Regulation of the sodium-potassium pump in cultured rat skeletal myotubes by intracellular sodium ions
The properties of the Na-K pump and some of the factors controlling its amount and function were studied in rat myotubes in culture. The number of Na-K pump sites was quantified by measuring the amount of [3H]ouabain bound to whole-cell preparations. Activity of the pump was determined by measuremen...
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E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
1989 |
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| Umfang: |
8 Ill. ; 3 Tab. 7 |
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| Reproduktion: |
Wiley InterScience Backfile Collection 1832-2000 |
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| Übergeordnetes Werk: |
in: Journal of Cellular Physiology - New York, NY [u.a.] : Wiley-Liss, 140(1989) vom: Jan., Seite 131-137 |
| Übergeordnetes Werk: |
volume:140 ; year:1989 ; month:01 ; pages:131-137 ; extent:7 |
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| 520 | |a The properties of the Na-K pump and some of the factors controlling its amount and function were studied in rat myotubes in culture. The number of Na-K pump sites was quantified by measuring the amount of [3H]ouabain bound to whole-cell preparations. Activity of the pump was determined by measurement of oua-bain-sensitive 86Rb-uptake and component of membrane potential. Chronic treatment of myotubes with tetrodotoxin (TTX), which lowers [Na]i, decreased the number of Na-K pumps, the ouabain-sensitive 86Rb uptake, and the size of the electrogenic pump component of Em. In contrast, chronic treatment with either ouabain or veratridine, which increases [Na+]i, resulted in an elevated level of Na-K pump sites. This effect was blocked by inhibitors of protein synthesis. Neither rates of degradation nor affinity of pump sites in cells treated with TTX, veratridine, or ouabain differred from those in control cells. The number and activity of Na-K pump sites were unaffected by chronic elevation in [Ca]i or chronic depolarization. We conclude that alterations in the level in intracellular Na ions play the major role in regulation of Na-K pump synthesis in cultured mammalian skeletal muscle. | ||
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(DE-627)NLEJ160799201 DE-627 ger DE-627 rakwb eng Regulation of the sodium-potassium pump in cultured rat skeletal myotubes by intracellular sodium ions 1989 8 Ill. 3 Tab. 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The properties of the Na-K pump and some of the factors controlling its amount and function were studied in rat myotubes in culture. The number of Na-K pump sites was quantified by measuring the amount of [3H]ouabain bound to whole-cell preparations. Activity of the pump was determined by measurement of oua-bain-sensitive 86Rb-uptake and component of membrane potential. Chronic treatment of myotubes with tetrodotoxin (TTX), which lowers [Na]i, decreased the number of Na-K pumps, the ouabain-sensitive 86Rb uptake, and the size of the electrogenic pump component of Em. In contrast, chronic treatment with either ouabain or veratridine, which increases [Na+]i, resulted in an elevated level of Na-K pump sites. This effect was blocked by inhibitors of protein synthesis. Neither rates of degradation nor affinity of pump sites in cells treated with TTX, veratridine, or ouabain differred from those in control cells. The number and activity of Na-K pump sites were unaffected by chronic elevation in [Ca]i or chronic depolarization. We conclude that alterations in the level in intracellular Na ions play the major role in regulation of Na-K pump synthesis in cultured mammalian skeletal muscle. Wiley InterScience Backfile Collection 1832-2000 Brodie, Chaya oth Sampson, S. R. oth in Journal of Cellular Physiology New York, NY [u.a.] : Wiley-Liss 140(1989) vom: Jan., Seite 131-137 (DE-627)NLEJ15907097X (DE-600)1478143-8 0021-9541 nnns volume:140 year:1989 month:01 pages:131-137 extent:7 http://dx.doi.org/10.1002/jcp.1041400116 text/html Deutschlandweit zugänglich GBV_USEFLAG_U ZDB-1-WIS GBV_NL_ARTICLE AR 140 1989 1 131-137 7 |
