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:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The calcium-regulating enzyme calcium adenosine triphosphatase (Ca-ATPase) was localized in the epithelium of amphibian urinary bladder by the one-step electron microscopic cytochemical procedure. The enzyme was identified along the basolateral border of the epithelial cells that comprise the bladder mucosa. The electron-dense precipitate indicating Ca-ATPase activity was seen in association with the outer leaflet of the basolateral plasmalemmae. Intracellularly, Ca-ATPase activity was seen in association with the mitochondrial matrix of the mitochondria-rich cells. Ca-ATPase was not seen along the apical microvillated border. Enzyme activity was also not seen after incubation in substrate-free media, calcium-free media, or incubation in the presence of vanadate. However, Ca-ATPase activity was evident when the calcium in the standard reaction medium was deleted in favor of magnesium. Addition of antidiuretic hormone (ADH; vasopressin) increased both the basolateral Ca-ATPase reaction and the mitochondrial reaction. Such data appear to indicate further that changes in cytosolic calcium ion concentration take place during the response of amphibian urinary bladder to the polypeptide hormone vasopressin.
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PMID:Electron microscopic cytochemical localization of Ca-ATPase in toad urinary bladder. 294 49

There appears to be two distinct natriuretic factors. One group, suspected since 1951 in overloaded dogs, had a low molecular weight: it belongs great affinity for ouabain, binds to digoxin antibodies and inhibits NA-K ATPase; this group seems heterogeneous in spite of the extraction of an amino glucosteroid-like substance from human urines. These factors are vasoconstrictor; the source is not still well known (hypothalamus ?). The atrial natriuretic factor (ANF) is a peptide about 20 to 25 amino acids and comes from a precursor of 152 amino acids, its synthesis was successful; secreted in the plasma from endocrine atrial granules, it causes striking natriuresis and diuresis and relaxes vascular and intestinal smooth muscle; it acts on guanylate cyclase but its renal mechanism of action is not well known; it constitutes an antagonist axe to ADH and RAA system. The relations between the two groups of natriuretic factors do not seem still very clear.
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PMID:[Natriuretic factors]. 295 21

Brain (Na+ + K+)-ATPase was protected by low concentrations of GSH from the inhibitory effect of pyrithiamin. The possible involvement of sulfhydryl groups in the inhibition was then studied by comparing the effect of pyrithiamin with that of N-ethylmaleimide on the enzyme. The treatment of rat brain (Na+ + K+)-ATPase with thesee inhibitors caused a significant decrease in reactivity of the enzyme to N-ethyl[3H]maleimide. N-Ethylmaleimide, like pyrithiamin, inhibited the partial reactions of (Na+ + K+)-ATPase system in parallel with the inhibition of the overall reaction. An SDS-polyacrylamide gel electrophoresis procedure indicated that pyrithiamin and N-ethylmaleimide inhibited Na+-dependent phosphorylation of the alpha(+) form of rat brain (Na+ + K+)-ATPase more than that of alpha, though the selectivity for the alpha(+) seemed to be higher with the former inhibitor than in the latter. The treatment also decreased sensitivity of the enzyme to ouabain inhibition. However, pyrithiamin- and N-ethylmaleimide-induced inactivations of the enzyme differed in the efficacy of GSH for protection and in the effect of the kind of ligands present during the reaction. Furthermore, pyrithiamin did not appear to interact directly with sulfhydryl groups, but caused the formation of disulfide in bovine brain (Na+ + K+)-ATPase. In contrast to N-ethylmaleimide, pyrithiamin did not affect the sulfhydryl-enzymes such as alcohol dehydrogenase and L-alanine dehydrogenase. It is concluded that pyrithiamin modifies the functional sulfhydryl groups of brain (Na+ + K+)-ATPase in a way different from N-ethylmaleimide and causes a structural change and inactivation of the enzyme.
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PMID:Involvement of sulfhydryl groups in the inhibition of brain (Na+ + K+)-ATPase by pyrithiamin. 298 20

