pubmed-article:3014906 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:3014906 | lifeskim:mentions | umls-concept:C0225828 | lld:lifeskim |
pubmed-article:3014906 | lifeskim:mentions | umls-concept:C0022245 | lld:lifeskim |
pubmed-article:3014906 | lifeskim:mentions | umls-concept:C0205409 | lld:lifeskim |
pubmed-article:3014906 | lifeskim:mentions | umls-concept:C0597484 | lld:lifeskim |
pubmed-article:3014906 | lifeskim:mentions | umls-concept:C0182537 | lld:lifeskim |
pubmed-article:3014906 | pubmed:issue | 1 Pt 2 | lld:pubmed |
pubmed-article:3014906 | pubmed:dateCreated | 1986-8-21 | lld:pubmed |
pubmed-article:3014906 | pubmed:abstractText | It has been suggested that catecholamines directly stimulate Na+-K+ pump activity in heart; however, these studies on multicellular preparations are confounded by possible alterations of extracellular K+ concentrations ([K+]o). We reinvestigated this problem by studying the effect of the beta-agonist isoproterenol (Iso) on intracellular Na+ activity (aiNa) in ventricular myocytes enzymatically isolated from rabbit heart. In 5 mM [K+]o, 0.1 microM Iso caused a 24.6 +/- 2.0% decrease of aiNa. Exposure to 1 microM Iso only caused a small additional decrease (27.8 +/- 2.4%), while a diminution of aiNa could already be noticed with only 10 nM Iso (12.8 +/- 1.9% diminution). Myocytes superfused with 15 mM [K+]o also exhibited a significant decrease of aiNa (22.9 +/- 3.6%) when exposed to 0.1 microM Iso. These data argue that accumulation of external K+ does not account for the effect of Iso on steady-state aiNa as postulated by Gadsby (Nature Lond. 306: 691-693, 1983). Furthermore, aiNa in myocytes superfused with 1.5 mM [K+]o decreased by only 8.7% on addition of 0.1 microM Iso. The latter observation suggests that the beta-agonist effect on aiNa regulation is directly or indirectly dependent on membrane potential and/or aiNa. Finally, kinetic analysis of the effect of 1 microM Iso on the decrease in aiNa on changing [K+]o from 1.5 to 5 mM demonstrated that the time course of aiNa recovery was accelerated by a factor of 1.9. This readily suggests that active Na+ transport is directly stimulated by Iso. The much greater relative effect of Iso on the time constant than on steady-state aiNa further indicates that Iso may also increase passive Na+ influx. | lld:pubmed |
pubmed-article:3014906 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:3014906 | pubmed:language | eng | lld:pubmed |
pubmed-article:3014906 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:3014906 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:3014906 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:3014906 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:3014906 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:3014906 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:3014906 | pubmed:month | Jul | lld:pubmed |
pubmed-article:3014906 | pubmed:issn | 0002-9513 | lld:pubmed |
pubmed-article:3014906 | pubmed:author | pubmed-author:BaumgartenC... | lld:pubmed |
pubmed-article:3014906 | pubmed:author | pubmed-author:DésiletsMM | lld:pubmed |
pubmed-article:3014906 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:3014906 | pubmed:volume | 251 | lld:pubmed |
pubmed-article:3014906 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:3014906 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:3014906 | pubmed:pagination | H218-25 | lld:pubmed |
pubmed-article:3014906 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
pubmed-article:3014906 | pubmed:meshHeading | pubmed-meshheading:3014906-... | lld:pubmed |
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pubmed-article:3014906 | pubmed:meshHeading | pubmed-meshheading:3014906-... | lld:pubmed |
pubmed-article:3014906 | pubmed:year | 1986 | lld:pubmed |
pubmed-article:3014906 | pubmed:articleTitle | Isoproterenol directly stimulates the Na+-K+ pump in isolated cardiac myocytes. | lld:pubmed |
pubmed-article:3014906 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:3014906 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:3014906 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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