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(DE-627)NLEJ160799201 DE-627 ger DE-627 rakwb eng Regulation of the sodium-potassium pump in cultured rat skeletal myotubes by intracellular sodium ions 1989 8 Ill. 3 Tab. 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The properties of the Na-K pump and some of the factors controlling its amount and function were studied in rat myotubes in culture. The number of Na-K pump sites was quantified by measuring the amount of [3H]ouabain bound to whole-cell preparations. Activity of the pump was determined by measurement of oua-bain-sensitive 86Rb-uptake and component of membrane potential. Chronic treatment of myotubes with tetrodotoxin (TTX), which lowers [Na]i, decreased the number of Na-K pumps, the ouabain-sensitive 86Rb uptake, and the size of the electrogenic pump component of Em. In contrast, chronic treatment with either ouabain or veratridine, which increases [Na+]i, resulted in an elevated level of Na-K pump sites. This effect was blocked by inhibitors of protein synthesis. Neither rates of degradation nor affinity of pump sites in cells treated with TTX, veratridine, or ouabain differred from those in control cells. The number and activity of Na-K pump sites were unaffected by chronic elevation in [Ca]i or chronic depolarization. We conclude that alterations in the level in intracellular Na ions play the major role in regulation of Na-K pump synthesis in cultured mammalian skeletal muscle. Wiley InterScience Backfile Collection 1832-2000 Brodie, Chaya oth Sampson, S. R. oth in Journal of Cellular Physiology New York, NY [u.a.] : Wiley-Liss 140(1989) vom: Jan., Seite 131-137 (DE-627)NLEJ15907097X (DE-600)1478143-8 0021-9541 nnns volume:140 year:1989 month:01 pages:131-137 extent:7 http://dx.doi.org/10.1002/jcp.1041400116 text/html Deutschlandweit zugänglich GBV_USEFLAG_U ZDB-1-WIS GBV_NL_ARTICLE AR 140 1989 1 131-137 7 |
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(DE-627)NLEJ160799201 DE-627 ger DE-627 rakwb eng Regulation of the sodium-potassium pump in cultured rat skeletal myotubes by intracellular sodium ions 1989 8 Ill. 3 Tab. 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The properties of the Na-K pump and some of the factors controlling its amount and function were studied in rat myotubes in culture. The number of Na-K pump sites was quantified by measuring the amount of [3H]ouabain bound to whole-cell preparations. Activity of the pump was determined by measurement of oua-bain-sensitive 86Rb-uptake and component of membrane potential. Chronic treatment of myotubes with tetrodotoxin (TTX), which lowers [Na]i, decreased the number of Na-K pumps, the ouabain-sensitive 86Rb uptake, and the size of the electrogenic pump component of Em. In contrast, chronic treatment with either ouabain or veratridine, which increases [Na+]i, resulted in an elevated level of Na-K pump sites. This effect was blocked by inhibitors of protein synthesis. Neither rates of degradation nor affinity of pump sites in cells treated with TTX, veratridine, or ouabain differred from those in control cells. The number and activity of Na-K pump sites were unaffected by chronic elevation in [Ca]i or chronic depolarization. We conclude that alterations in the level in intracellular Na ions play the major role in regulation of Na-K pump synthesis in cultured mammalian skeletal muscle. Wiley InterScience Backfile Collection 1832-2000 Brodie, Chaya oth Sampson, S. R. oth in Journal of Cellular Physiology New York, NY [u.a.] : Wiley-Liss 140(1989) vom: Jan., Seite 131-137 (DE-627)NLEJ15907097X (DE-600)1478143-8 0021-9541 nnns volume:140 year:1989 month:01 pages:131-137 extent:7 http://dx.doi.org/10.1002/jcp.1041400116 text/html Deutschlandweit zugänglich GBV_USEFLAG_U ZDB-1-WIS GBV_NL_ARTICLE AR 140 1989 1 131-137 7 |
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(DE-627)NLEJ160799201 DE-627 ger DE-627 rakwb eng Regulation of the sodium-potassium pump in cultured rat skeletal myotubes by intracellular sodium ions 1989 8 Ill. 3 Tab. 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The properties of the Na-K pump and some of the factors controlling its amount and function were studied in rat myotubes in culture. The number of Na-K pump sites was quantified by measuring the amount of [3H]ouabain bound to whole-cell preparations. Activity of the pump was determined by measurement of oua-bain-sensitive 86Rb-uptake and component of membrane potential. Chronic treatment of myotubes with tetrodotoxin (TTX), which lowers [Na]i, decreased the number of Na-K pumps, the ouabain-sensitive 86Rb uptake, and the size of the electrogenic pump component of Em. In contrast, chronic treatment with either ouabain or veratridine, which increases [Na+]i, resulted in an elevated level of Na-K pump sites. This effect was blocked by inhibitors of protein synthesis. Neither rates of degradation nor affinity of pump sites in cells treated with TTX, veratridine, or ouabain differred from those in control cells. The number and activity of Na-K pump sites were unaffected by chronic elevation in [Ca]i or chronic depolarization. We conclude that alterations in the level in intracellular Na ions play the major role in regulation of Na-K pump synthesis in cultured mammalian skeletal muscle. Wiley InterScience Backfile Collection 1832-2000 Brodie, Chaya oth Sampson, S. R. oth in Journal of Cellular Physiology New York, NY [u.a.] : Wiley-Liss 140(1989) vom: Jan., Seite 131-137 (DE-627)NLEJ15907097X (DE-600)1478143-8 0021-9541 nnns volume:140 year:1989 month:01 pages:131-137 extent:7 http://dx.doi.org/10.1002/jcp.1041400116 text/html Deutschlandweit zugänglich GBV_USEFLAG_U ZDB-1-WIS GBV_NL_ARTICLE AR 140 1989 1 131-137 7 |
