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)

The enzymatic response to injury appears as an increase in enzymatic activity in the periphery of burns and other injuries. The following processes constitute the enzymatic response: 1) release, 2) activation and 3) synthesis of enzymes. Processes 2) and 3) are dependent upon the fibroblast, which is an activated fibrocyte. Among the fibrocyte activators, and thus among the mediators of the enzymatic response, are histamine, serotonin, kinins, prostaglandins etc. The effects of non-steroidal anti-inflammatory drugs on the enzymatic response to burn injury were studied. Indomethacin, mefenamic acid or aspirin, suspended in carboxymethylcellulose, were given to rats by stomach tube. Controls received carboxymethylcellulose only. Circular burns were inflicted on anaesthetized animals which were killed 30 min, 2 h or 4 h after burning. The burns were studied histologically and enzyme histochemically by using the methods for prostaglandin synthetase, esterases, and adenosine triphosphatase. Aspirin had no effect on the enzymatic response. Mefenamic acid and indomethacin caused a less severe enzymatic response in the 4-h groups as compared to control rats.
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PMID:On the enzymatic response to injury and its mediators. 15 85

Salmonella typhimurium, an organism that invades intestinal mucosa but does not elaborate a traditional enterotoxin, evokes ileal secretion by causing alterations in active sodium and chloride transport mechanisms. To evaluate the possibility that these changes in transport might be related to the adenylate cyclase-cyclic AMP or NA+-K+-adenosine triphosphatase (ATPase) systems, mucosal adenylate cyclase, cAMP phosphodiesterase, Na+-K+ and Mg++ ATPase activities, and cAMP concentrations were measured in rabbit ileal loops infected with two strains of S. typhimurium. Strain TML invades the mucosa and evokes fluid secretion whereas strain SL 1027 invades but does not evoke secretion. Cholera toxin-stimulated loops were also studied. When compared to control loops, TML-infected mucosa demonstrated a marked increase in adenylate cyclase activity, in cAMP concentration, and no change in phosphodiesterase or ATPase activities. SL 1027-infected mucosa demonstrated no change in either adenylate cyclase or ATPase activities. Indomethacin pretreatment of cyclase activation. In contrast, indomethacin pretreatment of cholera toxin exposed animals resulted in only a partial reduction of secretion while not altering the stimulation of adenylate cyclase. These results suggest that: (1) S. typhimurium causes ileal secretion by stimulating adenylate cyclase; (2) mucosal invasion alone (SL 1027) is not sufficient to activate adenylate cyclase, and (3) Na+-K+-ATPase does not appear to be involved in salmonella-induced secretion. The mechanism of salmonella activation of adenylate cyclase is unclear but apparently differs from that of cholera toxin in that it is inhibited by indomethacin. This might be explained by the participation of prostaglandins in the salmonella activation process.
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PMID:Pathogenesis of Salmonella-mediated intestinal fluid secretion. Activation of adenylate cyclase and inhibition by indomethacin. 17 99

Prostacyclin (PGI2) did not alter the basal perfusion pressure in the isolated rat mesenteric arteries perfused with Krebs' solution, but produced a biphasic effect in arteries preconstricted with norepinephrine or arginine vasopressin: constriction, then prolonged dilation. Both these components of PGI2 effect were diminished in arteries denuded of their endothelia by a 10 min perfusion with distilled water or p-bromophenacyl bromide (10 microM). The present study elucidates the mechanism of these PGI2 actions. Indomethacin (0.28 microM) SQ 29548 (1 microM, thromboxane A2 receptor antagonist), saralasin (1 microM, angiotensin II receptor antagonist) or the free radical scavengers, superoxide dismutase (60 U/ml) and catalase (40 U/ml) did not inhibit the initial vasoconstriction, suggesting it was not mediated through endothelially generated thromboxane A2, angiotensin II or oxygen-derived free radicals. However, ethylene glycol bis(beta-aminoethyl ether)-N,N'-tetraacetic acid (50 microM; Ca++ chelating agent), 8-(diethyl-amino)octyl 3,4,5-trimethoxy benzoate (10 microM; intracellular Ca++ antagonist), or neomycin (5 mM; phospholipase-C inhibitor) abolished the vasoconstriction. Ouabain (0.5 mM) did not affect the vasodilation, but perfusion with excess (50 mM) or 0 K+ Krebs' solution abolished it, suggesting this PGI2 action involves changes in membrane K+ conductance via a mechanism independent of Na+/K+ adenosine triphosphatase. Vasodilation evoked by BRL 34915 (K+ channel activator) was similarly attenuated under these conditions, but not by ouabain. Furthermore, procaine (1 mM; nonspecific K+ channel inhibitor), but not apamin (0.5 microM) or tetraethylammonium (10 mM) blocked PGI2- and BRL 34915-induced vasodilation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanism of vascular actions of prostacyclin in the rat isolated perfused mesenteric arteries. 210 93

1. Indomethacin inhibits calcium-stimulated adenosine triphosphatase (Ca2+-ATPase), calcium, magnesium-stimulated adenosine triphosphatase (Ca2+,Mg2+-ATPase) and magnesium-stimulated adenosine triphosphatase (Mg2+-ATPase) activities in rat brain synaptic vesicles in vitro. 2. The Ca2+-ATPase activity is most strongly affected by this drug all of the activities of ATPases tested. 3. The decrease of Ca2+-ATPase activity by addition of indomethacin is due to a decrease of Vmax. 4. The Ki values for this drug for ATP and Ca2+ in Ca2+-ATPase were 1.13 mM and 0.68 mM, respectively.
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PMID:Effect of indomethacin on Ca2+-stimulated adenosine triphosphatase in the synaptic vesicles of rat brain in vitro. 621 40

The cytotoxic action of the S component of leukocidin from Staphylococcus aureus on rabbit polymorphonuclear leukocytes was supported by the following observations, (i) Leukocytes displayed a large chemotactic response to the S component (10(-10) M) as well as to the chemotactic factor N-formylmethionylleucylphenylalanine (10(-11) M). (ii) The S component stimulated high levels of phospholipase A2 activity in the cell membranes, with concomitant synthesis and release of prostaglandins. (iii) Uptake of 45Ca into leukocytes exposed to the S component was about double the rate of uptake into untreated cells. The increased 45Ca uptake into the cells was not inhibited by trifluoperazine and ruthenium red. (iv) Indomethacin and alloxazine, which had no effects on the binding of the S component to the cells, attenuated markedly the stimulation of phospholipase A2 activity, the syntheses of prostaglandins, and the increased uptake of 45Ca caused by the S component. The F component of leukocidin, bound to rabbit leukocytes with the aid of the S component, rapidly induced complete release of 86Rb from preloaded leukocytes. This release resulted from stimulation of ouabain-insensitive (Na+ + K+)-adenosine triphosphatase activity and inhibition of cyclic AMP-dependent protein kinase.
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PMID:Mode of action of staphylococcal leukocidin: effects of the S and F components on the activities of membrane-associated enzymes of rabbit polymorphonuclear leukocytes. 627 2