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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
1990-12-5
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pubmed:abstractText |
Spontaneous catecholamine (CA) release from bovine chromaffin cells maintained in primary tissue culture has been measured after pre-loading the cells with [3H]noradrenaline. Ouabain inhibited 86Rb+ uptake and increased 3H release in a concentration-dependent manner during a 60 min incubation period. Low external Na+ (5 mM: Li+ substitution) also increased 3H release. Whereas the 3H-releasing action of ouabain was maintained, the Li(+)-evoked release decreased with time. The effects of both ouabain and low Na+ solution on 3H release were completely inhibited by removal of Ca2+ from the external medium even though in Ca2(+)-free solution ouabain further inhibited 86Rb+ uptake into the cells. Readmission of Ca2+ to Na(+)-loaded cells (10-4 M-ouabain in Ca2(+)-free-1 mM-EGTA solution for 60 min) markedly increased the release of 3H. In the additional presence of diphenylhydantoin (DPH, 10-4 M) 3H release was significantly less on Ca2+ readmission. The 3H release from Na(+)-loaded cells was proportional to the concentration of Ca2+ readmitted. The 3H release was further increased from Na(+)-loaded cells in response to Ca2+ readmission when [Na+]o was lowered from 149 to 5 mM (Li+, choline+, Tris+ or sucrose substitution) though Li+ was less effective than the other Na+ substitutes. Potassium removal from the external medium significantly inhibited the 3H release evoked by Ca2+ readmission to Na(+)-loaded cells, even when [Ca2+]o was greater than normal (7.5 mM) or if Ca2+ was readmitted in low [Na+]o solution. Rb+, Cs+ or Li+ could substitute for K+ with the order of potency: Rb+ greater than or equal to K+ greater than Cs+ greater than Li+. A slight increase of external K+ (10.8 mM) potentiated the 3H release from Na(+)-loaded cells on Ca2+ readmission, but a higher concentration of K+ (149.4 mM) had the opposite action. The data is consistent with the hypothesis that ouabain-evoked CA release from bovine chromaffin cells is, in part, a consequence of an internal Na(+)-dependent Ca2+ influx. The evidence also suggests that there is Na(+)-Ca2+ competition at the external arm of the exchanger together with a monovalent cation activation site.
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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/Carrier Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Catecholamines,
http://linkedlifedata.com/resource/pubmed/chemical/Norepinephrine,
http://linkedlifedata.com/resource/pubmed/chemical/Ouabain,
http://linkedlifedata.com/resource/pubmed/chemical/Phenytoin,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium-Calcium Exchanger,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium-Potassium-Exchanging ATPase,
http://linkedlifedata.com/resource/pubmed/chemical/Tetrodotoxin
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0958-0670
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
75
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
573-86
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:2171585-Adrenal Glands,
pubmed-meshheading:2171585-Animals,
pubmed-meshheading:2171585-Calcium,
pubmed-meshheading:2171585-Carrier Proteins,
pubmed-meshheading:2171585-Catecholamines,
pubmed-meshheading:2171585-Cattle,
pubmed-meshheading:2171585-Cells, Cultured,
pubmed-meshheading:2171585-Chromaffin System,
pubmed-meshheading:2171585-Norepinephrine,
pubmed-meshheading:2171585-Ouabain,
pubmed-meshheading:2171585-Phenytoin,
pubmed-meshheading:2171585-Sodium,
pubmed-meshheading:2171585-Sodium-Calcium Exchanger,
pubmed-meshheading:2171585-Sodium-Potassium-Exchanging ATPase,
pubmed-meshheading:2171585-Tetrodotoxin
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pubmed:year |
1990
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pubmed:articleTitle |
Catecholamine release from bovine chromaffin cells: the role of sodium-calcium exchange in ouabain-evoked release.
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pubmed:affiliation |
Neuroscience Group, Faculty of Medicine, University of Newcastle, New South Wales, Australia.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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