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A quantitative analysis of cell volume and resting potential determination and regulation in excitable cells
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| Zeitschriftentitel: | The Journal of Physiology |
|---|---|
| Personen und Körperschaften: | , |
| In: | The Journal of Physiology, 559, 2004, 2, S. 459-478 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Wiley
|
| Schlagwörter: |
| author_facet |
Fraser, James A. Huang, Christopher L.‐H. Fraser, James A. Huang, Christopher L.‐H. |
|---|---|
| author |
Fraser, James A. Huang, Christopher L.‐H. |
| spellingShingle |
Fraser, James A. Huang, Christopher L.‐H. The Journal of Physiology A quantitative analysis of cell volume and resting potential determination and regulation in excitable cells Physiology |
| author_sort |
fraser, james a. |
| spelling |
Fraser, James A. Huang, Christopher L.‐H. 0022-3751 1469-7793 Wiley Physiology http://dx.doi.org/10.1113/jphysiol.2004.065706 <jats:p>This paper quantifies recent experimental results through a general physical description of the mechanisms that might control two fundamental cellular parameters, resting potential (<jats:italic>E</jats:italic><jats:sub>m</jats:sub>) and cell volume (<jats:italic>V</jats:italic><jats:sub>c</jats:sub>), thereby clarifying the complex relationships between them. <jats:italic>E</jats:italic><jats:sub>m</jats:sub> was determined directly from a charge difference (CD) equation involving total intracellular ionic charge and membrane capacitance (<jats:italic>C</jats:italic><jats:sub>m</jats:sub>). This avoided the equilibrium condition d<jats:italic>E</jats:italic><jats:sub>m</jats:sub>/d<jats:italic>t</jats:italic>= 0 required in determinations of <jats:italic>E</jats:italic><jats:sub>m</jats:sub> by previous work based on the Goldman‐Hodgkin‐Katz equation and its derivatives and thus permitted precise calculation of <jats:italic>E</jats:italic><jats:sub>m</jats:sub> even under non‐equilibrium conditions. It could accurately model the influence upon <jats:italic>E</jats:italic><jats:sub>m</jats:sub> of changes in <jats:italic>C</jats:italic><jats:sub>m</jats:sub> or <jats:italic>V</jats:italic><jats:sub>c</jats:sub> and of membrane transport processes such as the Na<jats:sup>+</jats:sup>–K<jats:sup>+</jats:sup>‐ATPase and ion cotransport. Given a stable and adequate membrane Na<jats:sup>+</jats:sup>–K<jats:sup>+</jats:sup>‐ATPase density (<jats:italic>N</jats:italic>), <jats:italic>V</jats:italic><jats:sub>c</jats:sub> and <jats:italic>E</jats:italic><jats:sub>m</jats:sub> both converged to unique steady‐state values even from sharply divergent initial intracellular ionic concentrations. For any constant set of transmembrane ion permeabilities, this set point of <jats:italic>V</jats:italic><jats:sub>c</jats:sub> was then determined by the intracellular membrane‐impermeant solute content (X<jats:sup>−</jats:sup><jats:sub>i</jats:sub>) <jats:italic>and</jats:italic> its mean charge valency (<jats:italic>z</jats:italic><jats:sub>X</jats:sub>), while in contrast, the set point of <jats:italic>E</jats:italic><jats:sub>m</jats:sub> was determined <jats:italic>solely</jats:italic> by <jats:italic>z</jats:italic><jats:sub>X</jats:sub>. Independent changes in membrane Na<jats:sup>+</jats:sup> (<jats:italic>P</jats:italic><jats:sub>Na</jats:sub>) or K<jats:sup>+</jats:sup> permeabilities (<jats:italic>P</jats:italic><jats:sub>K</jats:sub>) or activation of cation–chloride cotransporters could perturb <jats:italic>V</jats:italic><jats:sub>c</jats:sub> and <jats:italic>E</jats:italic><jats:sub>m</jats:sub> but subsequent reversal of such changes permitted full recovery of both <jats:italic>V</jats:italic><jats:sub>c</jats:sub> and <jats:italic>E</jats:italic><jats:sub>m</jats:sub> to the original set points. <jats:italic>Proportionate</jats:italic> changes in <jats:italic>P</jats:italic><jats:sub>Na</jats:sub>, <jats:italic>P</jats:italic><jats:sub>K</jats:sub> and <jats:italic>N</jats:italic>, or changes in Cl<jats:sup>−</jats:sup> permeability (<jats:italic>P</jats:italic><jats:sub>Cl</jats:sub>) instead conserved steady‐state <jats:italic>V</jats:italic><jats:sub>c</jats:sub> and <jats:italic>E</jats:italic><jats:sub>m</jats:sub> but altered their <jats:italic>rates</jats:italic> of relaxation following any discrete perturbation. <jats:italic>P</jats:italic><jats:sub>Cl</jats:sub> additionally determined the relative effect of cotransporter activity on <jats:italic>V</jats:italic><jats:sub>c</jats:sub> and <jats:italic>E</jats:italic><jats:sub>m</jats:sub>, in agreement with recent experimental results. In contrast, changes in X<jats:sub>i</jats:sub><jats:sup>−</jats:sup> produced by introduction of a finite permeability term to X<jats:sup>−</jats:sup> (<jats:italic>P</jats:italic><jats:sub>X</jats:sub>) that did not alter <jats:italic>z</jats:italic><jats:sub>X</jats:sub> caused sustained changes in <jats:italic>V</jats:italic><jats:sub>c</jats:sub> that were independent of <jats:italic>E</jats:italic><jats:sub>m</jats:sub> and that persisted when <jats:italic>P</jats:italic><jats:sub>X</jats:sub> returned to zero. Where such fluxes also altered the effective <jats:italic>z</jats:italic><jats:sub>X</jats:sub> they additionally altered the steady state <jats:italic>E</jats:italic><jats:sub>m</jats:sub>. This offers a basis for the suggested roles of amino acid fluxes in long‐term volume regulatory processes in a variety of excitable tissues.</jats:p> A quantitative analysis of cell volume and resting potential determination and regulation in excitable cells The Journal of Physiology |
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Wiley, 2004 |
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Wiley, 2004 |
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0022-3751 1469-7793 |
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0022-3751 1469-7793 |
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fraser2004aquantitativeanalysisofcellvolumeandrestingpotentialdeterminationandregulationinexcitablecells |
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2004 |
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Wiley |
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ai |
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ai |
| series |
The Journal of Physiology |
| source_id |
49 |
| title |
A quantitative analysis of cell volume and resting potential determination and regulation in excitable cells |
| title_unstemmed |
A quantitative analysis of cell volume and resting potential determination and regulation in excitable cells |
| title_full |
A quantitative analysis of cell volume and resting potential determination and regulation in excitable cells |
| title_fullStr |
A quantitative analysis of cell volume and resting potential determination and regulation in excitable cells |
| title_full_unstemmed |
A quantitative analysis of cell volume and resting potential determination and regulation in excitable cells |
| title_short |
A quantitative analysis of cell volume and resting potential determination and regulation in excitable cells |
| title_sort |
a quantitative analysis of cell volume and resting potential determination and regulation in excitable cells |
| topic |
Physiology |
| url |
http://dx.doi.org/10.1113/jphysiol.2004.065706 |
| publishDate |
2004 |
| physical |
459-478 |
| description |
