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)

Noradrenaline (10(-5)M) inhibits the summary RNA synthesis in isolated neurone nuclei. In the presence of the dissolvable cytoplasmic fraction noradrenaline effect is transformed: 3H-UTP inclusion into RNA is activated. Similar results were seen in experiments with adenosine-3',5'-cyclophosphate and previously with acetylcholine. The data obtained indicate the presence of the neurone cytoplasmic factor (factors) interacting with biogenic amines and cyclic nucleotides and influencing RNA synthesis in such a complex. In the cell-free system noradrenaline inhibits Na, K-ATPase synthesis, its effect being directed at RNA synthesis inhibition upon DNA gene of Na, K-ATPase. These findings allow a conclusion that a part of neurone genes undergo noradrenaline control: the expression of several ones is activated and of the other is inhibited--the former being higher than the latter, according to noradrenaline effect on the summary RNA synthesis. Noradrenaline does not influence the glial cell RNA and DNA syntheses.
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PMID:[Noradrenaline as a RNA and Na K ATPase biosynthesis regulator in the neurons]. 616

The activity of Na+, K+-ATPase was determined in synaptosomes and in pellets, (containing membranes, mitochondria and vesicles) and cytoplasm prepared from synaptosomes from rat cerebral cortex. The activity of the pellets was more than two fold higher than that of the synaptosomes or of their components and adding back the cytoplasm reduced the activity of the pellets. Noradrenaline did not affect the activity of the pellets but increased that of the synaptosomes in a dose-dependent fashion. It inhibited the activity of the membranes. Results indicate that synaptosomal Na+, K+-ATPase activity is low because of a factor in the cytoplasm and this factor is not present in synaptosome pellets. NA antagonises the activity of the factor.
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PMID:Stimulation and inhibition of synaptosome ATPases by noradrenaline. The involvement of cytoplasmic factor. 625 May 3

Effect of noradrenaline on kinetics of Na, K-ATPase activation in rat brain cortex was studied using ATP as a substrate and Na+ or K+ ions as cofactors. Noradrenaline (5 x 10(-5) M) increased the activating effect of ATP and Mg2+ as well as that of Na+ and K+. In presence of ATP and Mg2+ the hormone activated ATPase by the mixed type, and in response to Na+, K+ addition--by the non-competitive type. Noradrenaline appears to cause the conformational alterations in Na, K-ATPase molecule, which change the kinetics of the enzyme activation by ATP and the ions.
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PMID:[Mechanism of the activating action of noradrenaline on rat cerebral cortex Na, K-ATPase]. 625 90

Noradrenaline (NA) sensitizes rat brain (Na+ + K+)-ATPase to inhibition by ethanol (EtOH). This effect of NA increases with the degree of enrichment of the enzyme: 0.1 mM NA + 0.05 M EtOH produced 27% inhibition in whole brain homogenates, 40% in 2.5-fold purified P2 fractions, and 45% in 5-fold purified microsomal fractions. The sensitization by NA was prevented by 0.1 microM phentolamine but not by 100 microM propranolol. Adrenaline and phenylephrine also sensitized the enzyme to EtOH inhibition in all of the fractions but isoproterenol did not. For all three alpha agonists the degree of sensitization was concentration dependent and the degree of reversal of this effect varied with the concentration of phentolamine added. These findings suggest that the NA + EtOH interaction is a direct effect on the membrane, probably mediated by an alpha receptor modified perturbation of the membrane microenvironment of the enzyme.
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PMID:Alpha adrenoreceptor mediated alteration of ethanol effects on (Na+ + K+)-ATPase of rat neuronal membranes. 626 Mar 17

The effect of ascorbic acid and noradrenaline on the inhibition of synaptosomal membrane ATPase by vanadate has been studied. Ascorbic acid (2 x 10(-3) M) and noradrenaline (10(-4) M) partly reversed the inhibition by vanadate (10(-6) M); however, when both were administered together the inhibition was completely eliminated. Using electron spin resonance (ESR) spectroscopy, we detected that ascorbic acid (10(-3) M) caused a 42% of reduction of vanadate (10(-4) M). Noradrenaline (10(-4) M) alone also reduced vanadate (10(-4) M) partially. When ascorbic acid and noradrenaline were present together all the vanadate was reduced to vanadyl. The concentration of ascorbic acid present in the brain under physiological conditions is identical to that found effective in our experiments. We suggest that ascorbic acid may protect the ATPase, at least in part, from inhibition by vanadate as a consequence of reducing vanadate to vanadyl. In those tissues where noradrenaline is also present a complete reduction of endogenous vanadium can be presumed.
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PMID:Reduction of Vanadate by ascorbic acid and noradrenaline in synaptosomes. 626 31

