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)

Adenosine infusion produces sustained, reversible, controlled hypotension in humans, but markedly compromises renal function. Since adenosine inhibits renal perfusion and filtration via stimulation of intrarenal A1 receptors, we hypothesized that antagonism of A1-subtype receptors with the selective adenosine A1-receptor antagonist (+-)N6-endonorbornan-2-yl-9-methyladenine (N-0861) would attenuate adenosine-induced renal dysfunction while still allowing induction and maintenance of hypotension. Systemic and renal hemodynamic and excretory responses were measured in clearance studies conducted in six groups of anesthetized rats treated with: vehicle+saline, vehicle+adenosine, N-0861 (10 or 30 mumol/kg intravenously [i.v.])+saline, or N-0861 (10 or 30 mumol/kg i.v.),+adenosine. The A1-receptor antagonist had little effect on the magnitude, maintenance, or reversibility of controlled hypotension produced by adenosine infusion. Oliguria, hypofiltration, and electrolyte retention induced by adenosine infusion were attenuated in rats pretreated with N-0861. Adenosine A1-receptor antagonism also reduced the rebound hyperfiltration and hyperperfusion associated with cessation of adenosine infusion. N-0861 alone had only a modest effect on renal or systemic hemodynamics, but produced significant dose-related diuresis/natriuresis. These results suggest that coadministration of, or pretreatment with, a selective adenosine A1-receptor antagonist may attenuate the undesirable renal effects of adenosine while allowing maintenance of controlled hypotension.
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PMID:A selective adenosine A1 receptor antagonist attenuates renal dysfunction during controlled hypotension with adenosine in rats. 786 58

We investigated the effects of KW-3902 (8-noradamantan-3-yl-1,3-dipropylxanthine), a potent and selective adenosine A1-receptor antagonist, on lipopolysaccharide (LPS)-induced reduction of urine volume (UV) in anesthetized dogs, in comparison with those of furosemide. LPS was intravenously administered at a dose of 0.5 mg/kg; and the heart rate (HR), systemic blood pressure (BP), renal blood flow (RBF) and UV were measured every 15 min for 4 h. Administration of LPS continuously decreased HR, BP, RBF and UV. KW-3902, furosemide or their corresponding vehicle was given as a bolus injection 5 min after the LPS injection. Treatment with KW-3902 (1 mg/kg, i.v.) ameliorated the LPS-induced decline of UV and RBF. Furosemide (3.2 mg/kg, i.v.) tended to ameliorate the LPS-induced decline of UV but not RBF, the duration of the effect being shorter than that of KW-3902. These results suggest that KW-3902 can ameliorate the oliguria and the decrease in RBF during the early phase of LPS-induced shock. Endogenous adenosine may be involved in the endotoxin-induced oliguria via the adenosine A1-receptor.
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PMID:Effect of the selective adenosine A1-receptor antagonist KW-3902 on lipopolysaccharide-induced reductions in urine volume and renal blood flow in anesthetized dogs. 1113 32