<jats:p>This paper quantifies recent experimental results through a general physical description of the mechanisms that might control two fundamental cellular parameters, resting potential (<jats:italic>E</jats:italic><jats:sub>m</jats:sub>) and cell volume (<jats:italic>V</jats:italic><jats:sub>c</jats:sub>), thereby clarifying the complex relationships between them. <jats:italic>E</jats:italic><jats:sub>m</jats:sub> was determined directly from a charge difference (CD) equation involving total intracellular ionic charge and membrane capacitance (<jats:italic>C</jats:italic><jats:sub>m</jats:sub>). This avoided the equilibrium condition d<jats:italic>E</jats:italic><jats:sub>m</jats:sub>/d<jats:italic>t</jats:italic>= 0 required in determinations of <jats:italic>E</jats:italic><jats:sub>m</jats:sub> by previous work based on the Goldman‐Hodgkin‐Katz equation and its derivatives and thus permitted precise calculation of <jats:italic>E</jats:italic><jats:sub>m</jats:sub> even under non‐equilibrium conditions. It could accurately model the influence upon <jats:italic>E</jats:italic><jats:sub>m</jats:sub> of changes in <jats:italic>C</jats:italic><jats:sub>m</jats:sub> or <jats:italic>V</jats:italic><jats:sub>c</jats:sub> and of membrane transport processes such as the Na<jats:sup>+</jats:sup>–K<jats:sup>+</jats:sup>‐ATPase and ion cotransport. Given a stable and adequate membrane Na<jats:sup>+</jats:sup>–K<jats:sup>+</jats:sup>‐ATPase density (<jats:italic>N</jats:italic>), <jats:italic>V</jats:italic><jats:sub>c</jats:sub> and <jats:italic>E</jats:italic><jats:sub>m</jats:sub> both converged to unique steady‐state values even from sharply divergent initial intracellular ionic concentrations. For any constant set of transmembrane ion permeabilities, this set point of <jats:italic>V</jats:italic><jats:sub>c</jats:sub> was then determined by the intracellular membrane‐impermeant solute content (X<jats:sup>−</jats:sup><jats:sub>i</jats:sub>) <jats:italic>and</jats:italic> its mean charge valency (<jats:italic>z</jats:italic><jats:sub>X</jats:sub>), while in contrast, the set point of <jats:italic>E</jats:italic><jats:sub>m</jats:sub> was determined <jats:italic>solely</jats:italic> by <jats:italic>z</jats:italic><jats:sub>X</jats:sub>. Independent changes in membrane Na<jats:sup>+</jats:sup> (<jats:italic>P</jats:italic><jats:sub>Na</jats:sub>) or K<jats:sup>+</jats:sup> permeabilities (<jats:italic>P</jats:italic><jats:sub>K</jats:sub>) or activation of cation–chloride cotransporters could perturb <jats:italic>V</jats:italic><jats:sub>c</jats:sub> and <jats:italic>E</jats:italic><jats:sub>m</jats:sub> but subsequent reversal of such changes permitted full recovery of both <jats:italic>V</jats:italic><jats:sub>c</jats:sub> and <jats:italic>E</jats:italic><jats:sub>m</jats:sub> to the original set points. <jats:italic>Proportionate</jats:italic> changes in <jats:italic>P</jats:italic><jats:sub>Na</jats:sub>, <jats:italic>P</jats:italic><jats:sub>K</jats:sub> and <jats:italic>N</jats:italic>, or changes in Cl<jats:sup>−</jats:sup> permeability (<jats:italic>P</jats:italic><jats:sub>Cl</jats:sub>) instead conserved steady‐state <jats:italic>V</jats:italic><jats:sub>c</jats:sub> and <jats:italic>E</jats:italic><jats:sub>m</jats:sub> but altered their <jats:italic>rates</jats:italic> of relaxation following any discrete perturbation. <jats:italic>P</jats:italic><jats:sub>Cl</jats:sub> additionally determined the relative effect of cotransporter activity on <jats:italic>V</jats:italic><jats:sub>c</jats:sub> and <jats:italic>E</jats:italic><jats:sub>m</jats:sub>, in agreement with recent experimental results. In contrast, changes in X<jats:sub>i</jats:sub><jats:sup>−</jats:sup> produced by introduction of a finite permeability term to X<jats:sup>−</jats:sup> (<jats:italic>P</jats:italic><jats:sub>X</jats:sub>) that did not alter <jats:italic>z</jats:italic><jats:sub>X</jats:sub> caused sustained changes in <jats:italic>V</jats:italic><jats:sub>c</jats:sub> that were independent of <jats:italic>E</jats:italic><jats:sub>m</jats:sub> and that persisted when <jats:italic>P</jats:italic><jats:sub>X</jats:sub> returned to zero. Where such fluxes also altered the effective <jats:italic>z</jats:italic><jats:sub>X</jats:sub> they additionally altered the steady state <jats:italic>E</jats:italic><jats:sub>m</jats:sub>. This offers a basis for the suggested roles of amino acid fluxes in long‐term volume regulatory processes in a variety of excitable tissues.</jats:p> |
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| description | <jats:p>This paper quantifies recent experimental results through a general physical description of the mechanisms that might control two fundamental cellular parameters, resting potential (<jats:italic>E</jats:italic><jats:sub>m</jats:sub>) and cell volume (<jats:italic>V</jats:italic><jats:sub>c</jats:sub>), thereby clarifying the complex relationships between them. <jats:italic>E</jats:italic><jats:sub>m</jats:sub> was determined directly from a charge difference (CD) equation involving total intracellular ionic charge and membrane capacitance (<jats:italic>C</jats:italic><jats:sub>m</jats:sub>). This avoided the equilibrium condition d<jats:italic>E</jats:italic><jats:sub>m</jats:sub>/d<jats:italic>t</jats:italic>= 0 required in determinations of <jats:italic>E</jats:italic><jats:sub>m</jats:sub> by previous work based on the Goldman‐Hodgkin‐Katz equation and its derivatives and thus permitted precise calculation of <jats:italic>E</jats:italic><jats:sub>m</jats:sub> even under non‐equilibrium conditions. It could accurately model the influence upon <jats:italic>E</jats:italic><jats:sub>m</jats:sub> of changes in <jats:italic>C</jats:italic><jats:sub>m</jats:sub> or <jats:italic>V</jats:italic><jats:sub>c</jats:sub> and of membrane transport processes such as the Na<jats:sup>+</jats:sup>–K<jats:sup>+</jats:sup>‐ATPase and ion cotransport. Given a stable and adequate membrane Na<jats:sup>+</jats:sup>–K<jats:sup>+</jats:sup>‐ATPase density (<jats:italic>N</jats:italic>), <jats:italic>V</jats:italic><jats:sub>c</jats:sub> and <jats:italic>E</jats:italic><jats:sub>m</jats:sub> both converged to unique steady‐state values even from sharply divergent initial intracellular ionic concentrations. For any constant set of transmembrane ion permeabilities, this set point of <jats:italic>V</jats:italic><jats:sub>c</jats:sub> was then determined by the intracellular membrane‐impermeant solute content (X<jats:sup>−</jats:sup><jats:sub>i</jats:sub>) <jats:italic>and</jats:italic> its mean charge valency (<jats:italic>z</jats:italic><jats:sub>X</jats:sub>), while in contrast, the set point of <jats:italic>E</jats:italic><jats:sub>m</jats:sub> was determined <jats:italic>solely</jats:italic> by <jats:italic>z</jats:italic><jats:sub>X</jats:sub>. Independent changes in membrane Na<jats:sup>+</jats:sup> (<jats:italic>P</jats:italic><jats:sub>Na</jats:sub>) or K<jats:sup>+</jats:sup> permeabilities (<jats:italic>P</jats:italic><jats:sub>K</jats:sub>) or activation of cation–chloride cotransporters could perturb <jats:italic>V</jats:italic><jats:sub>c</jats:sub> and <jats:italic>E</jats:italic><jats:sub>m</jats:sub> but subsequent reversal of such changes permitted full recovery of both <jats:italic>V</jats:italic><jats:sub>c</jats:sub> and <jats:italic>E</jats:italic><jats:sub>m</jats:sub> to the original set points. <jats:italic>Proportionate</jats:italic> changes in <jats:italic>P</jats:italic><jats:sub>Na</jats:sub>, <jats:italic>P</jats:italic><jats:sub>K</jats:sub> and <jats:italic>N</jats:italic>, or changes in Cl<jats:sup>−</jats:sup> permeability (<jats:italic>P</jats:italic><jats:sub>Cl</jats:sub>) instead conserved steady‐state <jats:italic>V</jats:italic><jats:sub>c</jats:sub> and <jats:italic>E</jats:italic><jats:sub>m</jats:sub> but altered their <jats:italic>rates</jats:italic> of relaxation following any discrete perturbation. <jats:italic>P</jats:italic><jats:sub>Cl</jats:sub> additionally determined the relative effect of cotransporter activity on <jats:italic>V</jats:italic><jats:sub>c</jats:sub> and <jats:italic>E</jats:italic><jats:sub>m</jats:sub>, in agreement with recent experimental results. In contrast, changes in X<jats:sub>i</jats:sub><jats:sup>−</jats:sup> produced by introduction of a finite permeability term to X<jats:sup>−</jats:sup> (<jats:italic>P</jats:italic><jats:sub>X</jats:sub>) that did not alter <jats:italic>z</jats:italic><jats:sub>X</jats:sub> caused sustained changes in <jats:italic>V</jats:italic><jats:sub>c</jats:sub> that were independent of <jats:italic>E</jats:italic><jats:sub>m</jats:sub> and that persisted when <jats:italic>P</jats:italic><jats:sub>X</jats:sub> returned to zero. Where such fluxes also altered the effective <jats:italic>z</jats:italic><jats:sub>X</jats:sub> they additionally altered the steady state <jats:italic>E</jats:italic><jats:sub>m</jats:sub>. This offers a basis for the suggested roles of amino acid fluxes in long‐term volume regulatory processes in a variety of excitable tissues.</jats:p> |
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| series | The Journal of Physiology |
| source_id | 49 |
| spelling | Fraser, James A. Huang, Christopher L.‐H. 0022-3751 1469-7793 Wiley Physiology http://dx.doi.org/10.1113/jphysiol.2004.065706 <jats:p>This paper quantifies recent experimental results through a general physical description of the mechanisms that might control two fundamental cellular parameters, resting potential (<jats:italic>E</jats:italic><jats:sub>m</jats:sub>) and cell volume (<jats:italic>V</jats:italic><jats:sub>c</jats:sub>), thereby clarifying the complex relationships between them. <jats:italic>E</jats:italic><jats:sub>m</jats:sub> was determined directly from a charge difference (CD) equation involving total intracellular ionic charge and membrane capacitance (<jats:italic>C</jats:italic><jats:sub>m</jats:sub>). This avoided the equilibrium condition d<jats:italic>E</jats:italic><jats:sub>m</jats:sub>/d<jats:italic>t</jats:italic>= 0 required in determinations of <jats:italic>E</jats:italic><jats:sub>m</jats:sub> by previous work based on the Goldman‐Hodgkin‐Katz equation and its derivatives and thus permitted precise calculation of <jats:italic>E</jats:italic><jats:sub>m</jats:sub> even under non‐equilibrium conditions. It could accurately model the influence upon <jats:italic>E</jats:italic><jats:sub>m</jats:sub> of changes in <jats:italic>C</jats:italic><jats:sub>m</jats:sub> or <jats:italic>V</jats:italic><jats:sub>c</jats:sub> and of membrane transport processes such as the Na<jats:sup>+</jats:sup>–K<jats:sup>+</jats:sup>‐ATPase and ion cotransport. Given a stable and adequate membrane Na<jats:sup>+</jats:sup>–K<jats:sup>+</jats:sup>‐ATPase density (<jats:italic>N</jats:italic>), <jats:italic>V</jats:italic><jats:sub>c</jats:sub> and <jats:italic>E</jats:italic><jats:sub>m</jats:sub> both converged to unique steady‐state values even from sharply divergent initial intracellular ionic concentrations. For any constant set of transmembrane ion permeabilities, this set point of <jats:italic>V</jats:italic><jats:sub>c</jats:sub> was then determined by the intracellular membrane‐impermeant solute content (X<jats:sup>−</jats:sup><jats:sub>i</jats:sub>) <jats:italic>and</jats:italic> its mean charge valency (<jats:italic>z</jats:italic><jats:sub>X</jats:sub>), while