Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P20020 (adenosine triphosphatase)
 3,299 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Treatment with neuraminidase decreased the activity of Na+,K+-activated Mg2+-adenosine triphosphatase in plasma membranes isolated from experimental granulation tissue but not that of 5'-nucleotidase or leucine-beta-naphthylamidase. A temporary lowering of the pH of the plasma membrane suspension to 2-3 inactivated all three enzymes, which remained inactive after the pH had been readjusted to 7.4. Addition of dextran preparations to the membrane suspension decreased the activity of adenosine triphosphatase. Ethanol (0.4%) had a similar effect. These marker enzymes of plasma membranes were not affected by additions of hyaluronate, chondroitin sulfate, protein polysaccharide or soluble collagen. Serotonin stimulated the adenosine triphosphatase activity slightly. About 10-20% of the protein in the plasma membrane preparation was extracted with EDTA. This "fuzzy coat" fraction yielded a distinct gel-electrophoretic protein pattern. Hyaluronidase was not helpful in cleaving this surface layer from the plasma membranes.
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PMID:Properties of plasma membranes from granulation tissue with reference to extracellular matrix. 0 56

A spinal cord injury was produced in Wistar rats by extradural compression of the cord with a Sugita aneurysm clip for 5 seconds. During a 2-week observation period following the injury, the tissue norepinephrine (NE), dopamine (DA), and serotonin (5-HT) concentrations decreased uniformly at and below the injured site. The chemical denervation of NE or 5-HT neurons produced by the intraspinal injection of 6-hydroxydopamine (6-OHDA) or 5,7-dihydroxytryptamine (5,7-DHT) 2 weeks before the injury did not cause a marked difference in the extent of hemorrhagic necrosis of the spinal cord after trauma as compared to control animals without pretreatment. In the rats pretreated with 6-OHDA, NE was decreased to less than 30% of control (non-pretreated) values, and, beginning at 5 days after injury, motor performance (assessed quantitatively with the inclined-plane method) was significantly improved compared to results in the non-pretreated control rats. The rats pretreated with 5,7-DHT showed no change from control animals. Spinal cord samples from non-pretreated control animals obtained at the injury site 30 minutes after the compression injury showed a marked decrease in the activity of synaptosomal Na+-K+-ATPase (adenosine triphosphatase) of about 50%, and an increase in both thiobarbituric acid reaction substance (about 170%) and cyclic guanine monophosphate (about 150%). The NE-denervated rats showed no significant changes in these three parameters. The results indicated that NE released after crush injury may impair the neuronal cell membrane around the lesion site by induction of lipid peroxidation. The possible mechanisms by which released NE may alter membrane function are discussed.
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PMID:Role of monoamines in experimental spinal cord injury in rats. Relationship between Na+-K+-ATPase and lipid peroxidation. 298 70

In brain of adult and developing rats the Na+-K+-adenosine triphosphatase (Na+-K+-ATPase) system seems to react to serotonin (5-HT) changes induced pharmacologically. A 5-HT agonist (quipazine) elicits a response of the enzyme activity in the cerebral cortex in vivo, which is neutralized with a 5-HT antagonist (methysergide). This effect was observed from day 21 to adulthood. Also in a state of 5-HT receptor hypersensitivity (rats treated early with 5,6-dihydroxytryptamine), the response of Na+-K+-ATPase to the 5-HT agonist was higher than without neurotoxic lesion of 5-HT paths. These data suggest an involvement of the Na+-K+-ATPase system in 5-HT receptor sensitivity in the rat brain.
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PMID:A serotonin agonist-antagonist reversible effect on Na+-K+-ATPase activity in the developing rat brain. 629 93

Disturbance of central serotoninergic system has been suggested in Down's syndrome (DS). In this syndrome the 5-HT concentration in blood platelets is below normal, but the mechanism behind this has been controversial. Recently, evidence has accumulated indicating a decreased active transport of 5-HT possibly due to lowered activity of Mg++-dependent Na+-K+-stimulated adenosine triphosphatase. In the present study the kinetic analysis of 5-HT uptake by blood platelets from DS patients revealed a decreased Vmax, suggesting decreased transport function but an unchanged affinity to the uptake receptors, as indicated by normal Km values. The controls were mentally retarded patients from the same institute. The uptake continued in a linear fashion up to 20 min., suggesting an unchanged storage of 5-HT. Also the effect of zinc on the 5-HT uptake was studied; plasma zinc levels have been noted to be lowered in DS infants. In vitro zinc caused a dose-dependent inhibition of uptake at 10(-5) and 10(-4) M. In vivo, after 2 weeks treatment 135 mg/day orally no significant effect was noted.
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PMID:Nature of lowered 5-hydroxytryptamine uptake by blood platelets of patients with Down's syndrome. 645 3

Sodium/potassium-activated adenosine triphosphatase (Na+/K+-ATPase) activity in the kidney and brain is high, and is regulated by catecholamines. Na+/K+-ATPase activity is also high in the basolateral infoldings of the strial marginal cells, where it aids in maintaining the characteristic electrolyte composition of the endolymph. To clarify the involvement of humoral control in strial function, particularly the role of catecholamines, the K+-dependent p-nitrophenylphosphatase (K+-NPPase) activity of strial marginal cells was investigated in guinea pigs using a cerium-based cytochemical method. The effects of reserpine, serotonin (5-HT), norepinephrine (NE), epinephrine (EP), both alone and in combination, were studied. High doses of reserpine cause depletion of sympathetic substances. Strial K+-NPPase activity was decreased after reserpine or dopamine treatment, and was increased after 5-HT, NE, and EP treatment. After reserpinization, repeated treatment with 5-HT, NE, or EP led to detectable strial enzyme activity. Thus, exogenous 5-HT, NE, and EP were able to restore strial K+-NPPase activity in the reserpine-treated animals. These results suggested that biogenic amines regulate strial K+-NPPase activity. Thus, the function of the stria vascularis may be regulated by the opposing actions of these catecholamines, and 5-HT.
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PMID:Cytochemical localization of Na+/K+-ATPase activity in cochlear strial marginal cells after various catecholamine administrations. 1164 39