Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P20020 (adenosine triphosphatase)
 3,299 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

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

Previous studies have documented decreased levels of platelet sodium, potassium adenosine triphosphatase (Na+, K+ ATPase) enzyme activity in allergic subjects. The purpose of this study was to determine the effect of several drugs used to treat allergy and asthma on platelet Na+,K+ ATPase activity. Platelets from five allergic and five nonallergic subjects were incubated at 37 degrees C for 30 minutes with cortisol (1.0 to 3.6 micrograms/ml), theophylline (10 to 40 micrograms/ml), cromolyn (0.5 to 2.0 micrograms/ml), albuterol (3 to 24 ng/ml), chlorpheniramine (2.5 to 20 micrograms/ml), or diluent. The platelets were then rinsed, sonicated, serially centrifuged, and assayed for Na+,K+ ATPase activity nmol/min x micrograms protein by spectrophotometry. Mean activity (+/- 1 SEM) for the diluent incubation was 5.55 +/- 1.27 nmol/min x micrograms protein and 0.91 +/- 0.32 nmol/min x micrograms protein for the nonallergic and allergic subjects, respectively. The enzyme activity of allergic platelets (same units as above) increased after incubation with the following drugs: cortisol, 6.07 +/- 1.75 (p < 0.025) at 1.0 micrograms/ml, 7.55 +/- 1.36 (p < 0.005) at 1.4 micrograms/ml, and 5.95 +/- 0.91 (p < 0.025) at 1.8 micrograms/ml; cromolyn, 5.79 +/- 1.68 (p < 0.050) at 1.0 micrograms/ml; and albuterol, 4.43 +/- 1.61 (p < 0.05) at 12 ng/ml. Theophylline and chlorpheniramine did not have a similar effect on Na+,K+ ATPase activity. These data show that some of the drugs commonly used to treat allergic patients, especially anti-inflammatory agents, can increase the depressed platelet levels of Na+,K+ ATPase activity observed in allergic subjects. Modulation of Na+,K+ ATPase is a possible mechanism of action for these drugs in vivo.
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PMID:In vitro modulation of platelet sodium, potassium adenosine triphosphatase enzyme activity by antiallergy drugs. 839 60