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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
1986-1-6
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pubmed:abstractText |
Dose-response relations for the increase in the amplitude of Ca current (ICa) on external application of isoprenaline (ISP) and internally applied cyclic AMP (cAMP) or catalytic subunit of cAMP-dependent protein kinase (C subunit) were established in single ventricular cells of the guinea pig. An intracellular dialysis technique was used. The threshold concentration was for ISP 10(-9) M, for cAMP 3 microM (pipette concentration to which 10(-5) M 3-isobutyl-1-methylxanthine was added) and for C subunit around 0.4 microM (pipette concentration). The concentrations for the half-maximal effect were 3.7 X 10(-8) M (ISP), 5.0 microM (cAMP) and 0.95 microM (C subunit) and for the maximum effect 10(-6) M (ISP), 15-20 microM (cAMP) and 3-4 microM (C subunit). For all three agents the maximum increase in the Ca current density was similar (a factor of 3-4), suggesting that they converge on the same site of the Ca channel. Accordingly, the effects of cAMP and C subunit on ICa were non-additive to those of ISP. From these data the relationship both between concentrations of ISP and cAMP and between those of cAMP and active C subunit in terms of their effects on ICa could be estimated and were compared with those obtained in broken cell preparations. A competitive inhibitor of phosphorylation, 5'-adenylyl-imidodiphosphate (5 mM), greatly reduced the effects of ISP and C subunit on ICa. Cell dialysis with 3 mM adenosine-5'-(gamma-thio)-triphosphate, which produces a dephosphorylation-resistant phosphorylation, markedly potentiated the effects of ISP and cAMP on ICa.(ABSTRACT TRUNCATED AT 250 WORDS)
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP,
http://linkedlifedata.com/resource/pubmed/chemical/Ion Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Isoproterenol,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Adrenergic, beta
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0031-6768
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
405
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
285-93
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:2415919-Animals,
pubmed-meshheading:2415919-Calcium,
pubmed-meshheading:2415919-Cyclic AMP,
pubmed-meshheading:2415919-Dose-Response Relationship, Drug,
pubmed-meshheading:2415919-Guinea Pigs,
pubmed-meshheading:2415919-Ion Channels,
pubmed-meshheading:2415919-Isoproterenol,
pubmed-meshheading:2415919-Myocardium,
pubmed-meshheading:2415919-Protein Kinases,
pubmed-meshheading:2415919-Receptors, Adrenergic, beta
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pubmed:year |
1985
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pubmed:articleTitle |
On the mechanism of beta-adrenergic regulation of the Ca channel in the guinea-pig heart.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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