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(DE-627)NLEJ160799201 DE-627 ger DE-627 rakwb eng Regulation of the sodium-potassium pump in cultured rat skeletal myotubes by intracellular sodium ions 1989 8 Ill. 3 Tab. 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The properties of the Na-K pump and some of the factors controlling its amount and function were studied in rat myotubes in culture. The number of Na-K pump sites was quantified by measuring the amount of [3H]ouabain bound to whole-cell preparations. Activity of the pump was determined by measurement of oua-bain-sensitive 86Rb-uptake and component of membrane potential. Chronic treatment of myotubes with tetrodotoxin (TTX), which lowers [Na]i, decreased the number of Na-K pumps, the ouabain-sensitive 86Rb uptake, and the size of the electrogenic pump component of Em. In contrast, chronic treatment with either ouabain or veratridine, which increases [Na+]i, resulted in an elevated level of Na-K pump sites. This effect was blocked by inhibitors of protein synthesis. Neither rates of degradation nor affinity of pump sites in cells treated with TTX, veratridine, or ouabain differred from those in control cells. The number and activity of Na-K pump sites were unaffected by chronic elevation in [Ca]i or chronic depolarization. We conclude that alterations in the level in intracellular Na ions play the major role in regulation of Na-K pump synthesis in cultured mammalian skeletal muscle. Wiley InterScience Backfile Collection 1832-2000 Brodie, Chaya oth Sampson, S. R. oth in Journal of Cellular Physiology New York, NY [u.a.] : Wiley-Liss 140(1989) vom: Jan., Seite 131-137 (DE-627)NLEJ15907097X (DE-600)1478143-8 0021-9541 nnns volume:140 year:1989 month:01 pages:131-137 extent:7 http://dx.doi.org/10.1002/jcp.1041400116 text/html Deutschlandweit zugänglich GBV_USEFLAG_U ZDB-1-WIS GBV_NL_ARTICLE AR 140 1989 1 131-137 7 |
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Regulation of the sodium-potassium pump in cultured rat skeletal myotubes by intracellular sodium ions |
| abstract |
The properties of the Na-K pump and some of the factors controlling its amount and function were studied in rat myotubes in culture. The number of Na-K pump sites was quantified by measuring the amount of [3H]ouabain bound to whole-cell preparations. Activity of the pump was determined by measurement of oua-bain-sensitive 86Rb-uptake and component of membrane potential. Chronic treatment of myotubes with tetrodotoxin (TTX), which lowers [Na]i, decreased the number of Na-K pumps, the ouabain-sensitive 86Rb uptake, and the size of the electrogenic pump component of Em. In contrast, chronic treatment with either ouabain or veratridine, which increases [Na+]i, resulted in an elevated level of Na-K pump sites. This effect was blocked by inhibitors of protein synthesis. Neither rates of degradation nor affinity of pump sites in cells treated with TTX, veratridine, or ouabain differred from those in control cells. The number and activity of Na-K pump sites were unaffected by chronic elevation in [Ca]i or chronic depolarization. We conclude that alterations in the level in intracellular Na ions play the major role in regulation of Na-K pump synthesis in cultured mammalian skeletal muscle. |
| abstractGer |
The properties of the Na-K pump and some of the factors controlling its amount and function were studied in rat myotubes in culture. The number of Na-K pump sites was quantified by measuring the amount of [3H]ouabain bound to whole-cell preparations. Activity of the pump was determined by measurement of oua-bain-sensitive 86Rb-uptake and component of membrane potential. Chronic treatment of myotubes with tetrodotoxin (TTX), which lowers [Na]i, decreased the number of Na-K pumps, the ouabain-sensitive 86Rb uptake, and the size of the electrogenic pump component of Em. In contrast, chronic treatment with either ouabain or veratridine, which increases [Na+]i, resulted in an elevated level of Na-K pump sites. This effect was blocked by inhibitors of protein synthesis. Neither rates of degradation nor affinity of pump sites in cells treated with TTX, veratridine, or ouabain differred from those in control cells. The number and activity of Na-K pump sites were unaffected by chronic elevation in [Ca]i or chronic depolarization. We conclude that alterations in the level in intracellular Na ions play the major role in regulation of Na-K pump synthesis in cultured mammalian skeletal muscle. |
