Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:1.1.1.1 (alcohol dehydrogenase)
9,284 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

As aged polyuria is often observed in the IVCS strain of mouse, biochemical and histological studies were undertaken in order to clarify its etiology. Polyuria was observed at 7-8 months of age, and significant increases in water intake and urine volume were noted at 10-11 months of age. IVCS strain mice over one year old showed water intakes and urine volumes about five to six times greater than those in DDI strain mice. The osmolarity of urine excreted from polyuric mice was low compared with DDI strain mice, and elevations of sodium and potassium excretion were observed at an early stage of polyuria. At a more advanced stage of the disease, proteins of low molecular weight were excreted in most animals. Furthermore, depression of kidney response to ADH was recognized soon after onset of polyuria compared with normal IVCS strain mice. Thus, polyuria observed in IVCS strain mice may result from a functional defect of the renal tubules. In addition, significant deposition of amorphous substances, especially in the liver, kidney and spleen, occurred almost in parallel with polyuria. From these findings, it is obvious that mice of the IVCS strain exhibit characteristic polyuria and storage disease as they age.
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PMID:Clinical and pathogenic studies on aged polyuria in the IVCS strain of mouse. 401 46

Electrolytic lesion of the medio-ventral septal (MVS) area produces a sustained increase in daily water intake and urine output. This polyuria and hyperdipsia are associated with decreased levels of circulating radioimmunoassayable ADH. In addition, the usual ADH release to angiotensin II observed in normal controls and sham-lesioned rats was markedly blunted in MVS-lesioned animals.
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PMID:[Effects of septal lesions on the response of vasopressin to angiotensin II]. 403 4

The physiological basis for the polyuria and polydipsia occurring in some manic-depressive patients treated with lithium salts was studied in vivo and in vitro. Three lithium-treated polyuric patients, in whom other causes of a concentrating defect were excluded, had abnormal urinary concentrating abilities after a standard water depreviation test. Two of these patients failed to respond to exogenous vasopressin (ADH) and one had a subnormal response. The abilities of these patients to excrete solute-free water (C(H2O)) was comparable to normal subjects during steady-state water diuresis, suggesting no gross abnormalities in sodium transport. However, each of these patients demonstrated abnormally low capacities to reabsorb solute-free water (T(C) (H2O)) under hydropenic conditions after administration of hypertonic saline and vasopressin. These in vivo findings demonstrate at least a nephrogenic basis for the diabetes insipidus syndrome manifested by these three patients. The defect in water transport was further characterized in toad urinary bladders in vitro. Short-circuit current (I) and water flow (W) were studied under basal, ADH-stimulated, and cyclic adenosine 3',5'-monophosphate (c-AMP)-stimulated conditions. Increasing mucosal [Li(+)] progressively inhibited basal I, and both I and W induced by ADH. Significant inhibition of basal and ADH-induced I was observed at mucosal [Li(+)] < 1.1 mEq/liter, and of ADH-induced W at mucosal [Li(+)] = 11 mEq/liter. On the other hand, at these lithium concentrations, neither c-AMP-stimulated W nor I was inhibited. Increasing serosal [Li(+)] produced significant inhibition of basal I only at [Li(+)] at least 50-fold greater than at the mucosal (urinary) surface. These in vitro studies confirm that mucosal lithium inhibits the action of ADH, but not c-AMP. Hence, lithium appears to be a significant inhibitor of ADH-stimulated water flow, probably acts from the urinary surface, and appears to exert its effect at a site biochemically proximal to c-AMP action.
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PMID:Lithium-induced nephrogenic diabetes insipidus: in vivo and in vitro studies. 434 1

1. Acute changes in haematocrit were produced by exchange transfusion of dextran-in-saline or packed red cells.2. There were no significant changes in glomerular filtration rate, blood pressure, central venous pressure, heart rate, respiratory rate, blood volume or extracellular fluid volume following the exchange transfusions.3. Urine volume increased after haemodilution but decreased after haemoconcentration.4. The diuresis after haemodilution occurred despite an infusion of ADH or alcohol. Thus it could not be attributed to a change in circulating ADH level.5. There were two types of diuresis. The ;water diuretic' response was characterized by an increase in free water clearance with a reduction in urinary sodium concentration; the ;sodium diuretic' response by an increase in urinary sodium concentration but no change, or a fall, in free water clearance.6. The results were related to changes in medullary osmotic gradient found by other workers to occur when medullary blood flow rate is altered.
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PMID:The effect of acute changes in haematocrit in the anaesthetized dog on the volume and character of the urine. 535 36

Early gentamicin nephrotoxicity is characterized by a variety of renal transport abnormalities, including polyuria secondary to nephrogenic diabetes insipidus. To investigate whether gentamicin directly interferes with cellular mechanisms responsible for ADH responsivity as a possible contributing factor in this tubular transport alteration, the effect of gentamicin on ADH-stimulated water flow was examined in vitro in the toad urinary bladder. Gentamicin decreased ADH-stimulated osmotic water flow in a dose-dependent manner, with a threshold effect at approximately 0.5 mM. This inhibitory effect occurred only in response to submaximal concentrations of ADH, was reversible, and was preventable with Mg++. Additionally, gentamicin reduced theophylline-stimulated osmotic water flow but had no effect on cyclic AMP-induced water flow. These effects are consistent with a direct gentamicin-related decrease in ADH-responsive adenylate cyclase activity and suggest a mechanism that may contribute to the nephrogenic diabetes insipidus characteristic of early gentamicin nephrotoxicity and the nonoliguric acute renal failure that is a late toxic event occurring with the use of this antibiotic.
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PMID:The effect of gentamicin on antidiuretic hormone-stimulated osmotic water flow in the toad urinary bladder. 629 28

