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)

High Na+ intake has been proposed to induce a rise in the activity of a circulating inhibitor of the Na+, K+-pump. The effects on male Wistar rats of a high sodium diet (8 per cent NaCl) on the activity of such a plasma Na+, K+-ATPase inhibitor were investigated. Systolic blood pressure, body weight, urinary Na+ excretion, haematocrit, intraerythrocytic Na+ content and the activity of a Na+ dependent transport system, i.e. the uptake of 5-HT by blood platelets were measured in parallel. After one week, neither systolic blood pressure nor intraerythrocytic Na+ content were modified, but the ability of the plasma extracts to inhibit renal Na+, K+-ATPase increased (70.9 +/- 1.7 vs 76.3 +/- 2.1 mumol Pi/mg/h; p = 0.05). After two weeks, the plasma inhibitory activity, the systolic blood pressure and the intraerythrocytic Na+ content were higher than that of control animals (65.5 +/- 1.6 vs 79.1 +/- 2.8 mumol Pi/mg/h, p less than 0.001; 132 +/- 2 vs 114 +/- 4 mmHg, p. +/- 0.001 and 4.95 +/- 0.32 vs 3.81 +/- 0.36 mmol/l.cells, p less than 0.05). After three months, the ability of plasma extracts to inhibit the Na+ pump and the systolic blood pressure were still elevated (57.8 +/- 1.8 vs 72.9 +/- 1.8 mumol Pi/mg/h, p less than 0.001; 145 +/- 4 vs 118 +/- 2 mmHg, p less than 0.001) whereas intraerythrocytic Na+ content had returned to control levels and 5-HT uptake was not modified.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Chronic dietary sodium overload and release of a circulating Na+-K+ pump inhibitor]. 300 22

The effect of prenatal L-tryptophan supplementation on the serotonin (5-HT) synthesis and the activity of Na+,K+-ATPase in the cerebral cortex was studied during postnatal development, from birth up to day 30. A parallel and significant elevation of the serotonin content and the activity of tryptophan-5-hydroxylase was observed in the brain of infant rats born to mothers treated with L-tryptophan, as related to non-treated controls. The activity of Na+,K+-ATPase was also significantly elevated at the different ages studied throughout the developmental period, as related to controls. These results suggest an important role of L-tryptophan in the early regulation of the serotonin-synthesizing machinery, which lasts postnatally. Elevation of ATPase activity seems to be associated to the elevation in the activity of the 5-HT system.
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PMID:Brain serotonin synthesis and Na+,K+-ATPase activity are increased postnatally after prenatal administration of L-tryptophan. 300 68

In the search of sensitive models for actions of digitalis-like substances on intact cells or tissues, the effects of ouabain on human platelets were investigated. In a concentration-dependent manner ouabain 10(-8)-10(-4) M inhibited Na+-K+-ATPase activity measured as uptake of 86Rubidium (86Rb), with about 90% inhibition of the total uptake at ouabain greater than or equal to 10(-6) M. An almost identical concentration-effect curve was found for platelet uptake of 3H-serotonin (3H-5-HT). The platelet shape change reaction to exogenous 5-HT (1 X 10(-6) M) was suppressed by ouabain (10(-8)-10(-4) M) in a concentration-dependent manner, but with no clear maximum effect within the range tested. Aggregation induced by adenosine-di-phosphate (ADP 2 X 10(-6) M) was enhanced by ouabain 10(-8)-10(-6) M. At the highest concentration tested the rate of aggregation was increased by 31% and the change in light transmission by 54%. At low concentrations (less than 10(-9) M) of ouabain, there was a tendency towards increased aggregation as well as increased uptake of 86Rb, which may be a parallel to observations of positive inotropic effects of low concentration of glycosides, which do not inhibit Na+-K+-ATPase. The results show that human platelets can be used as a model tissue for studying effects of cardiac glycosides. This suggests that it may be useful for further investigations of the biological effects of agents with a similar effect profile, e.g. endogenous digitalis-like substances.
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PMID:Effects of ouabain on 86Rb-uptake, 3H-5-HT-uptake and aggregation by 5-HT and ADP in human platelets. 337 88

