:Female; D005665:Furosemide / Q000494:pharmacology*; D006439:Hemodynamics / Q000187:drug effects; D007213:Indomethacin / Q000494:pharmacology; D007668:Kidney / Q000098:blood supply / Q000187:drug effects*; D007684:Kidney Tubules / Q000187:drug effects; D008297:Male; D011458:Prostaglandins E / Q000494:pharmacology
D011458:Prostaglandins E; D005665:Furosemide; D007213:Indomethacin