The effects of cortisol excess on kidney function were studied in 8 normal conscious dogs. Cortisol was given orally until polyuria developed. Cortisol excess decreased urine osmolality (from 897 +/- 76 to 186 +/- 36 mosm. kg-1) and increased urine production (from 0.7 +/- 0.1 to 9.3 +/- 2.4 ml kg-1. h-1). The glomerular filtration rate increased by 23 +/- 9 per cent. Sodium and potassium concentrations in plasma were decreased. 66 Per cent of the increase in urine production was due to the increase in free water clearance and 34 per cent to the increased urea excretion. Cortisol excess apparently caused polyuria by inhibition of the action of ADH in the collecting duct, resulting in a decreased water and urea reabsorption. The decreased urea reabsorption possibly causes a smaller urea recirculation in the renal medulla and hence a decrease in concentrating capacity.
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PMID:The influence of cortisol excess on kidney function in the dog. 673 Feb 86

Male and female Long Evan rats and Brattleboro rats with ADH-deficient diabetes insipidus were treated with lithium administered in the diet for 12 weeks. The plasma lithium level was about 1 mmol/l in all groups. Lithium caused polydipsia and polyuria and lowering of renal concentrating ability in normal rats. In rats with ADH deficiency lithium tended to increase water intake, but did not influence spontaneous urine osmolality or maximal urine osmolality during water deprivation. The results indicate that the renal concentrating defect caused by lithium in rats can be explained by ADH-blockade as the only mechanism. However, there is circumstantial evidence that lithium in addition may stimulate thirst mechanisms by an ADH-independent action.
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PMID:Effects of lithium on water intake and renal concentrating ability in rats with vasopressin-deficient diabetes insipidus (Brattleboro strain). 683 12

Injections of 0.2 M LiCl i. p. (1 ml/100 g/day) induced polydipsia in rats drinking tap water. The plasma lithium concentration and its content in the erythrocytes, skeletal muscles, renal tissue were significantly higher in the rats drinking tap water as compared with rats drinking saline. No significant differences in the body volume of extracellular fluid, muscle water, Na, K content and their muscle intracellular concentrations were noted between the "lithium" and the control rats. Na content in the plasma and the renal cortex--medullar Na gradient were decreased in the "lithium" rats drinking tap water. The hyaluronic acid content in renal papilla was increased in all rats receiving lithium injections. After an injection of ADH the papillary hyaluronic acid content markedly decreased in control rats while it decreased only insignificantly in "lithium" rats. The impairment of the ability of urine concentrating and polyuria in "lithium" rats seems to be partly connected with an enhancement of the polymerization degree of renal papillar hyaluronic acid.
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PMID:[The effect of lithium on the tissue levels of electrolytes and hyaluronic acid levels in the kidney papilla in the rat]. 687 79

The effects of LVP, dDAVP, and dVDAVP on the water excretion of 14 vasopressin-sensitive and 2 ADH-resistant patients with diabetes insipidus were studied and compared. Findings showed that dDAVP and dVDAVP decreased the diuresis of all ADH-sensitive patients, and in those with diabetes insipidus, more markedly (7.6-fold) and for a longer duration (3.3-fold) than did LVP. From a comparison of the results, dVDAVP is at present one of the most effective preparations for reduction of polyuria in patients with ADH-sensitive diabetes insipidus.
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PMID:1-deamino-/4-valine-8-D-arginine/-vasopressin (dVDAVP), a new synthetic vasopressin analog for treating diabetes insipidus. 705 3

4-Methylpyrazole (4-MP), an alcohol dehydrogenase inhibitor, was administered to dogs to treat ethylene glycol (EG) intoxication. Eleven dogs were given 10.6 g of EG/kg of body weight; 5 dogs were treated with 4-MP 5 hours after EG ingestion and 6 dogs were treated with 4-MP 8 hours after EG ingestion. 4-Methylpyrazole was administered IV as a 50-mg/ml [corrected] solution in 50% polyethylene glycol: initial dose, 20 mg/kg; at 12 hours after initial dose, 15 mg/kg; at 24 hours after initial dose, 10 mg/kg; and at 30 hours after initial dose, 5 mg/kg. Physical, biochemical, hematologic, blood gas, serum and urine EG concentrations, and urinalysis findings were evaluated at 0, 1, 3, 6, 9, 12, 24, 48, 72 hours, and at 1 week and 2 weeks after EG ingestion. Dogs of both groups developed clinicopathologic signs associated with EG intoxication, including CNS depression, hyperosmolality, high anion gap metabolic acidosis, polydipsia, polyuria, calcium oxalate monohydrate and dihydrate crystalluria, and isosthenuria. Fractional excretion of sodium was increased in all dogs between 1 and 9 hours after EG ingestion, but remained increased beyond 24 hours only in the 2 dogs treated at 8 hours after EG ingestion that developed acute renal failure. All dogs treated 5 hours after EG ingestion recovered without morphologic, biochemical, or clinical evidence of renal impairment. Of the 6 dogs treated 8 hours after EG ingestion, 2 developed acute renal failure. One of the dogs treated 8 hours after EG ingestion remained isosthenuric for 2 months, but did not manifest any other signs of renal impairment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Efficacy of 4-methylpyrazole for treatment of ethylene glycol intoxication in dogs. 788 24


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