title: Allopurinol and enalapril failed to conserve urinary NOx and sodium in ischemic acute renal failure in spontaneously hypertensive rats.
abstract: BACKGROUND
  Ischemia-reperfusion-induced acute renal failure (ARF) is associated with a high mortality in patients with hypertension and with an unfavorable outcome of kidney transplants from marginal donors.
  
  
  OBJECTIVE
  The influence of allopurinol and enalapril on urinary nitrate/nitrite (UNOx), glomerular filtration rate, plasma and urinary sodium, and hemodynamic parameters was examined in spontaneously hypertensive rats (SHR) with ARF.
  
  
  METHODS
  ARF was induced by right-kidney removal and clamping the left renal artery for 40 min in 50 male 26-week-old SHR weighing 300 +/- 23 g. The rats were randomly allocated to five groups: (1) sham operated; (2) ARF; (3) ARF after pretreatment with 40 mg/kg allopurinol; (4) ARF after pretreatment with 40 mg/kg enalapril, and (5) ARF after pretreatment with 40 mg/kg allopurinol and 40 mg/kg enalapril. Creatinine clearance, UNOx (Griess reaction), cardiac output (dye dilution technique), mean arterial blood pressure, and renal blood flow were measured 24 h after reperfusion. Total vascular resistance and renal vascular resistance were calculated and compared between the groups.
  
  
  RESULTS
  A nonsignificant decrease was found in both daily UNOx excretion and creatinine clearance when pretreated ARF groups and the ARF group without pretreatment were compared (p > 0.05). Significantly lower plasma sodium values (139.5 +/- 4.86 mmol/l) in the allopurinol-pretreated ARF group were found than in the ARF group without pretreatment, in the ARF group pretreated with enalapril, and in the sham SHR group (p = 0.029). The urinary sodium loss was greater in the enalapril-pretreated than in the allopurinol-pretreated ARF group (p = 0.047). Allopurinol and/or enalapril pretreatment decreased total vascular resistance (p = 0.003) in comparison with the sham SHR group.
  
  
  CONCLUSIONS
  Neither allopurinol nor enalapril nor both were protective against ischemia-reperfusion injury in SHR, nor altered glomerular filtration rate and UNOx in a favorable direction.
authors.affiliation: Institute for Medical Research, Belgrade, Serbia. milan.r@EUnet.yu
authors.forename: Milan
authors.initials: M
authors.lastname: Radovic
authors.forename: Zoran
authors.initials: Z
authors.lastname: Miloradovic
authors.forename: Tamara
authors.initials: T
authors.lastname: Popovic
authors.forename: Nevena
authors.initials: N
authors.lastname: Mihailovic-Stanojevic
authors.forename: Djurdjica
authors.initials: D
authors.lastname: Jovovic
authors.forename: Mina
authors.initials: M
authors.lastname: Tomovic
authors.forename: Emina
authors.initials: E
authors.lastname: Colak
authors.forename: Sanja
authors.initials: S
authors.lastname: Simic-Ogrizovic
authors.forename: Ljubica
authors.initials: L
authors.lastname: Djukanovic
mesh_terms: D058186:Acute Kidney Injury / Q000209:etiology / Q000517:prevention & control / Q000652:urine*; D000493:Allopurinol / Q000008:administration & dosage*; D000818:Animals; D000959:Antihypertensive Agents / Q000008:administration & dosage; D000963:Antimetabolites / Q000008:administration & dosage; D004338:Drug Combinations; D004656:Enalapril / Q000008:administration & dosage*; D008297:Male; D009566:Nitrates / Q000652:urine*; D009573:Nitrites / Q000652:urine*; D051381:Rats; D011918:Rats, Inbred SHR; D015427:Reperfusion Injury / Q000150:complications / Q000378:metabolism* / Q000517:prevention & control; D012964:Sodium / Q000652:urine*; D016896:Treatment Outcome
chemical_list: D000959:Antihypertensive Agents; D000963:Antimetabolites; D004338:Drug Combinations; D009566:Nitrates; D009573:Nitrites; D000493:Allopurinol; D004656:Enalapril; D012964:Sodium