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 effect of synthetic (BHT, 2,2,5,7,8-pentamethyl-6-hydroxychroman) and natural (alpha-tocopherol) antioxidants on Ca++-transporting systems was compared in platelets, brain synaptosomes, and skeletal muscle sarcoplasmic reticulum. It was shown that synthetic antioxidants, in contrast to alpha-tocopherol, induced Ca++-release manifested in platelet aggregation, stimulation of 5-hydroxytryptamine release by synaptosomes, synaptosome depolarization and inhibition of Ca++-transport and Ca++-ATPase activity in the sarcoplasmic reticulum. The disturbances of Ca++-homeostasis induced by synthetic antioxidants are considered as molecular mechanisms of complications encountered upon their application.
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PMID:[Antioxidant-induced release of calcium in biological membranes]. 366 13

Strips of canine tracheal smooth muscle were studied in vitro to determine the effects of changes in the extracellular calcium (Cao) concentration on tonic contractions induced by acetylcholine and 5-hydroxytryptamine. Strips were contracted with graded concentrations of the above agents in 2.4 mM Ca, after which CaCl2 was administered to achieve final concentrations of 5.0, 10.0, and 20.0 mM. Increases in Cao to 5 mM or above caused significant relaxation of muscles contracted with 5-hydroxytryptamine but did not significantly relax muscles contracted with acetylcholine. Increases in Cao also caused significant relaxation of muscles contracted with low concentrations of K+ (20 or 30 mM). However, in 60 or 120 mM K+, increases in Cao resulted predominantly in muscle contraction. Inhibition of the Na+-K+-ATPase by ouabain (10(-5) M) or K+ depletion reversed the effects of Cao from relaxation to contraction in tissues contracted with 5-hydroxytryptamine. Increases in Cao also caused contraction rather than relaxation in the presence of verapamil (10(-6) M). We conclude that calcium has both excitatory and inhibitory effects on the contractile responses of canine tracheal smooth muscle. The inhibitory effects of Ca2+ appear to be linked to the activity of the membrane Na+-K+-ATPase.
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PMID:Effects of extracellular calcium on canine tracheal smooth muscle. 374 64

Resealed chromaffin-granule ;ghosts' were used to study the steady-state kinetics of catecholamine transport. The pump has a high affinity for (-)-noradrenaline, (-)-adrenaline, tyramine and 5-hydroxytryptamine (serotonin), but a lower affinity for (+)-noradrenaline. The measured rates of incorporation do not conform to Michaelis-Menten kinetics, but affinity constants for the former substrates are in the range 8-18mum. Reserpine is a potent inhibitor. Incorporation as a function of ATP concentration also fails to show simple kinetics; the affinity constant for ATP is deduced to be about 3mm at 1mm-MgCl(2). Adenylyl (betagamma-methylene)diphosphonate is a competitive inhibitor at low concentrations, but inhibits more strongly at high concentrations. The pump has a transition temperature at 29 degrees C and does not seem to be identical with the Mg(2+)-stimulated adenosine triphosphatase of chromaffin granules.
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PMID:Steady-state kinetics of catecholamine transport by chromaffin-granule "ghosts". 446 85

Antibodies raised against synaptosomal plasma membranes of rat hippocampus (anti-HPC IgG) caused inhibition of [3H]noradrenaline, [3H]5-hydroxytryptamine, [3H]GABA and [3H]aspartate uptake into S1 fractions and slices of hippocampus and cerebral cortex, but not those of caudate nucleus and hypothalamus. Similar inhibition was not observed on using antibodies against synaptosomal membranes of rat caudate nucleus. Anti-HPC IgG raised against synaptosomal membranes of hippocampus failed to alter both spontaneous and K+-evoked release of [3H]noradrenaline. They did not interfere with the binding of [3H]desipramine (the potent noradrenaline-uptake inhibitor) and with the binding of [3H]dihydroalprenolol, thus excluding any interaction of the antibodies with drug receptors which are located on either the pre- or postsynaptic membrane. The anti-HPC IgG inhibit the enzymatic activity of [Na+-K+-]ATPase by 30% upon incubation of the antibodies with crude membrane preparations. A comparison of their inhibitory effects with those of the neurotoxin 6-hydroxydopamine suggests that the corresponding hippocampal specific antigens are located at a presynaptic site.
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PMID:The effect of anti-synaptosomal membrane antibodies of neurotransmitter uptake. 611 32

