pubmed-article:2989364 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:2989364 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
pubmed-article:2989364 | lifeskim:mentions | umls-concept:C0027950 | lld:lifeskim |
pubmed-article:2989364 | lifeskim:mentions | umls-concept:C0597357 | lld:lifeskim |
pubmed-article:2989364 | lifeskim:mentions | umls-concept:C0001443 | lld:lifeskim |
pubmed-article:2989364 | lifeskim:mentions | umls-concept:C1158882 | lld:lifeskim |
pubmed-article:2989364 | lifeskim:mentions | umls-concept:C0205463 | lld:lifeskim |
pubmed-article:2989364 | lifeskim:mentions | umls-concept:C1551336 | lld:lifeskim |
pubmed-article:2989364 | lifeskim:mentions | umls-concept:C1709060 | lld:lifeskim |
pubmed-article:2989364 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:2989364 | pubmed:dateCreated | 1985-8-19 | lld:pubmed |
pubmed-article:2989364 | pubmed:abstractText | Adenosine specifically inhibits superoxide anion generation by N-formyl-methionyl-leucyl-phenylalanine-stimulated neutrophils without affecting either degranulation or "aggregation." We present data that also supports the hypothesis that adenosine engages a specific cell surface receptor to mediate inhibition of stimulated neutrophils. Theophylline (10 and 100 mu M), a competitive antagonist at adenosine receptors, reversed the effects of adenosine (0.1 mu M) on superoxide anion generation by stimulated neutrophils. The adenosine analogue 5'N-ethylcarboxamidoadenosine (NECA) was a more potent inhibitor of superoxide anion generation than either N6-phenylisopropyladenosine (PIA) or adenosine, an order of potency consistent with that previously demonstrated for adenosine A2 receptors. 2-Chloroadenosine inhibited superoxide anion generation at concentrations similar to NECA. [3H]-NECA and [3H]-2-chloroadenosine bound to a single receptor on intact neutrophils. The characteristics of the receptors for [3H]-NECA and [3H]-2-chloroadenosine were similar (Kd = 0.22 and 0.23 mu M, respectively; number of binding sites = 9.31 and 11.1 X 10(3) sites/cell, respectively). NECA, 2-chloroadenosine, adenosine, and PIA inhibited binding of [3H]-NECA with a rank order similar to that for inhibition of superoxide anion generation (NECA = 2-chloroadenosine greater than adenosine greater than PIA). There was 50% inhibition of superoxide anion generation by NECA at approximately 20% receptor occupancy. Adenosine, derived from damaged tissues, may serve as a specific, endogenous modulator of superoxide anion generation by activated neutrophils through interaction at this newly described receptor on human neutrophils. | lld:pubmed |
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pubmed-article:2989364 | pubmed:language | eng | lld:pubmed |
pubmed-article:2989364 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2989364 | pubmed:citationSubset | AIM | lld:pubmed |
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pubmed-article:2989364 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:2989364 | pubmed:month | Aug | lld:pubmed |
pubmed-article:2989364 | pubmed:issn | 0022-1767 | lld:pubmed |
pubmed-article:2989364 | pubmed:author | pubmed-author:HirschhornRR | lld:pubmed |
pubmed-article:2989364 | pubmed:author | pubmed-author:WeissmannGG | lld:pubmed |
pubmed-article:2989364 | pubmed:author | pubmed-author:CronsteinB... | lld:pubmed |
pubmed-article:2989364 | pubmed:author | pubmed-author:RosensteinE... | lld:pubmed |
pubmed-article:2989364 | pubmed:author | pubmed-author:KramerS BSB | lld:pubmed |
pubmed-article:2989364 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:2989364 | pubmed:volume | 135 | lld:pubmed |
pubmed-article:2989364 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:2989364 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:2989364 | pubmed:pagination | 1366-71 | lld:pubmed |
pubmed-article:2989364 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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pubmed-article:2989364 | pubmed:year | 1985 | lld:pubmed |
pubmed-article:2989364 | pubmed:articleTitle | Adenosine; a physiologic modulator of superoxide anion generation by human neutrophils. Adenosine acts via an A2 receptor on human neutrophils. | lld:pubmed |
pubmed-article:2989364 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:2989364 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:2989364 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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