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)

The authors made conspicuous in the rat the appearance of "diabetes insipidus" induced by two lithium salts: chloride and carbonate administered orally, with increasing doses in food. The polyuria, polydipsia and urinary hypotony are reversible and disappeared with stopping the treatment. The animals became insensible to the exogenous antidiuretic hormon during the treatment and progressively became sensible again during the following twenty days so suggesting a nephrogenic mechanism by lithium: either a loss of ADH activity, either the abolition of intrarenal osmotic pressure gradient.
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PMID:[Diabetes insipidus and exogenous antidiuretic hormone activity modifications by lithium in the rat]. 15 81

The diffusional and osmotic water permeability of collecting ducts in isolated papillae of rats' kidneys were measured in papillae taken from normal and lithium pretreated rats. The diffusional water permeability of collecting ducts in papillae from normal rats in the absence of ADH was 4.1 +/- 0.2 (S.E.M.) (n = 18) muM s-1 increasing to 7.2 +/- 0.6 mum s-1 with ADH. Values obtained with lithium (10 mM) in the medium, perfusate or both and in papillae taken from lithium pretreated rats did not differ significantly from the above. The cyclic AMP content of the papillae taken from normal rats was 83 +/- 6 pm mg protein in the absence of ADH and increased to 196 +/- 12 (n = 13) with 500 mu units ml-1 ADH. Lithium 10 mM in the medium did not alter this response. Papillae from lithium pretreated rats had a similar basal level of cyclic AMP but the increment in a lithium (10 mM) medium after ADH was significantly less. These results indicate that the impaired water handling of lithium treated rats is probably not due to a failure of the membrane to increase its permeability to water after ADH. Though lithium does alter the production of cyclic AMP this is not believed to be important regarding any alteration in water permeability. We believe it is probable that lithium interferes with sodium chloride transport at some more proximal nephron segment thereby producing the syndrome of polyuria.
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PMID:The effect of lithium on the permeability response induced in the collecting duct by antidiuretic hormone. 18 85

Renal, glomerular and tubular, factors responsible for the volume control of extracellular liquid were examined. The part played by angiotensin II in mediating the compensation of this liquid losses was studied in patients with spontaneous polyuria due to diencephalo-posthypophyseal diabetes insipidus or psychogenic polydipsia and healthy subjects with induced hypotonic polyuria. It was noted that: 1) acute expansion elicited a natriuretic response and increased distal sodium load, due to an increase in filtrate and relative inhibition of proximal reabsorption, or proximal inhibition if the filtrate was unchanged. The efficiency of distal sodium transport was often unchanged. 2) Return to sodium balance parity during prolonged expansion of volume, was accomplished by varying renal means, in accordance with the experimental model employed. Distal reabsorption was essentially depressed during prolonged saline load (secondary hypoaldosteronism). When protracted mineralcorticoid treatment was used, however, distal reabsorption was high, even in the escape stage, and its saturation required marked augmentation of the sodium load reaching the distal tubules. 3) Depletion of volume caused by protracted natriuretic treatment in spontaneous polyuria reduced both diuresis and sodium excretion. This resistance to the natriuretic effect of the drug followed intrarenal compensation that reduced the distal sodium load and encouraged reabsorption in some distal sites (secondary hyperaldosteronism). 4) Infusion of angiotensin II in sub- or pauci-pressor doses causes an isosmotic sodium saving, since it reduced the glomerular filtrate and increases the fraction of filtrate reabsorbed by the proximal tubules; the tubular effect is likely secondary to increased vascular, especially postglomerular resistance. In the healthy subject, angiotensin II leads to antidiuresis referable, on account of its intensity and longer time cycle, to ADH release angiotensin-dependent.
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PMID:[Physiological basis of homeostasis of the extracellular fluid volume]. 23 4

