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 production of oxygen-free radicals and their subsequent peroxidative action on membrane unsaturated fatty acids could be enhanced after subarachnoid hemorrhage. High-dose methylprednisolone (30 mg/Kg i.v.) treatment can antagonize acute SAH-induced brain hypoperfusion and protect the ultrastructural integrity of endothelial cell membranes. Experimental subarachnoid hemorrhage (SAH) was induced in anesthesized rats by slow injection of 0.3 ml of autologous arterial blood into cisterna magna. Tissue lipid peroxidation, quantified as thiobarbituric acid reactive material (TBAR) and Na(+)-K+ ATPase activity were assayed in three different rat brain areas (cerebral cortex, hippocampus and brain stem) of controls (without any surgical manipulation), sham-operated (0.3 ml. of mock CSF into cisterna magna) and after SAH induction, at 1 h, 6 h and 48 h. Na(+)-K+ ATPase activity decreased in the cerebral cortex at 1 h and 6 h and in brain stem at 1 h after SAH, while the same enzymatic activity was unchanged in the hippocampus. High-dose methyl-prednisolone treatment (started immediately after SAH induction) enhanced the Na(+)-K+ ATPase activity until control levels. There was no significant difference in lipid peroxide content between sham-operated and hemorrhagic animals; however, the injection itself induces a transient increase of TBAR (1 h after injection) and methylprednisolone treatment decreases the products of lipid peroxidation in all brain areas.
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PMID:Effects of high-dose methylprednisolone on Na(+)-K+ ATPase and lipid peroxidation after experimental subarachnoid hemorrhage. 217 70

Purified colony stimulating factor (CSF-1) stimulates the Na+,K+-ATPase activity of murine bone marrow-derived macrophages (BMM) and resident peritoneal macrophages (RPM) measured as ouabain-sensitive 86Rb+ uptake. Similar concentrations of CSF-1 stimulate the Na+,K+-ATPase activity and DNA synthesis in BMM whilst ouabain, a specific inhibitor of the Na+,K+-ATPase, also inhibits this CSF-1-mediated DNA synthesis. Other purified hemopoietic growth factors, granulocyte-macrophage CSF (GM-CSF) and interleukin-3 (IL-3), and the tumor promoter, 12-O-tetradecanoyl-phorbol-13-acetate (TPA), even though differing in their mitogenic capabilities, are also stimulators of the Na+,K+-ATPase activity in BMM and RPM. The non-mitogenic agents, lipopolysaccharide (LPS) and Concanavalin A (Con A), are also active. CSF-1 stimulation of the Na+,K+-ATPase was shown to be dependent on elevation of intracellular Na+ via an amiloride sensitive Na+-channel, most likely representing Na+/H+ exchange activity. Such stimulation of Na+,K+-ATPase activity via activation of the Na+/H+ exchange appears to be a necessary but insufficient early macrophage response for subsequent DNA synthesis.
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PMID:Activation and proliferation signals in murine macrophages: stimulation of Na+,K+-ATPase activity by hemopoietic growth factors and other agents. 244 3

Glucocorticoids have a well-known clinical effect on brain edema and intracranial hypertension, but the mechanism of action is still poorly understood. In the present report the effect of beta-methasone on choroid plexus transport and CSF formation was studied. Following 5 days of daily treatment with betamethasone the CSF production rate in rabbits was reduced by 43% as measured by ventriculo-cisternal perfusion with radioactive inulin. Accordingly, the transport capacity in the choroid plexus, measured in terms of choline uptake and accumulation in vitro, and the activity of Na+--K+-ATPase decreased in both rabbit (in the lateral ventricles by 31 and 31%, respectively) and rat (by 16 and 24%, respectively). Thus, the demonstrated influence of glucocorticoids on these functions of the choroid plexus seem to be important components in their therapeutic effect on intracranial hypertension.
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PMID:Corticosteroid action on choroid plexus: reduction in Na+-K+-ATPase activity, choline transport capacity, and rate of CSF formation. 255 68

