Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
|
pubmed:dateCreated |
1985-4-9
|
pubmed:abstractText |
Epinephrine is shown to stimulate heart cell beating by both alpha- and beta-adrenergic mechanisms. The beta-adrenergic effect undergoes desensitization in one to two minutes after beta-agonist addition. A beta-antagonist did not cause desensitization. The desensitization response is quantitatively related to the concentration of cAMP produced in the cells. The alpha-adrenergic component of epinephrine action does not undergo desensitization nor does it have effects on the beta-adrenergic stimulation of cell beating or cAMP production. Other alpha-agonists and antagonists also have no effect on cAMP production. Prostaglandin E1 increased cellular cAMP by a mechanism that was additive with the beta-adrenergic mechanism. Both prostaglandin E1 and beta-agonists caused phosphorylation of both glycogen phosphorylase and glycogen synthase. Prostaglandin E1 did not desensitize the cells to beta-adrenergic stimulation of cAMP. The data show that heart cells undergo a rapid homologous desensitization to beta-agonists when treated with epinephrine or isoproterenol. The desensitization is quantitatively related to the cellular cAMP concentration, but cAMP produced by another mechanism does not desensitize the cells. No alpha-adrenergic effects on the beta-induced desensitization were observed.
|
pubmed:grant | |
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adrenergic alpha-Agonists,
http://linkedlifedata.com/resource/pubmed/chemical/Adrenergic beta-Agonists,
http://linkedlifedata.com/resource/pubmed/chemical/Alprostadil,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP,
http://linkedlifedata.com/resource/pubmed/chemical/Epinephrine,
http://linkedlifedata.com/resource/pubmed/chemical/Prostaglandins E,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Adrenergic, beta
|
pubmed:status |
MEDLINE
|
pubmed:issn |
0746-3898
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
9
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
449-60
|
pubmed:dateRevised |
2007-11-14
|
pubmed:meshHeading |
pubmed-meshheading:6151955-Adrenergic alpha-Agonists,
pubmed-meshheading:6151955-Adrenergic beta-Agonists,
pubmed-meshheading:6151955-Alprostadil,
pubmed-meshheading:6151955-Animals,
pubmed-meshheading:6151955-Cells, Cultured,
pubmed-meshheading:6151955-Cyclic AMP,
pubmed-meshheading:6151955-Drug Resistance,
pubmed-meshheading:6151955-Epinephrine,
pubmed-meshheading:6151955-Heart,
pubmed-meshheading:6151955-Heart Rate,
pubmed-meshheading:6151955-Myocardium,
pubmed-meshheading:6151955-Prostaglandins E,
pubmed-meshheading:6151955-Rats,
pubmed-meshheading:6151955-Receptors, Adrenergic, beta
|
pubmed:articleTitle |
Homologous desensitization of rat heart cells to beta-adrenergic stimulation and the absence of alpha-adrenergic or prostaglandin E1 effects.
|
pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't
|