title: Renal hemodynamic and ureteral pressure changes in response to ureteral obstruction: the role of nitric oxide.
abstract: OBJECTIVE
  Triphasic changes in renal blood flow and ureteral pressure after unilateral ureteral obstruction have long been known. The contribution of nitric oxide to the decline in renal blood flow and ureteral pressure in unilateral ureteral obstruction was studied in this model using arginine infusion and by studying the effect of 2 inhibitors of nitric oxide synthase (NOS).
  
  
  METHODS
  Left ureteral obstruction was created in dogs. Renal blood flow and ureteral pressure were monitored. Groups 1 to 4 underwent unilateral ureteral obstruction and group 5 dogs underwent sham operation. Groups 2 to 5 received an infusion of arginine at hour 18 of obstruction that was sustained for 1 hour. In addition, NOS inhibitors were administered to dogs in groups 3 (N-monomethyl-L-arginine) and 4 (triamcinolone diacetate).
  
  
  RESULTS
  Arginine administration at 18 hours of obstruction caused a significant increase in renal blood flow and ureteral pressure compared to sham operated animals. Triamcinolone diacetate eliminated the increase in renal blood flow and ureteral pressure, whereas N-monomethyl-L-arginine did not, reflecting the competitive nature of its inhibition of NOS.
  
  
  CONCLUSIONS
  Arginine infusion 18 hours after unilateral ureteral obstruction led to increases in renal blood flow and ureteral pressure that were not seen in control animals. These results suggest that the nitric oxide system of the kidney is activated in unilateral ureteral obstruction. Since the addition of arginine is accompanied by an increase in renal blood flow and ureteral pressure, it further suggests that a lack of availability of substrate for NOS may explain the decrease in renal blood flow and ureteral pressure in obstruction. Providing substrate may be a way of maintaining renal blood flow in unilateral ureteral obstruction.
authors.affiliation: Department of Urology, James Buchanan Brady Foundation, Weill Medical College of Cornell University, New York, NY, USA.
authors.forename: Diane
authors.initials: D
authors.lastname: Felsen
authors.forename: David
authors.initials: D
authors.lastname: Schulsinger
authors.forename: Steven S
authors.initials: SS
authors.lastname: Gross
authors.forename: Francis Y
authors.initials: FY
authors.lastname: Kim
authors.forename: Donald
authors.initials: D
authors.lastname: Marion
authors.forename: E Darracott
authors.initials: ED
authors.lastname: Vaughan
mesh_terms: D000818:Animals; D004285:Dogs; D004791:Enzyme Inhibitors / Q000494:pharmacology; D009569:Nitric Oxide / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D052247:Nitric Oxide Synthase Type II; D011312:Pressure; D012079:Renal Circulation / Q000502:physiology*; D014221:Triamcinolone / Q000031:analogs & derivatives* / Q000494:pharmacology; D014513:Ureter / Q000187:drug effects / Q000503:physiopathology*; D014517:Ureteral Obstruction / Q000503:physiopathology*; D014665:Vasodilator Agents / Q000494:pharmacology; D019323:omega-N-Methylarginine / Q000494:pharmacology
chemical_list: D004791:Enzyme Inhibitors; D014665:Vasodilator Agents; D014221:Triamcinolone; D019323:omega-N-Methylarginine; D009569:Nitric Oxide; C030262:triamcinolone diacetate; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II