Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028961 (oliguria)
 1,847 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Platelet-activating factor (PAF-acether) has been shown to be produced by the kidney and to sharply reduce glomerular filtration rate (GFR) and renal plasma flow (RPF). Thus, PAF-acether could be a possible mediator of the reduction of GFR and RPF in ischemic-induced acute renal failure (ARF). We have assayed the effect of inhibiting the interaction of PAF-acether with its receptor using two specific PAF-acether antagonists, BN-52021 and alprazolam, on the evolution of the GFR and RPF, in the experimental model of ARF induced in rats by clamping the left artery for 60 min. In addition, we have measured arteriovenous differences in PAF-acether concentration, as well as PAF-acether content in glomeruli from rats with ARF pretreated or not with BN-52021. In metabolic cage studies, plasma creatinine increased more in the untreated than in the BN-52021-treated group, whereas creatinine clearance was higher in treated than in untreated rats. In acute clearance experiments, after renal artery clamping, untreated rats showed a marked oliguria and reduction of the inulin clearance (greater than 99%), which showed no recovery 90 min after clamp release, whereas GFR reached values above 0.1 ml/min in the rats treated with BN-52021 or alprazolam, with clearly significant statistical differences. Results of p-aminohippurate clearance were similar to those of GFR. Glomeruli from rats with ARF had greater amounts of PAF-acether than glomeruli from normal rats, whereas glomeruli from BN-52021-treated rats with ARF produced intermediate amounts. These results provide evidence for a role for PAF-acether in the genesis of this model of experimental ARF.
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PMID:Platelet-activating factor antagonists treatment protects against postischemic acute renal failure in rats. 232 16

We have examined the acute renal failure that occurs after uranyl nitrate administration in the rat and the specific effects of pretreatment of rats with angiotensin converting enzyme inhibitor (CEI), plasma volume expansion (PVE) after uranyl nitrate, and a combination of these treatments. We utilized a combination of micropuncture measurements of glomerular hemodynamics, cage studies, and histologic examination of renal tissue to evaluate the degree of acute renal failure in all groups studied. Uranyl nitrate (UN) (25 mg/kg body wt) administration caused a reduction in the nephron filtration rate (SNGFR) (39.4 +/- 1.6 to 24.8 +/- 2.9 nl X min-1 X g kidney wt-1, P less than 0.02) as a result of a major decrease in the glomerular ultrafiltration coefficient (LpA) from control values (greater than or equal to 0.085 +/- 0.008 to 0.035 +/- 0.007 nl X sec-1 X mm Hg-1 X g kidney wt-1, P less than 0.01). Treatments with CEI, PVE, and the combination of CEI and PVE in rats receiving UN restored 0.38 +/- LpA to normal values (greater than 0.061 +/- 0.009, 0.091 +/- 0.020, and 0.138 +/- 0.020 nl X sec-1 X mm Hg-1 X g kidney wt-1, respectively). Cage studies revealed that CEI treatment prevented oliguria and resulted in major volume losses and reduction in weight. However, rats died after a similar period after UN, but probably by different mechanisms. Analysis of renal ultrastructure revealed equivalent tubular damage in all experimental groups. Alterations in LpA after UN are functional in nature and are potentially preventable and reversible by a combination of treatments with CEI and PVE.
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PMID:Functional basis for the glomerular alterations in uranyl nitrate acute renal failure. 300 41