Hypothalamic lesions occasionally lead to excessive hypernatraemia and hyperosmolarity which cannot be explained by defective ADH secretion alone. As osmoregulation is a complex system the clinical features differ widely from one patient to another. In general central dysregulation of osmolarity is due to diffuse hypothalamic lesions, e.g. inflammatory inflammatory infiltration by histiocytosis X or by large suprasellar tumours. We report on a ten-year-old girl suffering from a suprasellar spongioblastoma and a twelve-year-old-girl, who had been operated for a large craniopharyngioma. Polyuria and polydipsia were not present. Whereas one patient presented hypernatraemic crises and showed normal osmolarity at the intervals, the other patient suffered from sustained hypernatraemia and hyperosmolarity. In the first patient water loading led promptly to clinical and laboratory normalisation. In the other case water loading failed to decrease hyperosmolarity but led to oedema. In the first patient hypernatraemic crises were combined with decreased serum potassium levels and elevated urinary aldosterone excretion. Therefore acute and long-term trials of spironolactone treatment were successful. Exogenous ADH-derivatives failed to normalize hyperosmolarity. In the other patient, however, DDAVP decreased the serum sodium level seen with small doses.
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PMID:[Hypothalamic hyperosmolarity in childhood (author's transl)]. 31 68

Angiotensin II is dipsogenic, and vasopressin (ADH) regulates renal water excretion. Together, these hormones govern overall mammalian water balance. The Brattleboro rat with inherited diabetes insipidus (DI) lacks ADH and is therefore a convenient model with which to elucidate mechanisms regulating water metabolism. In the present studies, angiotensin II has also been removed from DI rats by the administration of an inhibitor (captopril, SQ 14225; D-2-methyl-3-mercaptopropanoyl-L-proline) of the enzyme which converts angiotensin I, the relatively inert component of the renin-angiotensin system, to angiotensin II, the biologically active substance. SQ 14225 reduced the drinking rates, and after 6 days lowered peripheral plasma aldosterone concentrations were associated with hyperkalaemia. We conclude that the polydipsia of diabetes insipidus partly results from elevated plasma renin activities and angiotensin II concentrations seen in this syndrome. Further, the apparent hypoaldosteronism of DI Brattleboro rats reflects differences in both tissue usage of the steroid and adrenocortical sensitivities associated with polyuria, hyperosmolarity and possibly potassium wasting.
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PMID:Captopril (SQ 14225) depresses drinking and aldosterone in rats lacking vasopressin. 38 37

We have experienced with 50 cases of parasellar tumors, four cases of which had persistent thirst, polydipsia, polyuria, and reversible temporary hyponatremia secondary to hypernatriuresis. The mechanism of the syndrome in these four cases could not be explained by either that of the syndrome of hypernatremia or of the so-called SIADH. We tentatively named this syndrome as "CEREBRAL POLYURIC HYPONATREMIA" and the criteria of this syndrome as as follows: 1) persistent thirst, polydipsia polyuria, 2) reversible temporary hyponatremia secondary to hypernatriuresis, 3) exception of the following items--administration of uretic drugs, renal and adrenal dysfunction, hyperglycemia, hyperlipemia, overadministration of water, and poor administration of NaCl. The mechanism of this syndrome is presumed as follows: 1) compression by a tumor or surgical attack to the anterior hypothalamus, 2) disturbance of the mechanism of ADH secret-on, 3) extrasecretion of natriuretic factor possibly produced in the anterior hypthalamus, and 4) preservation of the thirst center.
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PMID:[Cerebral polyuric hyponatremia--discussion of a new syndrome with disturbance of electrolyte balance of central origin (author's transl)]. 55 42

Seven chronically prepared dogs (electromagnetic flow transducers around the pulmonary and left renal artery, left atrial catheter) maintained on a controlled sodium and water intake were studied. About 20 h after the last intake of food and water, the effects of i.v. methohexitone (initial dose: 6.10 +/- 0.84 mg/kg bw; sustaining infusion: 0.34 +/- 0.10 mg/min.kg bw) on renal excretion of sodium, potassium, urea and water as well as on several haemodynamic values were investigated over a period of 60 min (MP) after a control period (CP) of 60 min in the unanaesthetized state. In 18 of 19 experiments water diuresis (U/Posm less than 1) was observed between 20 and 40 min after starting the administration of methohexitone. Urine volume increased from 44 +/- 21 microliter/min.kg bw (CP) to 104 +/- 62 microliter/min.kg bw (MP).I.v. administration of arginine-vasopressin (ADH) completely abolished water diuresis. During MP, there was a decrease in cardiac output (-11%), stroke volume (-36%) and left atrial pressure (-27%), heart rate increased (+ 43%). Mean arterial blood pressure and renal blood flow did not change. It is assumed-as plasma osmolality did not change-that the central release of antidiuretic hormone is suppressed by methohexitone.
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PMID:[Water diuresis during methohexitone anaesthesia. Studies in chronically instrumented dogs (author's transl)]. 65 67

