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)

Reabsorption of osmotically free water (TmcH2O) was studied in 10 patients after renal transplantation. A rising or constant free water reabsorption was observed under hydropenia and increasing tubular solute load. These findings suggest that in the transplanted kidney the functioning nephrons respond in a normal way to plasma ADH-activity. The excretion of plasma-hypotonic urine reflects decreased antidiuretic activity as in overhydration rather than tubular unresponsiveness to ADH. The excretion of plasma-hypertonic urine indicates tubular reabsorption of osmotically free water due to ADH, and this in general rules out overhydration. Daily estimation of urinary and plasma osmolality will be useful in judging the actual state of hydration after renal transplantation.
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PMID:[Tubular response to antidiuretic plasma activity in the transplanted kidney (author's transl)]. 77 81

A study was performed on the effects of carbamazepine and of clofibrate in 7 cases of diabetes insipidus of high origin. In 4 cases the action of the two substances used in association was studied. Carbamazepine, in a dose of 0.60 g/day was effective in all cases with negativisation of free water clearance in 5 out of 7. Clofibrate, in a dose of 1.50 g/day was effective in 4 cases out of 7 with negativation of free water clearance in 2. Both medications act by provoking the secretion of anti-diuretic hormone by the hypothalamic/posterior pituitary centres and are thus only active if a minimal secretion of ADH is still possible. There is no apparent potentialisation of the two substances, which both require a minimal possibility of ADH secretion to be active. There is no diminution in the ADH secretor effect, since both products remain active for as long as they are given, making it possible to observe in 3 out of 7 cases spontaneous cure of the diabetes insipidus, allowing suppression of the treatment.
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PMID:[Comparative action of carbamazepine and clofibrate in diabetes insipidus. Study of 7 cases]. 80 54

The physiologic factors involved in vaseopressin (ADH) release and action are reviewed with emphasis on the interaction between osmotic and volume stimuli to the discharge of ADH. Abnormalities in reception of stimuli to ADH release, and in the impaired synthesis and release of ADH, are reviewed in relation to the causes of diabetes insipidus, and information on the biochemical changes which have been described in patients with nephrogenic diabetes insipidus is also discussed. We summarize the pathologic lesions and associated diseases found in 54 of our patients with diabetes insipidus. Criteria for establishing the diagnosis of diabetes insipdus are reviewed with emphasis on the dehydration test, including the importance of measuring plasma osmolality at the conclusion of water deprivation. Treatment of diabetes insipidus is briefly discussed with emphasis on the use of DDAVP and oral agents. The syndrome of inappropriate ADH secretion (SIADH) is reviewed including our experience with 39 patients. The differential diagnosis of SIADH, including the value of water loading and the measurement of ADH levels, is discussed. We comment on treatment of these patients including the use of investigational drugs. Lastly, we review the pharmacologic features and clinical relevance of some drugs which alter the release and action of ADH.
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PMID:Pathophysiologic and pharmacologic alterations in the release and action of ADH. 81 77

The effect of CPB on plasma ADH levels, urine flow, and urine osmolality was studied in nine patients. All patients received morphine, 1 mg. per kilogram, and 50 per cent nitrous oxide-50 per cent oxygen for anesthesia. CPB utilized a Travenol disposable bubble oxygenator and the prime consisted of 3 L. of Ringer's lactate. Measurements were made prior to induction of anesthesia , at 30 minutes following surgical incision, and at 15, 30, and 45 minutes during CPB. There were no statistically significant changes in mean arterial BP, cardiac index, serum sodium, or serum osmolality in any period. Urine flow increased from 0.99 +/- 0.3 ml. per minute to a high of 6.13 +/- 2.0 ml. per minute at 30 minute at 30 minutes on CPB (P less than 0.02). Urine osmolality declined from a control value of 691 +/- 142 mOsm. per kilogram to a low of 425 +/- 48 mOsm. per kilogram at 45 minutes on CPB (p less than 0.05). ADH levels rose from a control value of 4.3 +/- 1.5 to 13.0 +/- 3.3 pg. per milliliter with surgical stimulatiion (p less than 0.05). During CPB the ADH levels rose to a peak of 23.7 +/- 3.6 pg. per milliliter at 30 minutes (p less than 0.01) and were declining at 45 minutes. These data suggest that the stress of CPB results in an outpouring of ADH (or vasopressin) to function as a pressor to produce an increase in peripheral resistance. The ADH concentrations far exceed those required for normal physiologic control of water excretion and the urineflow will thus vary more with the hemodynamic changes than with the ADH levels.
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PMID:Antidiuretic hormone levels during cardiopulmonary bypass. 83 Oct 6

