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

The effect of clofibrate on the water metabolism was studied in rats with pituitary stalk lesion. It was found that this drug made the oliguria interphase much more marked and more prolonged. In rats anaesthetized with alcohol, clofibrate pre-treatment led to an enhancement of the effect of ADH. The experiments permit the conclusion that the presence of endogenous ADH is necessary for clofibrate antidiuresis. Its effect is presumably exerted via the mobilization of the ADH, but it can not be excluede that it also enhances the peripheral effect of ADH.
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PMID:Study of the antidiuretic effect of clofibrate in rat. 100 5

Methylmercury (MeHg) is a potent neurotoxicant and nephrotoxicant in several animal species including humans. Although the in vivo toxicity of MeHg per se is well known, the interaction between MeHg and other pollutants and with nutritional factors is not well understood. Since ethanol (EtOH) is a widely consumed toxicant which has been shown to enhance the histopathologic effects of MeHg on renal tissues, a study was undertaken to examine the effects of the combined administration to rats of MeHg and EtOH on renal function and on mercury distribution in body tissues. Forty-eight rats were divided into 6 treatment groups of 8 rats each. Rats in groups 1, 2 and 3 were given feed ad libitum, a restricted liquid diet of 70 mL/d or distilled water orally, respectively. Rats in groups 4, 5 and 6 were given 1.5 mg MeHg/kg bw, 2.0 g EtOH/kg bw, or 1.5 mg MeHg + 2.0 g EtOH/kg bw, respectively, by oral gavage daily for 45 d. All rats except those in group 1 (ad libitum) were fed 70 mL of liquid diet/d for the entire study period. The ingestion of MeHg + EtOH in combination induced a greater increase in renal weight compared to treatment with either MeHg + EtOH alone. Only those rats given MeHg in combination with EtOH exhibited oliguria and elevated blood urea nitrogen levels. Despite this antidiuresis, urinary concentrating ability was impaired in those rats given both MeHg and EtOH. In contrast, the ingestion of MeHg by itself caused the most rapid loss of glucose in urine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of administering methylmercury in combination with ethanol in the rat. 162 57

Levels of total amino compounds (ninhydrinpositive substances, n.p.s.) have been measured in the inner medullas of rats during acute water diuresis and following the induction of hypovolaemic oliguria by the injection (i.p.) of 30% polyethylene glycol 20,000 (PEG) in 0.9% saline. Mean medullary fluid n.p.s. concentrations fell from 26.5 mmol to 15.2 mmol Gly equiv/l (-43%) within 2.5 h from the onset of diuresis, while the mean calculated tissue osmolality decreased from 738 mosmol/kg (control) to 369 mosmol/kg H2O. By 24 h n.p.s. and osmolality had returned to control levels. By 0.5 h after injection of PEG the mean concentration of n.p.s. had increased from 26.4 mmol to 32.7 mmol Gly equiv/l (+24%) and by 4 h had reached 60.4 mmol Gly equiv/l (+19%). During this time the calculated mean tissue fluid osmolality rose from 696 to 1037 mosmol/kg H2O. Levels of n.p.s. did not increase further for up to 12 h. It is proposed that losses of amino compounds may make a significant contribution to the overall decrease in medullary cellular osmotic potential accompanying reduced tissue fluid osmolality, and that increased levels of these solutes may provide short-term osmoprotection during antidiuresis of rapid onset, in contrast to the more slowly accumulating methylamines and polyhydric alcohols.
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PMID:Alterations in renal inner medullary levels of amino nitrogen during acute water diuresis and hypovolaemic oliguria in rats. 189 36

Single injections of 15 microliter of 1 M NaCl or 2M sucrose into the carotid system of normal unanesthetized toads induced a rapid and significant decrease of urine production. This appears to be the first report on the existence of a Verney-like phenomena in a non-mammalian vertebrate. This antidiuresis was blocked out in the hypophysectomized diencephalic lesioned animal. Concurrently, small volumes (4 microliters) of 1 M NaCl but not 2 M sucrose also induced antidiuresis when injected into the midbrain tegmentum of normal but not of hypophysectomized diencephalic lesioned toads. Larger volumes (6 microliters) of 2 M sucrose were needed to induce a similar antidiuresis in normals. Furthermore, even larger volumes (more than 8 microliters) of any of both solutions were able to induce oliguria in normal as well as in hypophysectomized toads. On the basis of these results, the following conclusion would be drawn: the brain of the toad is able to detect ionic and osmotic stimuli, these stimuli apparently affect different receptors in the brain, the antidiuresis initiated by these mechanisms is dependent on diencephalic integrity.
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PMID:Antidiuretic responses to osmotic, ionic or volume stimulation of the brain in the unanesthetized toad, Bufo arenarum Hensel. 288 51

Adequate amniotic fluid (AF) volume is maintained by a balance of fetal fluid production (lung liquid and urine) and resorption (swallowing and intramembranous flow). Because fetal urine is the principle source of AF, alterations in urine flow and composition directly impact AF dynamics. Intra-amniotic 1-desamino-8-D-arginine vasopressin (DDAVP) is rapidly absorbed into fetal plasma and induces a marked fetal urinary antidiuresis. To examine the effect of intra-amniotic- DDAVP-induced fetal urinary responses on AF volume and composition, six chronically prepared ewes with singleton fetuses (gestation 128 +/- 2 days) were studied for 72 h after a single intra-amniotic DDAVP (50-microgram) injection. After DDAVP, fetal urine osmolality significantly increased at 2 h (157 +/- 13 to 253 +/- 21 mosmol/kg) and remained elevated at 72 h (400 +/- 13 mosmol/kg). Urinary sodium (33.0 +/- 4.5 to 117.2 +/- 9.7 meq/l) and chloride (26.0 +/- 2.8 to 92.4 +/- 8.1 meq/l) concentrations similarly increased. AF osmolality increased (285 +/- 3 to 299 +/- 4 mosmol/kg H2O), although there was no change in fetal plasma osmolality (294 +/- 2 mosmol/kg). Despite a 50% reduction in fetal urine flow (0.12 +/- 0.03 to 0.05 +/- 0.02 ml.kg-1.min-1 at 2 h and 0.06 +/- 0.01 ml.kg-1.min-1 after 72 h), AF volume did not change (693 +/- 226 to 679 +/- 214 ml). There were no changes in fetal arterial blood pressures, pH, PCO2, or PO2 after DDAVP. We conclude the following. 1) Intra-amniotic DDAVP injection induces a prolonged decrease in fetal urine flow and increases in urine and AF osmolalities. 2) Despite decreased urine flow, AF volume does not change. We speculate that, in response to DDAVP-induced fetal oliguria, reversed intramembranous flow (from isotonic fetal plasma to hypertonic AF) preserves AF volume.
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PMID:Ovine fetal adaptations to chronically reduced urine flow: preservation of amniotic fluid volume. 901 10