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)

Adenosine triphosphatase (ATPase) activities were compared in platelets of asthmatic and nonasthmatic children. Significantly elevated Mg2+- and Ca2+-dependent ATPase activities were found in particulate and soluble fractions of platelets from nonsteroid-treated asthmatic children compared to steroid-treated asthmatic and nonasthmatic children. The most pronounced increase (greater than twofold) occurred in the Ca2+-ATPase of the soluble fraction which contains platelet contractile protein. Intact cell surface of ecto ATPase activity was not significantly increased in platelets of asthmatic children. The findings are consistent with adrenergic imbalance in asthma involving depressed adenylate cyclase activity (beta-adrenergic) and increased ATPase activity (alpha-adrenergic) and may relate to abnormal platelet aggregation patterns.
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PMID:Increased adenosine triphosphatase activity in platelets of asthmatic children. 12 27

Changes in adenosine triphosphatase (ATPase) activity of the peripheral blood leukocytes were investigated in patients with bronchial asthma. Estimation of the leukocyte Mg++- and Ca++- dependent ATPases was carried out according to Hadden's method, incubating ATP with the membrane fraction of the leukocyte. The leukocyte ATPase activity was significantly elevated among asthmatic patients compared with control subjects. This elevated ATPase was seen in all asthmatics irrespective of acute attacks or the drug treatment. There was no clear correlation between the activity of ATPase and the percentage of leukocytes, neutrophils and eosinophils. There was no relationship between ATPase activity and adenyl cyclase activity of the same leukocytes from asthmatic patients.
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PMID:Leukocyte adenosine triphosphatase activity in human bronchial asthma. 18 9

Previous studies have identified changes of mechanical properties of airway smooth muscle (ASM) from a canine model of atopic airway hyperreactivity. These changes, including increased maximum shortening capacity (delta Lmax) and early shortening velocity (Vo), may be responsible for the airway hyperresponsiveness in asthma. We have suggested that these changes may be due to increased actomyosin ATPase activity, controlled via phosphorylation of the 20 kD myosin light chain (MLC20) by MLC kinase (MLCK). Therefore, ATPase activity, MLC20 phosphorylation, and MLCK content and activity were assessed in tracheal and bronchial smooth muscles (TSM and BSM) of ragweed pollen-sensitized dogs (S) and their littermate controls (C). Specific ATPase activities from STSM and SBSM were significantly higher than their control counterparts (CTSM, CBSM). Phosphorylation of MLC20 in STSM was greater both at rest and during electrical stimulation due to the increased amount of MLCK in STSM and SBSM by 30 and 25%, respectively. MLCK activity was also increased significantly in STSM and SBSM (from 46.99 +/- 8.33 and 42.85 +/- 5.92 to 91.9 +/- 6.43 and 64.12 +/- 7.88 32P mmol/mg fresh tissue weight/min respectively [mean +/- SEM]). When normalized to the amount of MLCK in the tissue, however, specific MLCK activity in STSM and SBSM was similar to that in controls. It is unlikely that myosin phosphatase plays any role in the changes of MLC20 phosphorylation in sensitized animals. Peptide mapping showed no visible change in primary structure of MLCK in STSM and SBSM compared with those of controls. We report that ASM actomyosin ATPase activity is increased in STSM and SBSM. The increased ATPase activity is the result of increased MLC20 phosphorylation, the latter likely resulting from the increased MLCK content, which may account for the hyperresponsiveness found in ASM from these animals.
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PMID:Ragweed sensitization-induced increase of myosin light chain kinase content in canine airway smooth muscle. 144 4

In our previous report, we demonstrated that the functions of phagocytes and lymphocytes were defective in patients with systemic lupus erythematosus (SLE). In an attempt to further clarify the defective mechanisms of these cells, 25 active SLE, 10 bronchial asthma patients (BA) on corticosteroids and 25 age and sex-matched normal individuals were investigated for the expression of membraneous C3b receptors, ionophore-induced 45Ca(2+)-uptake, mitochondrial potentials and phagocytic activity of neutrophils. We found decreased expression of C3b receptors on SLE PMN in both resting (37.2 +/- 3.7% of the normal controls) and FMLP-stimulated (68.3 +/- 7.1% of the normal controls) conditions, whereas the C3b receptor expression on BA-PMN receiving long-term steroid treatment was not different from normal controls. This suggests that the defective phagocytosis of SLE PMN is in the recognition, but not in the ingestion phase because of the normal function of Ca(2+)-influx and mitochondrial activity in SLE PMN. On the other hand, hyporesponsiveness to PHA stimulation (stimulation index: 127.4 +/- 46.3 in SLE vs. 311.2 +/- 30.4 in normals, p = 0.0077) was a distinct cell-mediated immune abnormality in our SLE patients. We measured the membrane potential of individual cells using 3,3'-dihexyloxacarbocyanin and found hyperpolarization in resting SLE lymphocytes. However, the membrane polarization of SLE lymphocytes became lower than that of normal cells after PHA stimulation for 3 days. A similar tendency was also found in Na(+)-K(+)-dependent ATPase activity in SLE lymphocytes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Defective expression of neutrophil C3b receptors and impaired lymphocyte Na(+)-K(+)-ATPase activity in patients with systemic lupus erythematosus. 166 18