The aim of the present experiments was to study the effects of the neurotransmitters acetylcholine, noradrenaline, 5-hydroxytryptamine, and dopamine on the Na+,K+-ATPase of rat brain synaptosomal fractions. It is shown that dopamine at low concentrations specifically inhibits the Na+,K+-ATPase of synaptic membranes from the brain regions rich in dopaminergic endings, but has no effect on the synaptosomal Na+,K+-ATPase from the other parts of brain. Acetylcholine and noradrenaline have similar specific effects on Na+,K+-ATPase from cholinergic and adrenergic synaptosomes. The Na+,K+-ATPase of synaptic membranes from the different brain regions, characterised by different distributions of cholinergic, adrenergic, and 5-hydroxytryptaminergic endings, show different reactions with neurotransmitters. These data indicate a functional significance of the effects of the neurotransmitters on the synaptosomal Na+,K+-ATPase.
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PMID:Functional significance of the effects of neurotransmitters on the Na+,K+-ATPase system. 614 22

1. Highly purified resealed chromaffin-granule ;ghosts' were assayed for ATPase and ATP-driven H(+)-translocation and 5-hydroxytryptamine-uptake activities, and for 5-hydroxytryptamine uptake driven by an imposed transmembrane H(+)-gradient. The effects of several inhibitors on these activities were studied. 2. Dicyclohexylcarbodi-imide inhibits all of these activities, but not in parallel; at low concentrations it decreases the permeability of the membrane to protons. 3. 4-Chloro-7-nitrobenzofuran (Nbf-Cl) and silicotungstate inhibit ATP-dependent activities, without effect on 5-hydroxytryptamine uptake driven by an imposed H(+)-gradient. 4. Tributyltin chloride inhibits all of the activities. 5. Treatment of the ;ghosts' with low concentrations of urea inhibits 5-hydroxytryptamine uptake and ATP-dependent generation of a transmembrane H(+)-gradient, without inhibiting ATPase activity. 6. Nbf-Cl and silicotungstate are without effect on the rate of leakage of 5-hydroxytryptamine from preloaded ;ghosts', whereas dicyclohexylcarbodi-imide and tributyltin chloride accelerate the rate of leakage. 7. Treatment of the membranes with (14)C-labelled Nbf-Cl labels several proteins; membranes treated with dicyclohexyl[(14)C]carbodi-imide are labelled predominantly in a protein of low molecular weight, which may be analogous to the mitochondrial H(+)-conducting proteolipid. 8. It is concluded that Nbf-Cl and silicotungstate inhibit the H(+)-translocating ATPase of the granule membrane; that dicyclohexylcarbodi-imide inhibits the ATPase, and inhibits 5-hydroxytryptamine accumulation by accelerating leakage of the amine; and that the effects of tributyltin chloride are due to inhibition of the ATPase, and collapse of the transmembrane H(+)-gradient through OH(-)-anion exchange.
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PMID:Inhibition of adenosine triphosphatase, 5-hydroxytryptamine transport and proton-translocation activities of resealed chromaffin-granule 'ghosts'. 625 64