The neuronal activity in spinal cord in response to electrical or adequate stimulation of afferent fibres increases extracellular K+ activity. The increase during a stimulation can reach 9-10 mM (so-called ceiling level) and persists for some time even when a stimulation is discontinued. The activation of a neuronal Na-K pump is a limiting factor in stimulation-evoked increase in extracellular K+ activity and in the time course of its recovery to the resting level. Drugs that affect either the neuronal activity (picrotoxin, strychnine, GABA, 5-HT) or activity of Na-K ATPase (oubain, naloxone, morphine, enkephalins) substantially change the K+ transience. Repetitive electrical stimulation of low threshold cutaneous afferents at frequency 1-100 Hz induced transient shrinkage of extracellular space in spinal dorsal horns by 5-75%. The increase in extracellular K+ activity depolarizes the membranes of neurones, glial cells, and primary afferent fibres and may eventually lead to either facilitation or inhibition of synaptic transmission. It is also suggested that the transient poststimulation changes in extracellular volume may alter synaptic potency in spinal cord.
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PMID:Modulation of spinal cord transmission by changes in extracellular K+ activity and extracellular volume. 362 Oct 32

The effects of serotonin and five other indoles were tested on the electrical parameters and ionic transport in the isolated toad lens. Serotonin, tryptophan and 5-hydroxy-L-tryptophan did not affect the electrical parameters of the lens at concentrations as high as 1 mM. Tryptamine, 5-methyltryptamine and 5-methoxytryptamine had dual effects: 1 mM in the posterior bathing solution depressed the potential difference of the posterior face of the lens, which resulted in an increase in the translenticular potential difference and short-circuit current; 1 mM in the anterior solution (in contact with the lens epithelium) produced a quick and pronounced reduction of the potential difference of the anterior face. This resulted in a 90-100% decline of the translenticular short-circuit current. Serotonin and tryptamine were then tested for their effect on the ATPases of lens epithelium. Both amines inhibited the enzymes with tryptamine at 5 mM completely inhibiting all ATPase activity. Since tryptophan is transported from the aqueous humor into the lens and may be converted by lens enzymes to serotonin and tryptamine, these findings may have physiological implications in cataractogenesis.
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PMID:Inhibition of ionic transport and ATPase activities by serotonin analogues in the isolated toad lens. 625 64

Previous results suggested a possible association between brain serotonin (5-HT) and Na+-K+-ATPase, in vivo. We extended the study to the developmental response of this enzyme to early 5-HT changes induced by early malnutrition and by a serotonin agonist. Agonist treatment produced a response of the enzyme activity at early stages of development in normal and malnourished brains. The induction of 5-HT changes through malnutrition could be playing an important role in the development and maturation of Na+-K+-ATPase activity, and brain 5-HT receptors could possibly be involved in such a response.
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PMID:Effects of malnutrition and quipazine on rat cerebral cortex ATPase activity during development. 625 73

Serotonin (10(-6)-10(-3) M) stimulates Na,K-ATPase in the rat brain cortex homogenate with a maximal effect at 10(-4) M. Deseril (10(-5) M), antagonist of serotonin receptors, removes the stimulating effect. Deseril has no influence on noradrenaline-induced ATPase activation; the alpha-adrenergic blocker phentolamine does not affect serotonin activation. The effects of the two transmitters are additive. It is assumed that the mediators interact with different membrane sites, serotonin activation being initiated via the serotonin receptors.
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PMID:[Sites responsible for stimulation of brain Na,K-ATPase by serotonin]. 627 36

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

Incubation of rat platelets with organotins inhibited their capacity to take up 5-hydroxytryptamine-14C (5-HT-14C) and stimulated the release of preloaded 5-HT-14C as well as endogenous 5-HT. Similar but less pronounced effects also were observed when platelets from rats treated intraperitoneally with organotins were examined. The relationships of organotin structure to 5-HT uptake inhibition and 5-HT release were similar, with the most active compounds being the trisubstituted derivatives bis(tri-n-butyltin) oxide, tri-n-butyltin chloride, tricyclohexyltin hydroxide, tri-n-propyltin chloride, and triphenyltin hydroxide. Scanning electron micrographs revealed increased platelet aggregation and shape change in organotin treated samples as compared to vehicle treated controls. It was suggested that the action of organotins on rat platelets was due, at least in part, to their known ability to interfere with ATPase mediated systems.
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PMID:Effects of organotins on rat platelets. 665


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