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)

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

1. A dye-linked alcohol dehydrogenase was purified 20-fold from extracts of Rhodopseudomonas acidophila 10050 grown anaerobically in the light on methanol/HCO3-. 2. The enzyme resembled many previously reported methanol dehydrogenases from other methylotrophic organisms in coupling to phenazine methosulphate, requiring ammonia as an activator, possessing a pH optimum of 9 and a mol.wt. of approx. 116000. In many other respects the enzyme showed singular properties. 3. The stability of the enzyme under various conditions of temperature and pH was studied. 4. Primary aliphatic amines containing up to nine carbon atoms (the longest tested) were better activators than ammonia. 5. A wide range of primary alcohols and aldehydes served as substrates, with apparent Km values ranging from 57 mM for methanol to 6 micron for ethanol. 6. O2 was an inhibitor competitive with respect to the alcohol substrate. In the presence of O2, apparent Km values of 145 mM were recorded for methanol. 6. Cyanide and alphaalpha'-bipyridine were inhibitors competitive with respect to the amine activator. 7. The properties of the enzyme from Rhodopseudomonas acidophila are compared with those of similar enzymes from other organisms, and implications of the salient differences are discussed.
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PMID:The dye-linked alcohol dehydrogenase of Rhodopseudomonas acidophila. Comparison with dye-linked methanol dehydrogenases. 64 93

Respones to bumetanide were studied in five ewes. During ADH infusion urine flow increased from less than 1-0 to approximately 11-5 cm3 min-1 within 30 min of intravenous injection of 0-02 mg kg-1 bumetanide and returned to approximately 2-0 cm3 min-1 within 3 h of dosing. The diuresis was accompanied by large increases in sodium and chloride excretion and smaller increases in potassium and free hydrogen ion excretion. Bicarbonate excretion and TCH20 were reduced. Plasma potassium and chloride concentrations decreased slightly while arterial bicarbonate pH and pCO2 slightly increased. A transient increase in GFR and RPF was followed by a small reduction in GFR. No change in CH20 was observed after bumetanide injection during water diuresis. Increasing the dose of bumetanide over the range 0-002 to 0-20 mg kg-1 resulted in more pronounced and prolonged responses. The results show that bumetanide is a potent diuretic in sheep with its main site of action on the ascending limb of Henle's loop.
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PMID:The effects of bumetanide on renal function and blood composition in sheep. 103 Aug 18

Differential interference contrast microscopic images were used to assess the cell volume regulatory increase (VRI) response of rat IMCD segments isolated from the mid-inner medullary region of pathogen-free Sprague-Dawley rats and perfused in vitro at 37 degrees C. In the absence of ADH. IMCD cells behaved in an osmometric fashion over the range of extracellular osmolalities 290 to 386 mOsm/kg H2O and had an osmotic space equal to 54.2% of total geometric volume. After initial shrinkage in hypertonic perfusing and bathing solutions (340 mOsm/kg H2O using sucrose), cell volume increased rapidly to the isotonic value only in tubules preincubated in ADH (100 microU/ml). The rates of VIR were: (-ADH) 0.0142 +/- 0.0046 nl.min-1.cm-1 or 0.30 +/- 0.10%/min and (+ADH) 0.7225 +/- 0.1278 nl.min-1.cm-1 or 15.42 +/- 2.31%/min (N = 4; P less than 0.01). An overshoot in cell volume was observed on return to isotonic media only in the ADH exposed tubules showing a hypertonic VRI response, indicating that IMCD cells accumulated solute during hypertonic VRI. In the absence of ADH, one mM dibutyryl cyclic AMP mimicked the effect of hormone on hypertonic VRI. This ADH-dependent VRI process required Na+ and (CO2 + HCO3-) in external media and was reduced or abolished by 0.1 mM amiloride, 0.1 mM 4,4'-diisothiocyanatostilbene-2,2-'-disulfonic acid (DIDS) in peritubular solutions. These data suggest that ADH-dependent, rapid hypertonic cell volume regulation in rat inner medullary collecting duct depends on NA+ uptake, which may be mediated by parallel Na+-H+ and an HCO3(-)-dependent. DIDS-sensitive pathway (such as, Cl+-HCO3- exchanger) in basolateral cell membrane. In addition, a luminal amiloride-sensitive pathway (most likely the cation-selective channel) may contribute to cell volume regulation in the rat IMCD.
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PMID:Rapid hypertonic cell volume regulation in the perfused inner medullary collecting duct. 255 37