The development of transport functions in the rabbit choroid plexus was followed postnatally up to 2 months after birth. The activity of ouabain-sensitive Na+, K+-ATPase in newborn rabbit choroid plexus composes about one-fourth (lateral and third ventricle) to one-half (fourth ventricle) of the activity in the adult animal, and it increases markedly within the first 3 weeks of early life. A similar profile of postnatal changes is observed for the capacity to take up and accumulate the organic base choline, which is about three to five times higher for the adult rabbit than for the newborn animal. This coincides with the maturation of the epithelial cells as well as with the development of the sympathetic nerve supply in the choroid plexus. The results suggest that energy-dependent translocation systems influenced by local sympathetic nerves in the choroid plexus, at the interface between blood and CSF, have a functional role shortly after birth.
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PMID:Early postnatal development of transport functions in the rabbit choroid plexus. 293 54

We have studied maturation of brain barrier systems in fetal, newborn, juvenile and adult rabbits. We have compared choroid plexus and brain Na+,K+-ATPase levels in each age group, as well as serum and CSF Na+ concentration as a measure of the ability of the choroid plexus to generate a gradient from blood to CSF. The choroid plexus appears functionally mature at all ages studied, both in ability to produce a Na+ gradient and in ATPase levels. In contrast, brain ATPase levels rose markedly with age. Kidney ATPase measured for comparison showed a pattern similar to brain.
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PMID:Choroid plexus, brain and kidney Na+,K+-ATPase: comparative activities in fetal, newborn and young adult rabbits. 628 98

Ouabain-sensitive Na+-K+-ATPase was measured spectrophotometrically in the lateral choroid plexuses of rabbit and rat. In the rabbit, a significant increase in the enzyme activity was seen at one week after unilateral sympathectomy (removal of the superior cervical ganglion), but not at three days or two weeks postoperatively, as compared with the intact, contralateral plexus. Unilateral sympathetic denervation of the rat's choroid plexus induced a nearly 40% decrease in Na+-K+-ATPase activity at 6 days after the operation, while no effect was seen after 12 days. The results agree with a local sympathetic inhibition of CSF production in rabbit (corresponding studies on rat have not been performed), and favor the assumption that the adrenergic nerves in the choroid plexus mediate direct effects on transport functions in the plexus epithelium.
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PMID:Sympathetic influence on sodium-potassium activated adenosine triphosphatase activity of rabbit and rat choroid plexus. 629 65

Ependymal epithelial cells from the choroid plexuses (CPs) separately of lateral (I + II), IIIrd and IVth ventricles of male Golden Hamsters were studied by electron microscopy and morphometry. The 16 hamsters were distributed between three injections groups: vehicle only, 25 micrograms and 2500 micrograms melatonin (M) by subcutaneous injection daily at L11 to L11.75 in a LD 14:10 daily photoperiod. After 28 consecutive daily injections, animals were killed and the CPs were dissected, fixed and prepared for electronmicroscopy. Thirteen measures of the CP ependymal cells were made, by planimetry, morphometry or direct counting or linear measurement on the EM prints. Effects of melatonin occurred only on the cells from the lateral ventricles. Here M at high dosage caused cell swelling (averaging 50% increase in area), and other cellular changes were graded in relation to M dosage. These were increased (to 26%) in mitochondrial area per cell, and increased (to 50%) in length of apical microvilli. Since in other work the latter form a major locus of ouabain-sensitive Na+, K+-ATPase, it is suggested that M may possibly have a stimulatory effects on transport and related CSF secretory activities by these cells.
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PMID:Stimulatory effects of melatonin on ependymal epithelium of choroid plexuses in golden hamsters. 713 Sep 80