The medullary thick ascending limb (MAL), but not the medullary collecting tubule (MCT), has been shown to have an impaired adenylate cyclase (AC) responsiveness to ADH and a selective hypoplasia in Brattleboro diabetes insipidus (DI) rats. Since chronic ADH administration has been found to increase epithelium volume and basolateral membrane surface area in MAL but not in MCT, we investigated whether chronic ADH infusion would affect the hormone-sensitive AC and the Na-K-ATPase activity--two markers of the basolateral membrane--in single micro-dissected portions of thick ascending limb and collecting tubule in DI rats. Results indicate that 1. in MAL of ADH-treated rats, AC responses to in vitro AVP and glucagon and Na-K-ATPase activity increased to the same extent as did epithelium volume (60-80%); 2. changes in the other segments were independent of any morphological alteration. In the cortical thick ascending limb, AVP and glucagon-sensitive AC decreased by 30-40% whereas Na-K-ATPase activity did not change. In the collecting tubule, AC response to in vitro AVP was not altered by ADH-treatment but glucagon-sensitive AC dropped by 50% and Na-K-ATPase activity doubled, independently of any variation in plasma aldosterone and glucagon levels. These results show that, in the MAL, the ADH-induced variations in enzyme activity are a reflection of the enlargement of the basolateral membrane surface area. Further studies are needed to clarify the origin of enzymatic alterations in the other segments.
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PMID:Influence of chronic ADH treatment on adenylate cyclase and ATPase activity in distal nephron segments of diabetes insipidus Brattleboro rats. 299 94

In this report the disturbances in biochemistry of the heart muscle exposed to alcohol are delineated. All elements of cellular substructures are affected. In plasma membranes, (Na+ + K+)-activated ATPase (EC 3.6.1.3) is inhibited. Mitochondrial damage consists in diminished respiratory function and calcium uptake and binding. High-energy phosphates remain intact. Alcohol also affects the malate-aspartate shuttle. Acetaldehyde, a metabolite of ethanol, has a direct effect on myocardial protein synthesis through microsomal inhibition; however, the development of cardiac hypertrophy is not affected. Malfunction of sarcoplasmic reticulum is evidenced by disturbances in calcium binding and uptake. Effects of ethanol on the contractile machinery are deficiencies in the turnover rate of chemical into mechanical energy (diminished Vmax), and in the number of cross-bridges formed (P0). It increases stiffness of series elastic elements. There is diminished fatty acid oxidation with increased esterification. The involvement of CoA synthetase (EC 6.2.1.1), palmityl-carnitine transferase (EC 2.3.1.7), and pyruvate dehydrogenase complex in disturbed fatty acid oxidation is not certain. The role of catalase in myocardial ethanol oxidation was examined. Ethanol activates myocardial catalase-H2O2 complex (EC 1.11.1.6). The biochemical basis of fetal alcohol syndrome is low hepatic alcohol dehydrogenase (EC 1.1.1.1) activity during fetal life.
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PMID:Effect of alcohol on the heart and cardiac metabolism. 628 54

The effect on transepithelial Na transport of tizolemide was investigated in isolated frog skin (Rana temporaria). It was found that tizolemide (2-5 mM, serosal side) decreased transepithelial Na transport (measured as short circuit current and as net sodium flux) within 60 min to 25-40% of the control level resulting from reduction of the unidirectional sodium influx. Intracellular recording with microelectrodes revealed that these changes were associated with depolarization of the intracellular space to less than 40% of the control values (averaging - 71.7 +/- 5.1 mV) which is a consequence of a decrease in conductance of the basolateral border to about 25% of the control values. The conductance of the apical border was only slightly reduced. It is suggested that tizolemide blocks the partial conductance of potassium at the basolateral border which secondarily diminishes transepithelial Na transport due to a decrease of the driving force for apical border Na entry. A certain degree of inhibition of the Na-K-ATPase by tizolemide cannot be excluded. When vasopressin (ADH) was added to frog skin after treatment with tizolemide, the response was markedly reduced compared to that of untreated control preparations. Under these conditions, the conductance of the basolateral border increased while the apical border remained little influenced by the hormone--opposite to the response of frog skins under control conditions. It is concluded that the mode of action of ADH is more complex than has been recognized hitherto and includes effects at the basolateral border.
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PMID:Tizolemide-induced changes of passive transport components across the basolateral membrane of isolated frog skin. 628 44

Maternal ethanol consumption produces a reduction in postnatal growth. We have studied especially changes of liver and brain. This reduction is more marked if the alcoholic offspring are maintained with their biological mothers than if they are kept with surrogate mothers. Rats exposed prenatally to alcohol show a marked accumulation of fat in the liver and a significant proliferation of liver endoplasmic reticulum. No change in the postnatal development of liver alcohol (ADH) and acetaldehyde dehydrogenases (ALDH) (high and low Km) is observed in offspring from alcoholic mothers, with the exception of slightly higher ALDH (low Km) for the offspring that remain with alcoholic mothers. The postnatal development of the liver (Na+-K+) ATPase is also similar in control and alcoholic groups. However, in the case of the enzyme from the brain, a lower ATPase activity is observed in the group derived from alcoholic mothers. Interestingly, at 20 days of postnatal period, an induction of the ATPase (from liver and brain) was observed when the group of offspring from alcoholic mothers were kept on an alcohol diet.
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PMID:Effects of prenatal and postnatal exposure of rats to alcohol: changes in (Na+-K+) ATPase. 629 87