The cases of diabetes insipidus (DI) after surgery of intracranial aneurysms were reported and discussed. 1. Of 112 patients operated on for intracranial arterial aneurysm (microsurgical approach), four patients (3.6%) showed DI in the postoperative period. In 3 cases of these 4, the aneurysms located on the anterior communicating artery and the remaining one was the posterior inferior cerebellar artery. 2. The exact mechanism of occurrence of DI is obscure. We suppose that not only vascular spasm of branches of the anterior cerebral and anterior communicating arteries supplying to the paraventricular and preoptic nucleus, but also surgical trauma with direct tissue injury might explain the symptoms. 3. All patients showed a monophasic type of DI which started 1 to 4 days after surgery and lasted from 6 up to 9 days. 4. Two patients with DI showed decreased plasma ADH values below 0.6 microunits/ml in the few days prior to the appearance of abnormally large amount of urinary output. Therefore, once the diagnosis of postoperative DI is made, the patients should be managed promptly with the replacement therapy of Aqueous pitressin. 5. A slow continuous infusion of Aqueous pitressin in the range of 1 to 1.5 IU/hr effectively reduce the polyuria which were not controlled by intermittent intramuscular injections.
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PMID:[Diabetes insipidus after surgery of intracranial arterial aneurysms--with special reference to the human ADH and aldosterone secretion (author's transl)]. 72 83

In anaesthesized dogs given large doses of ADH and DOC and subjected to acute left renal denervation, urine flow (V) and sodium excretion (UNaV) rose significantly in response to bilateral carotid artery clamping in both the intact (p less than 0.05) and the denervated kidney (p less than 0.001). This was associated with significant (p less than 0.05) increases of the tubular rejection fraction of sodium (TRFNa) while creatinine clearance (Ccr) remained unchanged. Following a second control period, carotid occlusion was repeated, while perfusion pressure in the left kidney was kept constant by aortic constriction. In this case the diuretic and natriuretic response in the right kidney occurred in the same fashion as previously, and no significant change in V, UNaV, or TRFNa was observed in the left kidney. The amount of free water reabsorbed in the collecting duct (TcH2O) was not consistently altered by carotid occlusion. It is concluded that acute renal denervation augments the pressure diuresis that follows carotid occlusion. The failure of carotid polyuria to occur when renal perfusion pressure is kept constant points to the importance of mechanical factors. Still, a wash-out of the medullary osmotic gradient seems to be an unlikely mechanism.
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PMID:Mechanism of carotid-occlusion diuresis. 75 93

1. A lithium chloride (1.1 g/kg) supplemented diet was given to Long Evans (LE) and Brattleboro (DI) rats to investigate its actions in the presence (LE) and absence (DI) of vasopressin. 2. During the first 24 h, Li-supplemented LE rats displayed an initial water deficit (drinking less than renal output), increased plasma antidiuretic (ADH) titres and slightly increased plasma renin activities (PRA) and plasma osmolarities. Such changes were qualitatively similar to those seen in rats fed a normal diet, but deprived of water for 24 hours. After 12 days, the Li-supplemented rats had elevated plasma ADH titres, but reduced pituitary oxytocic and antidiuretic activities. 3. The urinary losses of Na, K and Cl exceeded dietary intakes in LE rats on the introduction of the Li-supplement, and the urinary osmolarity fell by 50%. Electrolyte balances were gradually re-established, although drinking and urine production increased in parallel to reach twice the control values by day 12 of the supplement. 4. Aldosterone and corticosterone secretory rates and their peripheral plasma concentrations were unchanged both after 24 h and 28 days of the Li-supplement. 5. Li elicited no water deficit or saluresis in DI rats, and although the polyuria and polydipsia were exacerbated, urinary osmolarity did not change over the 12 day observation period. 6. Li increased Ca excretion in both rat types; after 12 days the PRA of DI but not LE animals were increased. 7. It is concluded that the overall renal actions of Li are tempered by vasopressin rather than adrenocorticosteroids.
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PMID:Time course of lithium-induced alterations in renal and endocrine function in normal and Brattleboro rats with hypothalamic diabetes insipidus. 85 9


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