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

The syndrome of inappropriate ADH secretion ("SIADH") was first recognized 1935 by Roth et al. and described in detail 1957 by Schwartz et al. The clinical symptoms (hyponatremia, hypertonicity of urine and inability to excrete a water load) are caused by inadequately elevated ADH secretion under a variety of situations and diseases. Some recent work was focused on the pathogenesis of this syndrome and new clinical findings (low plasma levels of uric acid and potassium) as well as special forms ("SIADH" without elevated vasopressin levels in plasma) are thought to be of relevance. New therapeutical recommendations will be discussed.
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PMID:[The syndrome of inappropriate secretion of vasopressin (SIADH) (author's transl)]. 85 83

This study was undertaken to evaluate the effect of dopamine (D) on renal water excretion. Intravenous (i.v.) infusion of D (7.5 microgram/kg per min) was associated with a significant, reversible increase in free water excretion (CH2O) and a decrease in urinary osmolality (Uosmol). These changes, however, were associated with significant increases in renal blood flow (RBF), glomerular filtration rate (GFR), and urinary sodium excretion (UNaV). These increases could have been responsible for the diuretic response to D. To examine whether D has a direct effect on vasopressin (ADH) release, D was infused into one common carotid artery at a dose equal to one-fourth the i.v. dose. No effects on CH2O and Uosmol were observed. To examine whether D might have an antagonistic effect on ADH a single bolus of ADH (100 mU) was given to the same hypophysectomized dogs with and without D infusion. The antidiuretic response to ADH was the same, whether or not D was given concomitantly. The net changes in Uosmol and CH2O in response to ADH were not significantly different. Taken together, the present results provide no evidence for a direct effect of D on ADH release nor do they indicate an interference with the peripheral action of ADH. The dopamine-induced diuresis is probably the result of increased solute excretion. This, in turn, is the result of the combined effects of dopamine on increasing renal blood flow, GFR, and sodium excretion.
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PMID:Mechanism of dopamine-induced diuresis in the dog. 87 87

Infusions (20 microliter/min) of hypertonic (0.3 M) NaCl and angiotensin II (1 ng/kg min-1) in isotonic (0.15 M) NaCl were made for 1 h in the hydrated goat during fully developed water diruesis. Either H2O or deuterium (D2O) WAS USED AS SOLVENT. A pronounced antidiuretic response, outlasting the infusion period by 30 min or more, was seen when the substances were dissolved in H2O. Only a weak inhibition of the water diuresis, which was extinguished during the infusion period, was obtained when D2O was used as the solvent. The infusion of 0.3 M NaCl/H2O invariably induced drinking in one of the goats, which, however, showed no drinking response to the infusions of 0.3 M NaCl/D2O. The possibility is discussed that D2O (perhaps by its inhibitory effect on (Na+-K+)-ATPase activity) reduced the sensitivity of juxtaventricular receptors regulating ADH-release and water intake.
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PMID:Deuterium induced extinction of ADH-release in response to intracerebroventricular infusions of hypertonic NaCl and angiotensin. 89 28

The effect of bradykinin on the renal medullary osmotic gradient was evaluated in anesthetized dogs which were undergoing water diuresis and which received a unilateral renal arterial infusion of bradykinin. The effect of the peptide on the medullary osmotic gradient was determined by analysis of medullary tissue electrolyte and urea concentrations and by analysis of changes in urine osmolality induced by vasopressin. Bradykinin decreased the total osmolality per kg H2O in tissue from inner medulla and papilla (-18.7 +/- 6% and -19.3 +/- 8%) and increased fractional water excretion (3.8 +/- 1.3%). Furthermore, a direct relationship between changes in free water clearance and changes in papillary tissue, osmolality was found. Finally, the increase in urine osmolality after ADH was significantly less in vasodilated than in control kidneys. These results indicate that bradykinin can diminish the medullary osmotic gradient during water diuresis in the dog. Thus, a bradykinin-induced increase in free water clearance may be accounted for by other than an inhibition of proximal tubular sodium reabsorption.
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PMID:Effect of bradykinin on the renal medullary osmotic gradient in water diuresis. 90 88

Two female reindeer were hydrated by administration of (10% of b.wt.) water into the rumen. The diuretic response was very fast and strong but the urea and electrolyte excretion were little affected. Dehydration was carried out by not giving the reindeer water for 48 h. This water deprivation caused a loss of up to 20% of their body weight. The urine osmolality did not exceed 840 mosm/kg H2O, although the plasma osmolality rose from 300 to 346 and 368 mosm/kg H2O respectively. The plasma and urine urea concentrations were elevated during dehydration, while the urine urea excretion did not increase. Urine sodium concentration did not increase. When the urine flow rate, after two days of water deprivation, decreased to half of the original, the urine Na+ concentrations, instead of increasing, went down to half of the original. So did the potassium excretion. When ADH was injected intravenously into hydrated animals a dose of 30 mU of ADH was needed to induce antidiuresis or increased excretion of potassium. The resistance to ADH and the low relative thickness of the medulla confirm the limited capacity of reindeer kidney to concentrate urine or to excrete a solute load. On the other hand, reindeer is able rapidly to excrete surplus water without affecting the electrolyte or nitrogen balance.
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PMID:Responses of reindeer to water loading, water restriction and ADH. 92 Feb 4


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