Noradrenaline (N) sensitizes rat brain (Na+ + K+)-ATPase to inhibition by low concentrations of ethanol (E). Only 1-N and not d-N was effective. The sensitization is also produced by other alpha-adrenergic agonists (adrenaline, phenylephrine), but not by isoproterenol, and is prevented by phentolamine but not by propranolol. The sensitization is greater with partially purified enzyme than with crude homogenates. N + E, like much higher concentrations of E alone, produced competitive inhibition with respect to K+ but uncompetitive or mixed inhibition with respect to Na+, Mg++ and ATP, and a reduced "physiological efficiency" of ATP utilization. All these changes were abolished by increasing K+ to 20 mM. After 3-week E treatment, with or without withdrawal, the N + E interaction was markedly reduced, though basal ATPase activity was increased only after withdrawal. Temperature-dependence studies (Arrhenius plots) indicated that sensitization occurs by alteration of activation energy only above the transition temperature. These findings suggest that alpha-agonists fluidize membrane lipids and thus facilitate conformational change of the enzyme by E, resulting in inhibition.
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PMID:Acute and chronic catecholamine-ethanol interactions on rat brain (Na+ + K+)-ATPase. 626 96

Unilateral chemical lesion of the nucleus locus coeruleus in rats produced unilateral depletion of ipsilateral cortical norepinephrine. Norepinephrine depletion was not associated with changes in "resting" metabolic balance of the cerebral cortex, as determined by in situ reflection spectrophotometry of the redox state of cytochrome oxidase. Norepinephrine depletion, however, caused slowing of the transient metabolic response to sudden increases in energy demand produced by direct cortical electrical stimulation. The effect was apparent in the redox state of both cytochrome oxidase and NAD, the latter being measured, also in situ, by reflection microfluorometry. These results demonstrate that norepinephrine has a role in modulating the response to increased metabolic demand in the cerebral cortex. Norepinephrine may mediate its effect by potentiating Na+, K+-ATPase or through its effects on vascular reactivity, or both.
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PMID:Norepinephrine depletion alters cerebral oxidative metabolism in the "active" state. 626 26

Noradrenaline (NA) and isopropyladrenaline in a dose of 11 microM/kg were shown to activate in vivo Na+, K+-ATPase and Mg2+-ATPase in the mouse renal microsomal fraction. NA (10(-6) M) increased the activity of Na+, K+-ATPase in vitro and did not affect the activity of Mg2+-ATPase in the hepatic and renal microsomal fractions. NA did not significantly affect in vivo the mitochondrial ATPases activity in the presence of various stimulators (Mg, dinitrophenol, bicarbonate) and inhibitors (oligomycin, bicyclohexyl carbodiimide) in the mouse liver and kidneys. cAMP (10(-6) M) activated Na+, K+-ATPase in vitro reduced the activity of Mg2+-ATPase in the microsomal fraction, and did not change the activity of the mitochondrial ATPases in the mouse liver and kidneys. The following scheme of the mechanism of catecholamine (CA) effect on Na+, K+-ATPase is suggested: CA leads to beta-adrenoreceptors leads to adenylate cyclase leads to cAMP leads to protein kinase leads to Na+, K+-ATPase. The mechanism of Mg2+-ATPase regulation is discussed.
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PMID:[Catecholamine regulation of the liver and kidney ATPase activity in mice]. 627 63

Superfusion of the isolated Pacinian corpuscles from cat mesenterium with solutions containing dibutyril-cAMP or theophylline caused an increase in spike activity and a decrease in receptor potential amplitude and firing potential threshold. An opposite effect was observed after catecholamine application. It was suggested that the effect of catecholamines on the Pacinian corpuscles is accompanied by a decrease in the cAMP level in a sensory nerve terminal. Norepinephrine decreased the adenylate cyclase activity and activated Na+, K+-ATPase in homogenates of Pacinian corpuscles. The effect of norepinephrine on Na+, K+-ATPase could be eliminated by phentolamine and was not sensitive to propranolol. A possible participation of alpha-adrenoreceptors in modulating catecholamine effect on electrical activity of the Pacinian corpuscles is discussed.
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PMID:[Analysis of the modulating effect of catecholamines on electrogenesis in an isolated mechanoreceptor]. 628 1

The aim of the study reported was to explore differences in neuro-effector characteristics of the resistance vessels from normotensive and hypertensive rats (WKY and SHR), which from five to twelve weeks of age had been exposed to either low-sodium (0.5 mM/100 g food), control-sodium (5 mM/100 g) or high-sodium (50 mM/100 g) diet. Isolated small mesenteric arteries (diameter 150-200 microM) were mounted in a two-vessel Mulvany-Halpern myograph. Noradrenaline sensitivity was similar in all arteries. Frequency-response curves of SHR arteries were steeper than in WKY. In both strains low-sodium curves were displaced to higher frequencies with little difference between control and high-sodium curves. Inhibition of the Na-K-ATPase with ouabain enhanced neurogenic responses more than noradrenaline responses, but to similar extents in all sodium groups. The results suggest that chronic low-sodium diet substantially reduces the total adrenergic transmitter release per impulse.
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PMID:Effects of low and high Na diets on cardiovascular dynamics in normotensive and hypertensive rats: neuroeffector characteristics of the resistance vessels. 659 94


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