The intracellular levels of sodium, potassium, and free calcium, as well as red blood cell transport of 86Rb (a radioactive potassium analogue) and 45Ca were measured in patients with bronchial asthma (BA). The intracellular content of sodium was 10-20% higher in patients with BA, though the differences in the present sample (7 controls and 18 BA patients) failed to be significant (p less than 0.05). The differences were most pronounced in infection-dependent BA and not eliminated during glucocorticoid hormone therapy. The activity of the Na+, K+ pump, as assessed by the values of an ouabain-inhibited component of 86Rb entry, was increased by 10-20% (p less than 0.05) in BA patients and of Na+, K+ cotransport (an ouabain-sensitive furosemide-inhibited component of 86Rb entry), by 35-45% (p less than 0.25). The passive red blood cell membrane permeability in BA patients (an ouabain + furosemide-insensitive component of 86Rb) remained unchanged. The quin-2-loaded red blood cell entry rate for 45Ca was decreased by 5-10%. In the absence of a Ca(2+)-ATPase inhibitor (0.5 mM orthovanadate), these differences were greatly significant (p less than 0.005). In addition, the patients with BA showed a 10% reduction in free calcium levels; however, the differences were insignificant (p less than 0.25), which might be caused by Ca-pump activation. As in the experiments with Na+ level measurements, the greatest differences in red blood cell Ca(2+)-balance control were recorded in patients with infection-dependent BA and independent of glucocorticoid hormone therapy. Possible mechanisms of involvement of the changes found in monovalent cation and Ca2+ transport in the pathogenesis of BA were also discussed.
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PMID:[The transport of monovalent ions and calcium in the erythrocytes of patients with bronchial asthma]. 188 40

Recent studies have shown that inhaled frusemide exerts a protective effect against various bronchoconstrictor stimuli in asthma including exercise, fog and allergen. Since mast cell activation seems to be a component of bronchoconstriction by these stimuli it is possible that inhibition of mediator release accounts for some or all of the inhibitory effects of frusemide in asthma. Since inhaled adenosine 5'-monophosphate (AMP) is another stimulus that produces bronchoconstriction by augmenting mast cell mediator release, we have investigated the ability of this drug to antagonise the airway effects of inhaled AMP and methacholine in a randomized, placebo-controlled, double-blind study of 12 asthmatic subjects. Inhaled frusemide (approximately 28 mg) administered 5 min prior to challenge increased the provocation concentration of inhaled AMP and methacholine required to reduce forced expiratory volume in one second (FEV) by 20% from baseline from 30 to 96 mg.ml-1 (p less than 0.01) and from 1.1 to 1.8 mg.ml-1 (p less than 0.01), respectively. The protection that frusemide afforded against AMP was significantly greater than that against methacholine (p less than 0.05). These data suggest that inhaled frusemide may serve as a functional antagonist against a smooth muscle spasmogen, such as methacholine, possibly by augmenting prostanoid generation. Its more potent activity against AMP and other bronchoconstrictor stimuli, that are considered to involve mast cell mediators, suggests an additional action on mast cell functions possibly at the level of the Ca++/Mg(++)-ATPase.
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PMID:Inhibition of adenosine 5'-monophosphate- and methacholine-induced bronchoconstriction in asthma by inhaled frusemide. 215 Oct 34

A decrease in activity of Ca2(+)-ATPase and activation of Na+, K(+)-ATPase, correlating with elevation in content of phosphatidyl inositol and phosphatidyl serine, were detected in erythrocyte membranes of patients with the infectional-allergic form of bronchial asthma. Microviscosity of the erythrocyte membranes, estimated by fluorescence spectra of pyrene, was not altered, while negative charge as shown by ANS- fluorescence, was slightly increased on the membrane surface. Euphylline, intal, levamizole and glucocorticosteroid were found to regulate the ATPases activity in vivo and in vitro.
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PMID:[Structural-functional properties of erythrocyte membranes in patients with infectious-allergic bronchial asthma]. 253 46

