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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
4 Pt 2
|
| pubmed:dateCreated |
1994-11-18
|
| pubmed:abstractText |
The goal of this study was to assess beta-adrenergic receptor (beta-AR) signaling mechanisms in mediating physiological responses to sympathomimetic amines after 45 min coronary artery occlusion followed by 45 min reperfusion. At this time, isoproterenol (Iso) infusion (0.1 microgram/kg-1.min-1, n = 5) increased percent wall thickening in previously ischemic subendocardium (Endo) more than in nonischemic Endo (12.6 +/- 1.2 vs. 7.2 +/- 0.6%, P < 0.05), whereas forskolin (25 nmol.kg-1.min-1, n = 6) elicited the opposite effect (3.6 +/- 0.6 vs. 10.4 +/- 2.8%, P < 0.05). During Iso and forskolin infusions increases in regional myocardial blood flow in the previously ischemic zone were similar to the nonischemic zone. In all groups, total beta-AR density was depressed in previously ischemic Endo compared with nonischemic Endo (65 +/- 7 vs. 82 +/- 8 fmol/mg, P < 0.05), but the fraction of beta-AR binding agonist with high affinity increased (82 +/- 4 vs. 49 +/- 1%, P < 0.05). The changes in beta-AR were associated with a decrease in Iso-stimulated adenylyl cyclase (22 +/- 8%), a decrease in guanosine 5'-triphosphate (GTP)-stimulatory protein (Gs) (23 +/- 6%), and a decrease in inhibitory G proteins (16 +/- 4%). However, regional Endo functional responsiveness to beta-AR stimulation was enhanced in reperfused myocardium in response to Iso but not to forskolin. Thus the mechanism of increased number of beta-AR binding agonist with high affinity in previously ischemic myocardium predominated over persistent downregulation of total beta-AR density and reductions in Gs and adenylyl cyclase activity and correlated best with the physiological response to beta-AR stimulation. These data may also suggest that Iso exerts an action distal to adenylyl cyclase in previously ischemic myocardium.
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| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Forskolin,
http://linkedlifedata.com/resource/pubmed/chemical/GTP-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Isoproterenol,
http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Adrenergic, beta
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Oct
|
| pubmed:issn |
0002-9513
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
267
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
H1578-88
|
| pubmed:dateRevised |
2007-11-15
|
| pubmed:meshHeading |
pubmed-meshheading:7943405-Amino Acid Sequence,
pubmed-meshheading:7943405-Animals,
pubmed-meshheading:7943405-Blood Pressure,
pubmed-meshheading:7943405-Coronary Vessels,
pubmed-meshheading:7943405-Dogs,
pubmed-meshheading:7943405-Electrophoresis, Polyacrylamide Gel,
pubmed-meshheading:7943405-Female,
pubmed-meshheading:7943405-Forskolin,
pubmed-meshheading:7943405-GTP-Binding Proteins,
pubmed-meshheading:7943405-Heart,
pubmed-meshheading:7943405-Heart Rate,
pubmed-meshheading:7943405-Hemodynamics,
pubmed-meshheading:7943405-Isoproterenol,
pubmed-meshheading:7943405-Male,
pubmed-meshheading:7943405-Molecular Sequence Data,
pubmed-meshheading:7943405-Myocardial Ischemia,
pubmed-meshheading:7943405-Myocardial Reperfusion,
pubmed-meshheading:7943405-Myocardium,
pubmed-meshheading:7943405-Peptide Fragments,
pubmed-meshheading:7943405-Receptors, Adrenergic, beta,
pubmed-meshheading:7943405-Signal Transduction,
pubmed-meshheading:7943405-Time Factors,
pubmed-meshheading:7943405-Ventricular Function, Left
|
| pubmed:year |
1994
|
| pubmed:articleTitle |
Mechanisms mediating responsiveness to beta-adrenergic stimulation after coronary reperfusion in conscious dogs.
|
| pubmed:affiliation |
Department of Medicine, Harvard Medical School, Brigham and Women's Hospital, Boston 02115.
|
| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|