The short-term (30 days) effects of lithium carbonate on ADH secretion, urinary enzyme secretion (specific markers of tubular damage), fractional excretion of sodium, calcaemia, calciuria and fractional reabsorption of phosphate, plasma and urinary Ca, urea and creatinine clearance were assessed in 15 female patients with emotional disorders. An immediate increase in diuresis was noted. At least in the acute initial phase, this phenomenon appears to be caused by inhibited ADH incretion. No significant variation were noted in calciuria or the fraction of sodium secretion but there was a significant increase of enzymuria, confirming the potential nephrotoxicity of lithium treatment.
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PMID:[Lithium and the kidney. Acute effects on ADH secretion and enzymuria]. 286 50

We studied the effects of cyclic AMP (cAMP) on HCO-3 transport by rabbit cortical collecting tubules perfused in vitro. Net HCO-3 secretion was observed in tubules from NaHCO3- loaded rabbits. 8-Bromo-cAMP-stimulated net HCO-3 secretion, whereas secretion fell with time in control tubules. Both isoproterenol and vasopressin (ADH) are known to stimulate adenylate cyclase in this epithelium; however, only isoproterenol stimulated net HCO-3 secretion. The mechanism of cAMP-stimulated HCO-3 secretion was examined. If both HCO-3 and H+ secretion were to occur simultaneously in tubules exhibiting net HCO-3 secretion, cAMP might increase the net HCO-3 secretory rate by inhibiting H+ secretion, by stimulating HCO-3 secretion, or both. These possibilities were examined using basolateral addition of the disulfonic stilbene (4,4'-diisothiocyanostilbene-2,2'-disulfonate (DIDS). In acidifying tubules from NH4Cl-loaded rabbits, DIDS eliminated HCO-3 reabsorption, a result consistent with known effects of DIDS as an inhibitor of H+ secretion. In contrast, cAMP left acidification (H+ secretion) intact. DIDS applied to HCO-3 secretory tubules failed to increase the HCO-3 secretory rate, indicating minimal H+ secretion in HCO-3 secreting tubules. Thus, inhibition of H+ secretion by cAMP could not account for the cAMP-induced stimulation of net HCO-3 secretion. cAMP-stimulated HCO-3 secretion was reversibly eliminated by 0 Cl perfusate, whereas luminal DIDS had no effect. Bath amiloride (1 mM) failed to eliminate cAMP-stimulated HCO-3 secretion when bath [Na+] was 145 mM or 5 mM. cAMP depolarized the transepithelial voltage. The collected fluid [HCO-3] after cAMP could be accounted for by electrical driving forces, suggesting that cAMP stimulates passive HCO-3 secretion. However, cAMP did not alter HCO-3 permeability measured under conditions expected to inhibit transcellular HCO-3 movement (0 Cl- solutions and bath DIDS). This measured HCO-3 permeability was not high enough to account, by passive diffusion, for the HCO-3 fluxes observed in Cl-containing solutions. We conclude the following: cAMP increased net HCO3- secretion by stimulating HCO3- secretion and not by inhibiting H+ secretion; this HCO3- secretion may have occurred by Cl-HCO3- exchange; Na+-H+ exchange appeared not to play a role in basolateral H+ extrusion under these conditions; and the stimulation of HCO3- secretion by isoproterenol, but not ADH, suggests the existence of separate cell cAMP pools or cellular heterogeneity in this cAMP response.
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PMID:Cyclic adenosine monophosphate-stimulated bicarbonate secretion in rabbit cortical collecting tubules. 298 40