Brain pial microvessels have previously been demonstrated to have blood-brain barrier properties. The potential difference (PD) across exposed brain pial microvessels, 20-60 microns in diameter and superfused with artificial CSF, has been measured in anaesthetised rats using glass microelectrodes. The PD on insertion into venous vessels, V(in), was 3.2 mV lumen negative, and in arterial vessels it was higher at 4.5 mV. Superfusion with high K(+)-CSF, made by replacing Na+ with K+, caused a positive deflection in PD, VK+, whereas reducing the Na+ alone, by replacing Na+ by Tris-HCl, made the lumen more negative. These two effects were additive. Studies on venous vessels showed that ouabain had no effect on V(in) and only affected VK+ under conditions of low Na pre-exposure. Neither histamine nor cimetidine had any effect on V(in) or VK+ whereas tetraethylammonium, a K(+)-channel blocker, reduced VK+ by 20%. These experiments demonstrate that changes in PD caused by changing abluminal Na+ or K+ are due predominantly to movement of ions through channels in the endothelial cell membranes, and that actions that alter the activity of the Na+,K(+)-ATPase or reduce the resistance of the paracellular pathway in parallel with increased membrane permeability have less effect on the PD.
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PMID:Transendothelial electrical potential across pial vessels in anaesthetised rats: a study of ion permeability and transport at the blood-brain barrier. 752 22

Brain and CSF potassium concentrations are well regulated during acute and chronic alterations of plasma potassium. In a previous study, we have shown that during chronic perturbations, regulation is achieved by appropriate adaptation of potassium influx, but that the degree of such adaptation during acute perturbations is much less. To elucidate further potential regulatory mechanisms, rats were rendered acutely or chronically hyper- or hypokalemic (range 2.7-7.6 mM). Measurements were made of brain and CSF water and ion contents to examine whether regulation occurred by modulation of K+ uptake into parenchymal cells. Furthermore, the permeability-surface area products (PSs) of 22Na+ were determined, because changes in K+ efflux fia Na+,K(+)-ATPase on the brain-facing side of the blood-brain barrier might be reflected in modified Na+ permeability. Brain and CSF K+ concentrations and Na PS were all independent of chronic changes in plasma K+ and acute hypokalemia, suggesting that neither modulation of parenchymal K+ uptake nor K+ efflux via the Na+,K(+)-ATPase is involved in extracellular K+ regulation in these conditions. In contrast, Na PSs were increased by 40% (p < 0.05) in acute hyperkalemia. This was accompanied by a slight loss of tissue K+ and water from the intracellular space. These results suggest that increased potassium influx in acute hyperkalemia is compensated by stimulation of K+ efflux via Na+,K(+)-ATPase. A slight degree of overstimulation, as indicated by a net loss of tissue K+, leads us to hypothesize that other factors, apart from the kinetic characteristics of Na+,K(+)-ATPase, may regulate this enzyme at the blood-brain barrier.
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PMID:Mechanisms of brain ion homeostasis during acute and chronic variations of plasma potassium. 786 Jun 67

Considerable, but as yet still controversial evidence indicates the presence, in mammalian tissues of endogenous digitalis-like factors (EDLFs) which inhibit cell membrane Na+, K(+)-adenosine triphosphatase (Na+, K(+)-ATPase) and which may cross-react with anti-digitalis antibodies. The aim of this study was to evaluate the effect of antibodies against cardiac glycosides on Na+, K(+)-ATPase in human erythrocytes. For this purpose, we measured the effect of antibodies against two different cardiac glycosides (anti-ouabain rabbit antiserum and anti-digoxin Fab fragments) on the activity of the Na+, K(+)-ATPase, as measured by erythrocyte rubidium-86 (86Rb) uptake, in subjects who had never come into contact with exogenous cardiac glycosides, and compared these results with the effect of two control rabbit sera: a normal serum and an antiserum to a non-related antigen. Anti-ouabain rabbit antiserum and anti-digoxin Fab fragments induced a significantly greater percentage change in 86Rb uptake in the erythrocytes than the two control sera (ANOVA followed by multiple comparison by the Games-Howell test). The average percentage change was +11.8 +/- 16.3% (n = 19) (mean +/- SD) for anti-ouabain antiserum +10.8 +/- 15.6% (n = 23) for anti-digoxin Fab fragments, -1.68 +/- 11.2% (n = 11) for anti-rhGM-CSF antiserum, and -5.8 +/- 11.7 (n = 10) for normal control serum. In a subgroup of ten subjects in whom the 3 antisera were tested simultaneously, the stimulation of erythrocyte 86Rb uptake induced by the two antidigitalis antibodies correlated significantly (r = 0.906, p = 0.001, n = 10).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The stimulatory effect on human erythrocyte rubidium-86 uptake by anti-cardiac-glycoside antibodies. 857 8


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