in contrast, the set point of <jats:italic>E</jats:italic><jats:sub>m</jats:sub> was determined <jats:italic>solely</jats:italic> by <jats:italic>z</jats:italic><jats:sub>X</jats:sub>. Independent changes in membrane Na<jats:sup>+</jats:sup> (<jats:italic>P</jats:italic><jats:sub>Na</jats:sub>) or K<jats:sup>+</jats:sup> permeabilities (<jats:italic>P</jats:italic><jats:sub>K</jats:sub>) or activation of cation–chloride cotransporters could perturb <jats:italic>V</jats:italic><jats:sub>c</jats:sub> and <jats:italic>E</jats:italic><jats:sub>m</jats:sub> but subsequent reversal of such changes permitted full recovery of both <jats:italic>V</jats:italic><jats:sub>c</jats:sub> and <jats:italic>E</jats:italic><jats:sub>m</jats:sub> to the original set points. <jats:italic>Proportionate</jats:italic> changes in <jats:italic>P</jats:italic><jats:sub>Na</jats:sub>, <jats:italic>P</jats:italic><jats:sub>K</jats:sub> and <jats:italic>N</jats:italic>, or changes in Cl<jats:sup>−</jats:sup> permeability (<jats:italic>P</jats:italic><jats:sub>Cl</jats:sub>) instead conserved steady‐state <jats:italic>V</jats:italic><jats:sub>c</jats:sub> and <jats:italic>E</jats:italic><jats:sub>m</jats:sub> but altered their <jats:italic>rates</jats:italic> of relaxation following any discrete perturbation. <jats:italic>P</jats:italic><jats:sub>Cl</jats:sub> additionally determined the relative effect of cotransporter activity on <jats:italic>V</jats:italic><jats:sub>c</jats:sub> and <jats:italic>E</jats:italic><jats:sub>m</jats:sub>, in agreement with recent experimental results. In contrast, changes in X<jats:sub>i</jats:sub><jats:sup>−</jats:sup> produced by introduction of a finite permeability term to X<jats:sup>−</jats:sup> (<jats:italic>P</jats:italic><jats:sub>X</jats:sub>) that did not alter <jats:italic>z</jats:italic><jats:sub>X</jats:sub> caused sustained changes in <jats:italic>V</jats:italic><jats:sub>c</jats:sub> that were independent of <jats:italic>E</jats:italic><jats:sub>m</jats:sub> and that persisted when <jats:italic>P</jats:italic><jats:sub>X</jats:sub> returned to zero. Where such fluxes also altered the effective <jats:italic>z</jats:italic><jats:sub>X</jats:sub> they additionally altered the steady state <jats:italic>E</jats:italic><jats:sub>m</jats:sub>. This offers a basis for the suggested roles of amino acid fluxes in long‐term volume regulatory processes in a variety of excitable tissues.</jats:p> A quantitative analysis of cell volume and resting potential determination and regulation in excitable cells The Journal of Physiology |
| spellingShingle | Fraser, James A., Huang, Christopher L.‐H., The Journal of Physiology, A quantitative analysis of cell volume and resting potential determination and regulation in excitable cells, Physiology |
| title | A quantitative analysis of cell volume and resting potential determination and regulation in excitable cells |
| title_full | A quantitative analysis of cell volume and resting potential determination and regulation in excitable cells |
| title_fullStr | A quantitative analysis of cell volume and resting potential determination and regulation in excitable cells |
| title_full_unstemmed | A quantitative analysis of cell volume and resting potential determination and regulation in excitable cells |
| title_short | A quantitative analysis of cell volume and resting potential determination and regulation in excitable cells |
| title_sort | a quantitative analysis of cell volume and resting potential determination and regulation in excitable cells |
| title_unstemmed | A quantitative analysis of cell volume and resting potential determination and regulation in excitable cells |
| topic | Physiology |
| url | http://dx.doi.org/10.1113/jphysiol.2004.065706 |