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)

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

1. In conscious rabbits an i.v. infusion of 30 or 60 microgram E. coli pyrogen/kg body wt. decreased urine flow from control of 1.13 +/- 0.11 (S.E. of mean) ml./min to 0.43 +/- 0.09 ml./min while urine osmolality increased from 212 +/- 16 to 679 +/- 82 m-osmole/kg H2O. Clearances of exogenous creatine and p-aminohippurate did not change significantly. 2. Plasma antidiuretic activity (rat bio-assay) increased from control of 15.5 +/- 4.2 to 56.8 +/- 5.5 muu./ml. at the top of antidiuresis. 3. Comparable urine flow and osmolality changes were evoked by a pyrogen dose of only 0.2 microgram per animal injected into the lateral cerebral ventricle. 4. The results suggest that in the rabbit pyrogen stimulates ADH release by an unknown central mechanism.
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PMID:Antidiuretic action of intravenous and intracerebral pyrogen in conscious rabbits. 36 8

A systematic study has been undertaken to improve the understanding of water regulation in premature babies who are artificially ventilated. Thirty nine premature babies, 16 normal (Group N, GA 31.4 weeks, B/W 1622 g) and 23 with respiratory distress syndrome who were ventilated with or without continuous positive pressure (Group V, GA 31 weeks, BW 1505 g) have been studied. Plasma osmolalities were the same in both groups (284 and 282 mosM/Kg H2O) but there were significant differences (p less than 0.001) between the urine osmolalities N = 150.6 +/- 19.6 V = 294 +/- 25.9 mosM/Kg H2O) and the plasma ADH levels of the two groups (N = 2.9 +/- 0.4 pg/ml, V = 12.2 +/- 2.4 pg/ml). There was a significant correlation between the urine osmolality and the plasma ADH level but not between plasma osmolality and the plasma ADH level. Several hypotheses can be proposed but none are satisfactory.
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PMID:[Plasma vasopressin in premature infants on mechanical ventilation]. 37 63

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

Ethanol and drugs can affect each other's absorption, distribution, metabolism, and excretion. When ingested together, ethanol can increase drug absorption by enhancing the gastric solubility of drugs and by increasing gastrointestinal blood flow. However, high concentrations of ethanol induce gastric irritation causing a pyloric spasm which in turn may delay drug absorption and/or reduce bioavailability. The 'quality' of the alcoholic beverage, independent of its ethanol content, can contribute to altered absorption of a drug. Ethanol is not bound to plasma proteins extensively enough to modify drug distribution. However, serum albumin levels in chronic alcoholics may be abnormally low so that some drugs, e.g. diazepam, have an increased volume of distribution. In addition to the amount ingested, the duration of regular intake determines the effect of ethanol on drug metabolism. Acute intake of ethanol inhibits the metabolism of many drugs but long term intake of ethanol at a high level (greater than 200g of pure ethanol per day) can induce liver enzymes to metabolise drugs more efficiently. At the present time there are no accurate means, with the possible exception of liver biopsy, to clinically predict the capacity of an alcoholic to metabolise drugs. Several drugs can inhibit the metabolism of ethanol at the level of alcohol dehydrogenase. Individual predisposition determines the severity of this drug-ethanol interaction. During its absorption phase, ethanol inhibits the secretion of antidiuretic hormone and is also able to induce increased excretion of a drug through the kidneys. However, chronic alcoholics with water retention may show reduced excretion of drugs via this route. At the pharmacodynamic level, ethanol can enhance the deleterious effects of sedatives, certain anxiolytics, sedative antidepressants and antipsychotics and anticholinergic agents, on performance. Mechanisms of lethal interactions between moderate overdoses of ethanol and anxiolytics/opiates/sedatives are poorly understood. On the other hand, certain peptides, 'nonspecific' stimulants, dopaminergic agents and opiate antagonists can antagonise alcohol-induced inebriation to a significant degree.
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PMID:Drug interactions with alcohol. 38 74

The activity of demeclotetracyclin, and ADH antagonist, is studied in 11 ethylic patients with cirrhosis of the liver, under a large hydric diet (1500 cm3). The prescription of the cyclin (600 mg daily) is always determined by a fall of the urinary osmolarity (-36%) and by a dramatic improvement of the free water clearance (+ 60%); consecutively, we observe an increase of natremia in 8 out of 9 cases. Associated with Spironolactone (200 mg daily) the anti-ADH activity persists (the free water clearance becomes positive in 5 out of 10 patients), in spite of the natriuretic activity of anti-aldosterone ; a minimal fall of the natremia is observed in only 2 cases. The indication of Demeclotetracyclin in the curative or preventive treatment of the hyponatremia of the liver cirrhosis is discussed.
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PMID:[Use of demeclotetracycline in the treatment of hyponatremia in cirrhotic ascitis]. 40 86