Contraction of tracheal smooth muscle requires the binding of Ca2+ to calmodulin, which then binds to and activates MLCK. The Ca2+-calmodulin-MLCK complex catalyzes the phosphorylation of myosin, which causes contraction by stimulating actin-activated Mg2+-ATPase activity of myosin. Myosin phosphorylation appears to be a transient event that is responsible for a high velocity of shortening. The mechanism responsible for maintenance of isometric force is unknown, although a second Ca2+-dependent mechanism with a greater sensitivity to Ca2+ than the activation of MLCK has been hypothesized. Force would be maintained through the slow cycling of nonphosphorylated cross-bridges or a small population of phosphorylated cross-bridges. Tracheal smooth muscle utilizes both extracellular and intracellular pools of Ca2+ for contraction. Moreover, the membrane channels through which extracellular Ca2+ passes have been subdivided into potential-dependent channels (PDCs) and receptor-operated channels (ROCs) independent of membrane potential. The relative extent to which extracellular and intracellular sources of Ca2+ as well as PDCs and ROCs are utilized depends on the agonist used for contraction, its concentration, and the type and location of the smooth muscle being investigated. Calcium antagonists such as verapamil and nifedipine, which reportedly block PDCs but not ROCs, are much better inhibitors of tracheal smooth muscle contractions induced by serotonin than those induced by acetylcholine, histamine, and leukotriene D4, indicating an effect of these latter three agents on ROCs. Relaxation of tracheal smooth muscle following stimulation of beta-adrenergic receptors most likely results from an increase in cAMP that stimulates a cAMP-dependent protein kinase to catalyze a protein phosphorylation that leads to relaxation by decreasing the intracellular concentration of Ca2+. The primary mechanisms whereby cAMP is thought to reduce intracellular Ca2+ to effect relaxation include: activation of a calmodulin-sensitive Ca2+ ATPase in the plasma and sarcoplasmic reticulum membranes, and extrusion of Ca2+ by a Na+-Ca2+ exchange mechanism coupled to Na+-K+-ATPase in the cell membrane. A more controversial mechanism for relaxation that bypasses Ca2+ might involve the dephosphorylation of myosin. Leukotrienes are released by various stimuli, including immunologic challenge, and have been considered as important mediators of bronchoconstriction in allergic asthma.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Tracheal smooth muscle. 301 93

Challenges with ouabain and histamine were performed a week apart in 10 patients with asthma and 5 normal subjects. Concentrations were increased cumulatively until specific airway conductance decreased by 30% or the maximal concentration of 1.0% was reached. At low concentrations, ouabain induced bronchodilatation in six patients who had asthma. Bronchodilatation gradually decreased with increasing concentrations and was followed by bronchoconstriction in two patients with asthma who had high airway sensitivity to histamine. Ouabain caused only bronchoconstriction in three patients with severe asthma. The normal subjects showed mild bronchodilatation or no response to ouabain. Several possible biochemical mechanisms may be responsible for the bronchodilatory response to low doses of ouabain, such as stimulation of adenylate cyclase or (Na+,K+)-adenosine triphosphatase. The absence of a bronchodilatory response to ouabain in patients with severe asthma suggests an impairment in the activity of these enzymes.
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PMID:Airway responses to inhaled ouabain in subjects with and without asthma. 301 88

Adenosine triphosphatase (ATPase) activities were compared in leukocytes of asthmatic and nonasthmatic children. Both Mg(2+)- and Ca(2+)-dependent ATPase activities were significantly elevated in two membrane fractions (59 to 66%) and in a superntant fraction (68 to 72%) prepared from sonicated leukocytes of asthmatic subjects. Intact cell surface or ecto ATPase was also elevated (67 to 76%) in asthmatic leukocytes. Alternate day glucocorticosteroid therapy was associated with leukocyte ATPase activities intermediate between those for asthmatics not receiving steroids and for nonasthmatic control subjects. Incubation of normal leukocytes with 10(-8) M hydrocortisone or leukocyte membranes with 10(-4)-10(-3) M hydrocortisone in vitro also resulted in decreased ATPase activities. The elevated leukocyte ATPase activities appear to relate to the adrenergic imbalance in asthma previously characterized by reduced beta adrenergic responsiveness of adenylate cyclase and suggest the possibility of more than one enzymatic abnormality intrinsic to the asthmatic condition.
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PMID:Increased adenosine triphosphatase in leukocytes of asthmatic children. 427 34


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