| abstract_unstemmed |
The properties of the Na-K pump and some of the factors controlling its amount and function were studied in rat myotubes in culture. The number of Na-K pump sites was quantified by measuring the amount of [3H]ouabain bound to whole-cell preparations. Activity of the pump was determined by measurement of oua-bain-sensitive 86Rb-uptake and component of membrane potential. Chronic treatment of myotubes with tetrodotoxin (TTX), which lowers [Na]i, decreased the number of Na-K pumps, the ouabain-sensitive 86Rb uptake, and the size of the electrogenic pump component of Em. In contrast, chronic treatment with either ouabain or veratridine, which increases [Na+]i, resulted in an elevated level of Na-K pump sites. This effect was blocked by inhibitors of protein synthesis. Neither rates of degradation nor affinity of pump sites in cells treated with TTX, veratridine, or ouabain differred from those in control cells. The number and activity of Na-K pump sites were unaffected by chronic elevation in [Ca]i or chronic depolarization. We conclude that alterations in the level in intracellular Na ions play the major role in regulation of Na-K pump synthesis in cultured mammalian skeletal muscle. |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">NLEJ160799201</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20210707044850.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">070201s1989 xx |||||o 00| ||eng c</controlfield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ160799201</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Regulation of the sodium-potassium pump in cultured rat skeletal myotubes by intracellular sodium ions</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">1989</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="b">8 Ill.</subfield><subfield code="b">3 Tab.</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">7</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">The properties of the Na-K pump and some of the factors controlling its amount and function were studied in rat myotubes in culture. The number of Na-K pump sites was quantified by measuring the amount of [3H]ouabain bound to whole-cell preparations. Activity of the pump was determined by measurement of oua-bain-sensitive 86Rb-uptake and component of membrane potential. Chronic treatment of myotubes with tetrodotoxin (TTX), which lowers [Na]i, decreased the number of Na-K pumps, the ouabain-sensitive 86Rb uptake, and the size of the electrogenic pump component of Em. In contrast, chronic treatment with either ouabain or veratridine, which increases [Na+]i, resulted in an elevated level of Na-K pump sites. This effect was blocked by inhibitors of protein synthesis. Neither rates of degradation nor affinity of pump sites in cells treated with TTX, veratridine, or ouabain differred from those in control cells. The number and activity of Na-K pump sites were unaffected by chronic elevation in [Ca]i or chronic depolarization. We conclude that alterations in the level in intracellular Na ions play the major role in regulation of Na-K pump synthesis in cultured mammalian skeletal muscle.</subfield></datafield><datafield tag="533" ind1=" " ind2=" "><subfield code="f">Wiley InterScience Backfile Collection 1832-2000</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Brodie, Chaya</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Sampson, S. R.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">in</subfield><subfield code="t">Journal of Cellular Physiology</subfield><subfield code="d">New York, NY [u.a.] : Wiley-Liss</subfield><subfield code="g">140(1989) vom: Jan., Seite 131-137</subfield><subfield code="w">(DE-627)NLEJ15907097X</subfield><subfield code="w">(DE-600)1478143-8</subfield><subfield code="x">0021-9541</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:140</subfield><subfield code="g">year:1989</subfield><subfield code="g">month:01</subfield><subfield code="g">pages:131-137</subfield><subfield code="g">extent:7</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1002/jcp.1041400116</subfield><subfield code="q">text/html</subfield><subfield code="z">Deutschlandweit zugänglich</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">ZDB-1-WIS</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_NL_ARTICLE</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">140</subfield><subfield code="j">1989</subfield><subfield code="c">1</subfield><subfield code="h">131-137</subfield><subfield code="g">7</subfield></datafield></record></collection>
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