The uptake of C14-urea into everted and noneverted bladder sacs was compared, over short time periods (up to 2 min), with the transepithelial urea fluxes. This method allowed the study of the time course of urea uptake and distribution, while previously this problem was only studied in steady-state conditions. When mucosal uptake was studied no accumulation of C14-urea inside the tissue was observed, indicating that the mucosal border could be the limiting step. Comparative studies of urea and inulin uptake from the serosal side showed that urea equilibrated with the water epithelial cells in less than 30 sec. This accumulation suggested again that the mucosal border is an effective barrier for urea translocation. The kinetics of the increase in urea permeability induced by antidiuretic hormone was also studied and it was similar (T1/2:4.3 min) to the kinetics of the increase in water permeability induced by the hormone (T1/2:5.6 min). A strong parallelism was also observed between the time course of the increases in water and urea permeabilities induced by medium hypertonicity (T1/2 25 and 26 min, respectively). The values obtained for the permeability coefficient ktrans), either at rest or under ADH were similar to those previously reported employing steady-state techniques (28+/-8 and 432+/-25 cm-sec-1-10(-7), respectively).
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PMID:Urea uptake and translocation in toad urinary bladder: the effect of antidiuretic hormone. 40 46

1. The effects of hypertonic saline infusion into the third ventricle were investigated in ten monkeys which were pre-operated, trained, and used in the conscious state under controlled conditions. 2. In non-hydrated monkeys, intraventricular infusion of NaCl 1.0 M, 0.01 ml./min for 30 min did not affect urine volume or Na output but produced a small increase in urine osmolality. Comparable infusion of NaCl 0.15 M had no effect on any parameter. 3. In monkeys undergoing water diuresis (with i.v. infusion of 5% dextrose), intraventricular hypertonic saline produced large reciprocal changes in urine volume and osmolality while urine Na showed no significant change. The effects on urine volume and osmolality were greater than those of lysine-vasopressin 30 m-u./kg i.v. 4. The absence of natriuresis after intraventricular hypertonic saline infusion in the monkey was in notable contrast to the results reported in lower species. However, the data suggested that the infusion probably released ADH as in other species.
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PMID:Search for a natriuretic mechanism sensitive to sodium in the brain of the monkey. 41 58

Experiments were carried out in different segments of the intestine of unanaesthetised rats to assess the effect of vasopressin on intestinal absorptive processes. The following data were observed. (1) Within a physiological range of doses (Aziz, 1969), ADH diminished the net sodium absorption mainly by reducing the unidirectional sodium influx, whereas the behaviour of the efflux was not uniform. (2) The unidirectional volume fluxes showed the same behaviour as did the sodium fluxes. (3) ADH produced an oral-aboral gradient (jejunum greater than ileum greater than colon). (4) ADH did not significantly change the transfer of actively transported sugars; it did influence, however, passively transported substances. (5) During the intravenous application of ADH, a substance was secreted into the perfusion solution which diminished the absorption of volume and electrolytes. (6) Cyclic AMP acted on intestinal absorption in the same way as did ADH. In view of these results two mutually independent transport pathways for sodium and water are supposed, one of which is influenced by ADH or cAMP. Based on a two membrane model, an ADH mechanism is discussed: the permeability of the luminal membrane system is enhanced in the presence of vasopressin.
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PMID:Intestinal absorption under the influence of vasopressin: studies in unanaesthetised rats. 42 21

The pathogenesis of the rare hypernatremia, usually described in the literature as "neurogenic" or "essential" hypernatremia, consists of defective thirst mechanism either alone or in combination with impaired osmoregulation of ADH release. As etiology, disturbances of the neoplastic, vascular and degenerative type and malformations in the hypothalamic area are known. In patients with the hypodipsia-hypernatremia syndrome, dysfunction of the anterior pituitary lobe, obesity, abnormal regulation of body temperature, psychomotor retardation and episodic muscular weakness are frequently encountered as additional abnormalities. A 6-year-old patient is described with hypodipsia-hypernatremia syndrome manifest for 3 years. Besides hypernatremia, hypodipsia and the relative insensitivity of the osmoreceptors regulating ADH release, elevated body temperature, polyphagia and obesity, partial hypothalamic-hypophyseal dysfunction, lethargy and psychomotor retardation are the principal findings. An inflammatory lesion or one occupying an intracranial space was not demonstrable until now. Under forced water intake and hypocaloric diet the patient has progressed well with nearly complete normalization of the hypernatremia, body temperature and obesity.
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PMID:Hypodipsia-hypernatremia syndrome. 42 94


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