Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lithium intoxication was induced in rats by intraperitoneal administration of lithium chloride in a daily dose of 200 mg/kg (0.22 LD50) for 6 days. Polyuria connected with pathological changes in the epithelium of the convoluted tubules and depression of the antidiuretic hormone--acid mucopolysaccharides system in the area of the straight kidney tubules was observed on the 6th day of the experiments. Oligouria and death of some of the animals on the 7th experimental day was caused by severe lesions the kidney structure. Further observation (30 days) demonstrated that, along with the regeneration processes, there developed a marked sclerosing ofthe kidney tissue. A conclusion was drawn that severe lithium intoxication was associated with the development of acute renal insufficiency. Functional reserves of the kidneys after the cessation of lithium chloride administration remained lowered for a long period.
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PMID:[Role of the kidneys in the pathogenesis of lithium poisoning]. 13 80

Lithium (Li+) chloride, 2 to 3 mEq. per kilogram of body weight, was administered intraperitoneally to normal Wistar rats daily for 4 to 66 days. This resulted in a marked reduction in urine osmolality (Uosm.) and increase in the excretion of water, Na+, K+, uric acid, and phosphate. The excretion of uric acid and potassium was a direct function of UNaV. The magnitude of depression in urine osmolality was significantly related to the rate of excretion of lithium in the urine, suggesting that the change in water reabsorption is dependent on the presence of the ion in the luminal side of the tubule. During 2 per cent saline diuresis, Li+-treated rats achieved less fractional free water reabsorption (TcH2O/GFR times 100) at any level of fractional osmolar clearance (Cosm./GFR times 100) than normal rats. On the other hand, during 0.225 per cent saline diuresis, fractional free water clearance (CH2O/GFR times 100) was normal over a wide range of fractional urine flow (V/GFR times 100), indicating intact function of the ascending limb of the loop of Henle. The intravenous infusion of vasopressin (VP) or dibutyryl cyclic-adenosine monophosphate (dcAMP) to Li+-treated rats resulted in a modest rise in Uosm. and a reduction in V/GFR times 100 and CH2O/GFR times 100. Although the response to VP appeared earlier than that to dibutyryl cyclic-AMP, the magnitude of the changes in Uosm., V/GFR times 100, and CH2O/GFR times 100 was eventually the same with both substances. Comparison between normal and Li+-treated rats revealed that the response to both VP and dibutyryl cyclic-AMP was blunted, albeit to a greater extent in the former. Inhibition by Li+ of adenylate cyclase will only partially explain the present data. Impairment in the release of endogenous VP or a block distal to the formation of cyclic-AMP must have played a role. In view of a normal diluting capacity and the increase in the excretion of phosphate and uric acid, it is suggested that Li+, when administered chronically in the present doses, inhibits proximal tubular reabsorption.
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PMID:Renal effects of lithium administration in rats: alterations in water and electrolyte metabolism and the response to vasopressin and cyclic-adenosine monophosphate during prolonged administration. 16 79

1 The effect of intravenous infusion of lithium, 2.56 mumol/min on the antidiuretic responses to antidiuretic hormone (ADH), adenosine triphosphate (ATP), 3'-5' adenosine cylic monophosphate (cyclic AMP) and theophyline was studied in water-loaded, alcohol-anaesthetized rats. 2 Lithium reversibly inhibits the antidiuretic response to all concentrations of ADH, depressing the maximum response but not changing the amount required for half maximal response. 3 The rate of increase of serum lithium relates more clearly to the inhibitory effect than does the serum concentration. 4 Sodium concentrations in the renal papilla seem to fall when serum lithium levels are rising. 5 Lithium inhibits the antidiuretic response to ATP and cyclic AMP but does not inhibit the response to theophyline.
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PMID:The effects of lithium ions on the antidiuretic action of vasopressin in the rat. 17 68

The acute effects of intraperitoneal lithium on the phosphaturic responses to parathyroid hormone (PTH) and pharmacologic doses of vasopressin were studied in rats. Lithium significantly inhibited the phosphaturic response to PTH at a dosage of 90 mug/kg/hr but did not affect the response to 30 mug/kg/hr. Conversely, lithium eliminated the phosphaturic response to vasopressin at a dosage of 300 mU/kg/hr but did not affect the response to dibutyryl adenosine 3', 5'-monophosphate (db-cAMP), 10 mg/kg/hr. Renal lithium content was increased substantially after the larger dose of PTH and was diminished slightly after db-cAMP and the larger dose of vasopressin. The latter two treatments also inhibited renal lithium reabsorption whereas the smaller dose of vasopressin and both dosages of PTH did not. These results indicate that lithium interferes with the phosphaturic responses to certain dosages of pth and vasopressin and suggest that renal lithium reabsorption and tissue lithium uptake may in part determine the extent of this cation-hormonal interaction. In addition, a competitive type of interaction between lithium and vasopressin is postulated.
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PMID:Selective lithium inhibition of hormonal phosphaturic responses. 17 56

