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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6 Pt 2
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pubmed:dateCreated |
1995-1-27
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pubmed:abstractText |
Hypoxic pulmonary vasoconstriction is refractory to beta-adrenergic receptor (beta-AR)-mediated pulmonary vasodilation. We hypothesized that hypoxic pulmonary arteries release adenosine (Ado) that antagonizes beta-AR-mediated pulmonary vasodilation. Using isolated rat pulmonary artery rings, we investigated 1) the effect of hypoxia and exogenous Ado on beta-AR-mediated pulmonary vasodilation, 2) the intracellular site of dysfunctional beta-AR-mediated pulmonary vasodilation in hypoxia, and 3) the Ado receptor subtype responsible for dysfunction of beta-AR-mediated pulmonary vasodilation. Hypoxia attenuated normal beta-AR-mediated pulmonary vasodilation to isoproterenol (97.5 +/- 0.8 vs. 71.5 +/- 2.3%, P < 0.01). In contrast, forskolin induced the same vasorelaxation in hypoxic pulmonary rings as controls (P = 0.09). Incubation of normoxic rings with Ado attenuated the vasorelaxation response induced by beta-AR stimulation (71.5 +/- 5.9%, P < 0.01), similar to the effect observed in hypoxia. Both nonspecific Ado receptor blockade (8-sulfophenyl-theophylline) and specific A1-receptor blockade (8-cyclopentyl-1,3-dimethylxanthine) restored the vasorelaxation response of hypoxic rings induced by beta-AR stimulation (93.3 +/- 2.3 and 92.2 +/- 2.8%, P < 0.01). The effects of hypoxia and Ado were reproduced by a specific A1 agonist (2-chloro-N6-cyclopentyladenosine), demonstrating impaired vasorelaxation induced by beta-AR stimulation in normoxia (70.6 +/- 4.5%, P < 0.01). From these data, we conclude that hypoxia antagonizes beta-AR-mediated pulmonary vasodilation via an Ado A1-receptor mechanism.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/2-chloro-N(6)cyclopentyladenosine,
http://linkedlifedata.com/resource/pubmed/chemical/Adenosine,
http://linkedlifedata.com/resource/pubmed/chemical/Forskolin,
http://linkedlifedata.com/resource/pubmed/chemical/Isoproterenol,
http://linkedlifedata.com/resource/pubmed/chemical/Oxygen,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Adrenergic, beta,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Purinergic P1
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0002-9513
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
267
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
H2179-85
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:7810717-Adenosine,
pubmed-meshheading:7810717-Animals,
pubmed-meshheading:7810717-Forskolin,
pubmed-meshheading:7810717-Isoproterenol,
pubmed-meshheading:7810717-Oxygen,
pubmed-meshheading:7810717-Pulmonary Artery,
pubmed-meshheading:7810717-Rats,
pubmed-meshheading:7810717-Rats, Sprague-Dawley,
pubmed-meshheading:7810717-Receptors, Adrenergic, beta,
pubmed-meshheading:7810717-Receptors, Purinergic P1,
pubmed-meshheading:7810717-Vasodilation
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pubmed:year |
1994
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pubmed:articleTitle |
Adenosine A1-receptor mechanisms antagonize beta-adrenergic pulmonary vasodilation in hypoxia.
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pubmed:affiliation |
Department of Surgery, University of Colorado Health Sciences Center, Denver 80262.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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