Hypercalcemia is associated with impaired urinary concentrating ability. To explore the mechanism(s) by which hypercalcemia impairs chloride transport in the loop of Henle, we carried out in vivo microperfusion of the loop segment in Sprague-Dawley rats rendered acutely hypercalcemic (12.1 +/- 0.1 mg/dliter) by calcium gluconate infusion. Control rats were infused with sodium gluconate and had normal plasma calcium (8.0 +/- 0.2 mg/dliter). Compared to control, fractional chloride reabsorption was decreased (61 +/- 4 to 50 +/- 3%; P less than 0.05) and early distal chloride increased 74 +/- 6 to 98 +/- 3 mEq/liter (P less than 0.001) in hypercalcemia. During hypercalcemia, infusion of verapamil failed to increase fractional chloride reabsorption (49 +/- 4%; P less than 0.05) or decrease early distal chloride (95 +/- 2; P less than 0.05) toward control values. Similarly, indomethacin did not improve fractional chloride reabsorption (48 +/- 4%; P less than 0.05) or distal chloride concentration (93 +/- 7; P less than 0.05). In control rats infused with Ringers HCO3, the addition of calcium 8.0 mEq/liter to the perfusate increased early distal calcium (9.22 to 3.11 mEq/liter) but was associated with no change in fractional chloride reabsorption (-6 +/- 6%) and a slight decrease in early distal chloride (-9 +/- 3 mEq/liter; P less than 0.05). These data are consistent with the hypothesis that an elevated plasma, not luminal calcium, concentration impairs chloride reabsorption in the loop segment, primarily the ADH-stimulated component. This may have an important role in the urinary concentrating defect of hypercalcemia.
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PMID:Role of the loop segment in the urinary concentrating defect of hypercalcemia. 348 71

Experiments on 220 albino rats showed that lithium carbonate, chloride and nicotinate had different capacities to suppress ethanol dependence induced by a three-month administration of alcohol, with lithium nicotinate showing the greatest activity. The efficacy of the drugs correlated with the normalization of the activity of alcohol dehydrogenase, catalase and the levels of nicotinamide coenzymes and lipid peroxides in the brain, liver and kidneys. The drug administration was attended by an increased EEG synchronization, expanded range of perceived frequencies and enhanced synchronization energy. The above changes occurred with all lithium salts, being, however, most prominent with lithium nicotinate.
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PMID:[Comparative evaluation of the suppressive effects of lithium preparations in the treatment of experimental chronic habituation to alcohol]. 608 85

An SH reactive agent, N-ethylmaleimide (NEM), if introduced in the serosal bath (10(-4) M), stimulates the short circuit current (SCC) across the frog skin. This effect is due to an increase of Na active transport, because is inhibited by ouabain (10(-4) M). A stimulatory action on Cl- or HCO3- secretion can be ruled out because the rise in SCC occurs also in the absence of Cl- or HCO3-. It is known that NEM inhibits the ADH action by forming covalent bounds with SH groups of ADH membrane receptors (1). Thus it is possible that this binding should mimic the ADH action on SCC. In order to test this hypothesis, we studied the effect of serosal NEM on SCC both in the absence and in the presence of I midazol (20 mM), an activator of the cyclic AMP phosphodiesterase. Imidazol treatment decreases the effect of NEM on SCC. Thus we conclude that NEM serosal treatment is able to mimic some ADH effects, by using the same ways of the ormone action.
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PMID:[Effect of N-ethylmaleimide, introduced in to the serous fluid, on the active transport of sodium through the skin of Rana esculenta]. 660 55

The aim of this article is to consider how a large quantity of potassium (K+) can be excreted without the development of hyperkalemia. The hypothesis will focus on interactions between K+ and HCO3- primarily within the kidneys. It is speculated that the absorption of K+ from the gastrointestinal tract is accompanied by an initial addition of HCO3- to the body; this in turn could, via intrarenal events, promote the delivery of HCO3- to the cortical collecting duct (CCD), where interactions may permit the development of a very high rate of excretion of K+. To test one portion of this hypothesis, studies were performed in sheep because they normally consume approximately 10-fold more K+ per kilogram body weight than do humans. In the absence of a significant degree of anabolism, there is only a limited potential to shift K+ acutely into cells. Hence, an extremely large capacity to excrete K+ is required to avoid a severe degree of hyperkalemia. The excretion of K+ depends primarily on the ability to have a sustained rise in the (K) in each liter of luminal fluid exiting the CCD to very high levels and to have a large number of liters of fluid exit the terminal CCD while antidiuretic hormone is acting. A reasonable approximation of this CCD flow rate can be obtained by examining the osmole excretion rate when ADH acts. Because these sheep excreted 1,650 mosmol (2 L x 827 mosm/kg H2O) per day, a minimum estimate for volume delivery out of the CCD is 5 to 6 L/day.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Potassium excretion: a story that is easy to digest. 787 41


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