Salt and water balance in vertebrates in controlled by the release of two blood borne hormones: aldosterone and antidiuretic (ADH). It is the purpose of this chapter to review the mechanisms (at the plasma membrane level) by which these hormones cause an increase in salt (sodium) and water movement in the target tissues. The primary effect of aldosterone is to increase the Na+ permeability of the lumen-facing (apical) membrane by activation of pre-existing quiescent channels at short times, and by the incorporation of newly synthesized channels after prolonged exposure. Other effects might involve an increase in energy supply and synthesis of Na+-K+ ATPase which is responsible for Na+ extrusion from cell cytoplasm to blood. Similarly, ADH stimulates pre-existing quiescent apical membrane Na+ channels. The second effect of ADH is to increase epithelial water permeability. Evidence strongly suggests that water channels exist in cytoplasmic vesicles which, upon ADH challenge, fuse into the apical membrane causing a rapid increase in apical membrane hydraulic conductivity. The movements of vesicles are dependent on an intact cytoskeleton. Regulation of electrolyte and non-electrolyte transport will be discussed in the light of the above two mechanisms.
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PMID:Control of Na+ and water absorption across vertebrate "tight epithelia by adh and aldosterone. 631 91

The concept of a hypermetabolic state to explain metabolic tolerance to ethanol grew from the recognition that the rate of alcohol metabolism is, in general, limited by the rate at which mitochondria can reoxidize reducing equivalents and thus by the rate at which oxygen can be consumed by the liver. This relationship appears to be most important in conditions in which the alcohol dehydrogenase (ADH)/QO2 ratio is high and is not in conflict with observations suggesting that ADH can, under certain conditions, constitute a rate-determining step for ethanol metabolism in rodents. Liver preparations from animals fed alcohol chronically, in which an increase in ethanol metabolism is shown, consume oxygen at higher rates. This effect, concerning which there is discrepancy among investigators, depends on the type of preparation. Thyroid hormones play a permissive role in the development of the hypermetabolic state, while increased circulating levels of these hormones are not required. Antithyroid drugs inhibit both metabolic tolerance in vivo and the hypermetabolic state. While the hypermetabolic state requires an increased ATP utilization in the form of an adenosine triphosphatase, or an inhibition of ATP synthesis, the different mechanisms proposed for such an effect do not quantitatively account for the increases in oxygen consumption. In humans and animals chronically exposed to ethanol, but withdrawn, oxygen tensions in blood leaving the liver are significantly reduced. In some situations, low oxygen tensions in zone 3 of the hepatic acinus can reach critical hypoxic levels and may lead to cell necrosis. Studies in which the effectiveness of propylthiouracil is tested in human alcoholic hepatitis are discussed.
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PMID:Hypermetabolic state and hypoxic liver damage. 632 88

1. The redox state of mitochondrial NAD was monitored fluorometrically as a function of active ion transport work in the isolated doubly perfused bullfrog kidney. 2. Initial experiments to measure the O2 consumption (QO2) of small pieces from the bullfrog kidney gave a basal QO2 - 3.0 (+/- 0.43) nmoles O2/mg dry wt. min. Addition of 50 microM-ouabain inhibited QO2 by 72.7%. Subsequent addition of the mitochondrial uncoupler 1799 stimulated QO2 by 226%, while cyanide totally inhibited respiration. 3. Ion transport functional parameters and NADH fluorescence were simultaneously monitored during systematic reductions in perfusate PO2 to test the sufficiency of O2 delivery to the isolated perfused frog kidney. No significant changes in transport functions or fluorescence were observed until the PO2 dropped to 184 mm Hg or below. O2 tensions of 184 mm Hg or below caused decreases in G.F.R. and transport functions which were accompanied by an increase in NADH fluorescence. The lack of changes in kidney function in the PO2 range 550-340 mmHg suggested that the tissue is adequately oxygenated at the normal perfusate PO2 of 550 mmHg. 4. The relationship between active transport rate and NAD redox levels was studied by increasing transport work (via increased G.F.R. or ADH) or by decreasing transport work (via decreased G.F.R. or ouabain) while simultaneously monitoring the NAD redox state of the intact tissue fluorometrically. In all cases, an increase in work caused a net oxidation of NAD while a decrease in work caused a reduction of NAD. 5. It is concluded that the NADH fluorescence responses are indicative of mitochondrial active to passive transitions in response to changes in active transport work. The aerobic production of ATP and the normally functioning Na-K-ATPase appear to be essential to maintain active transport and to elicit the appropriate state transitions. Thus, ATP (and, possibly, ADP and Pi) may be part of the coupling mechanism linking active ion transport and aerobic metabolic rate in the kidney.
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PMID:Coupling of aerobic metabolism to active ion transport in the kidney. 696 4


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