Chromaffin granule membrane vesicles accumulate large amounts of catecholamines against their concentration gradients. This process is ATP-dependent, reserpine, FCCP and nigericin sensitive. Carrier-mediated, reserpine-sensitive accumulation has also been demonstrated in the absence of ATP when a pH gradient (delta pH) is artificially generated across the membrane. Crude preparation of 5-hydroxytryptamine storage vesicles from rat brain or from pig platelets showed similar requirement of a transmembrane pH gradient for accumulation of the amine. The catecholamine transporter from chromaffin granules has been solubilized by the use of detergents in the presence of phospholipids. Removal of the detergent either by Sephadex filtration or by dialysis results in the formation of proteoliposomes which catalyze delta pH-dependent, reserpine-sensitive catecholamine accumulation. Under proper conditions, the solubilized H+-translocating ATPase has been incorporated into the same proteoliposomes with the catecholamine transporter, and ATP-dependent transport has been measured. The reconstituted protein shows specificity and affinity towards catecholamines similar to the native one.
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PMID:Active transport of biogenic amines in chromaffin granule membrane vesicles. 645 80

Dense granules, the storage organelles for 5-hydroxytryptamine in blood platelets, have been isolated from porcine platelets and are shown to transport 5-hydroxytryptamine in response to a transmembrane proton gradient (delta pH). Transport in the absence of delta pH is minimal, and it is shown that a rapid increase in transport takes place as delta pH increases. Direct measurements with [14C]methylamine show a delta pH of 1.1 units (acid inside) for intact granules. Osmotically active ghosts of dense granules from which 95% of the endogenous 5-hydroxytryptamine content has been released have also been prepared. Ghosts swell in the presence of ATP and Mg2+, and this swelling is shown to be due to the entry of protons via a process linked to ATP hydrolysis. Proton entry is also apparently linked to anion penetration in ghosts. Steady-state 5-hydroxytryptamine transport in ghosts is stimulated approx. 3-fold on the addition of ATP to the incubation medium, and the stimulation of 5-hydroxytryptamine transport in ghosts correlates with the formation of a transmembrane delta pH. Ghosts generate a delta pH of 1.1-1.3 pH units (acid inside) in the presence of 5 mM-ATP/2.5 mM-MgSO4. delta pH is generated within 3 min at 37 degrees C and is dissipated by the ionophore nigericin and by NH4Cl. It is shown that an Mg2+-stimulated ATPase activity is present on the ghost membrane, and inhibition of the ATPase leads to a corresponding decrease in 5-hydroxytryptamine transport. The results presented support the idea that 5-hydroxytryptamine transport into platelet dense granules is dependent on the presence of a transmembrane delta pH and, together with previous findings by others, suggest a generalized mechanism for biogenic amine transport into subcellular storage organelles.
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PMID:Participation of a transmembrane proton gradient in 5-hydroxytryptamine transport by platelet dense granules and dense-granule ghosts. 645 80

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

The effects of N-methylmaleimide (N-MtM), a vacuolar H(+)-ATPase inhibitor, were evaluated in the putamen of the cat to study the in vivo transport mechanisms of dopamine (DA), 5-hydroxytryptamine (5-HT), and their metabolites 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), and 5-hydroxyindolacetic acid (5-HIAA), using the brain focal microdialysis technique combined with HPLC. The addition of N-MtM to the perfusate altered invariably the flux of the DOPAC, HVA, and 5-HIAA in a similar pattern, resulting in a decrease of the extracellular levels of such metabolites, its extent being N-MtM concentration dependent, thus indicating that the mechanism(s) of such a decrease is (are) related most likely to decreased transport from the intracellular to the extracellular space as the consequence of the inhibition of the vacuolar H(+)-ATPase of DA and 5-HT neurons by the N-MtM. Furthermore, N-MtM masked the release of DA and 5-HT produced by KCl 120 mmol/l. Indeed, N-MtM increased the extracellular levels of such transmitters to values exceeding 4 to 6 times of those produced by KCl 120 mmol/l alone, which suggests that vacuolar H(+)-ATPase is probably involved also in the retention and/or reuptake process of DA and 5-HT.
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PMID:H(+)-ATPase and transport of DOPAC, HVA, and 5-HIAA in monoamine neurons. 767 13


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