The effect of lithium on the urine concentrating response to antidiuretic hormone (ADH) and the excretion of ADH has been studied in rats and man. The maximum urine osmolarity following 18 h dehydration and Pitressin (5 u) was decreased in three out of four patients during lithium treatment compared to their response to the same test in the absence of lithium. In a fifth patient, tested only during lithium treatment, the urine remained hypotonic to plasma throughout this test. Lithium increased the excretion of ADH in non-polyuric patients from 9-22 mu/24 h in the absence of lithium to 36-202 mu/24 - during lithium treatment. In four patients with lithium-induced polyuria, a diuretic acting on the distal tubules, clorexolone, reduced the polyuria. Lithium increased urine volume and the excretion of ADH in four rats receiving lithium in their diet. The response to exogenous ADH was decreased during lithium administration.
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PMID:Lithium and the antidiuretic hormone. 78 47

The usual treatment for recurrent syndrome of inappropriate secretion of antidiuretic hormone has been fluid restriction. Recently White and Fetner described an adult with SIADH successfully managed with lithium carbonate. Described here is a child with recurrent SIADH who was diagnosed as having an acute hyponatremic episode and who then relapsed twice in a two-month period while chronic fluid restriction was attempted. He has now been maintained on 300 mg/day of lithium carbonate and is asymptomatic with normal serum sodium concentration and urine osmolalities. Lithium appears to be effective in the management of recurrent SIADH and may allow control in a patient who cannot comply with long-term fluid restriction.
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PMID:Treatment of recurrent syndrome of inappropriate secretion of antidiuretic hormone with lithium. 83 44

The etiology, diagnosis and management of lithium-induced diabetes insipidus (LIDI) is discussed, including the presentation of a case report. It is suggested that lithium provokes LIDI by decreasing the responsive ness of the kidney to the antidiuretic hormone. Lithium-induced polyuria may be managed by concomitant treatment with a thiazide diuretic or discontinuation of the lithium. Caution must be employed, however, when using thiazides with lithium as these diuretics decrease renal clearance of lithium.
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PMID:Lithium-induced nephrogenic diabetes insipidus. 94 67

Lithium, an established inhibitor of antidiuretic hormone action, was used (as the carbonate salt) to treat a patient with the syndrome of inappropriate secreation of antidiuretic hormone. The patient was studied by balance technics, and after a stablized hyponatremic state developed, 0.9 g of lithium carbonate was administered daily. A prompt water diuresis ensued, with correctionof hyponatremia in two days. Discontinuation of the drug resulted in a gradual return of the hyponatremic state. No change in urinary cyclic AMP occurred during the period of lithium effect. Lithium carbonate may be an effective treatment for both the acute and the chronic forms of the syndrome.
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PMID:Treatment of the syndrome of inappropriate secretion of antidiuretic hormone with lithium carbonate. 111 Jul 24

Lithium ion provides a useful and specific form of chemotherapy for manic and hypomanic episodes, although its antimanic effect may be delayed for as long as a week or more, requiring the use of an antipsychotic agent in the initial period to control the behavior of very disturbed patients. The mechanisms of action of lithium remain obscure, but probably involve effects on neuronal and hormone-target cell membranes. Lithium has interesting antithyroid and anti-antidiuretic hormone effects that are potentially useful medically. The main limitation of the use of lithium is its narrow therapeutic index and requirement of close medical supervision. The most promising aspects of the use of lithium are its encouragement of better psychiatric diagnosis and its "prophylactic" effectiveness in at least reducing the frequency and severity of manic and depressive attacks in manin-depressive illness.
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PMID:Lithium salts: 1970-1975. 116 89

Lithium may induce all clinical physiological abnormalities of the polydipsia- polyuria syndrome. Authors describe a 61-year-old woman patient in whom permanent disturbance of the water metabolism, nephrogenic diabetes insipidus (NDI) was caused by lithium treatment, lasting longer than 10 years. The partial resistance of the fluid disturbance to vasopressin has been investigated by the administration of supramaximal doses of dDAVP. Considering the known antidiuretic effect of indomethacin, authors compared antidiuruetic activity of indomethacin and piroxicam (Hotemin) by studying standard parameters of water metabolism/free water clearance ect.) It was found that piroxicam, on mg basis a more effective antiinflammatory compound, was less antidiuretic then indomethacin. It was concluded, that there is no close parallelism between the structure and antiinflammatory and antidiuretic activity of nonsteroid antiinflammatory drugs. In the opinion of authors nonsteroid antiinflammatory drugs may have a role in the treatment of lithium-induced NDI, though, the establishment of the safety use of such therapy requires further studies.
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PMID:[Lithium-induced chronic water-metabolism disorder (nephrogenic diabetes insipidus)]. 192 71


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