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Control of L‐type calcium current during the action potential of guinea‐pig ventricular myocytes
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| Zeitschriftentitel: | The Journal of Physiology |
|---|---|
| Personen und Körperschaften: | , |
| In: | The Journal of Physiology, 513, 1998, 2, S. 425-442 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Wiley
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| Schlagwörter: |
| author_facet |
Linz, Klaus W. Meyer, Rainer Linz, Klaus W. Meyer, Rainer |
|---|---|
| author |
Linz, Klaus W. Meyer, Rainer |
| spellingShingle |
Linz, Klaus W. Meyer, Rainer The Journal of Physiology Control of L‐type calcium current during the action potential of guinea‐pig ventricular myocytes Physiology |
| author_sort |
linz, klaus w. |
| spelling |
Linz, Klaus W. Meyer, Rainer 0022-3751 1469-7793 Wiley Physiology http://dx.doi.org/10.1111/j.1469-7793.1998.425bb.x <jats:p> <jats:list list-type="explicit-label"> <jats:list-item><jats:p>During an action potential the L‐type Ca<jats:sup>2+</jats:sup> current (<jats:styled-content><jats:italic>I</jats:italic><jats:sub>Ca,L</jats:sub></jats:styled-content>) activates rapidly, then partially declines leading to a sustained inward current during the plateau phase. The reason for the sustained part of <jats:styled-content><jats:italic>I</jats:italic><jats:sub>Ca,L</jats:sub></jats:styled-content> has been investigated here.</jats:p></jats:list-item> <jats:list-item><jats:p>In the present study the mechanisms controlling the <jats:styled-content><jats:italic>I</jats:italic><jats:sub>Ca,L</jats:sub></jats:styled-content> during an action potential were investigated quantitatively in isolated guinea‐pig ventricular myocytes by whole‐cell patch clamp. To measure the actual time courses of <jats:styled-content><jats:italic>I</jats:italic><jats:sub>Ca,L</jats:sub></jats:styled-content> and the corresponding L‐type channel inactivation (<jats:styled-content><jats:italic>f</jats:italic><jats:sub>AP</jats:sub></jats:styled-content>) during an action potential, action potential‐clamp protocols combined with square pulses were applied.</jats:p></jats:list-item> <jats:list-item><jats:p>Within the first 10 ms of the action potential the <jats:styled-content><jats:italic>I</jats:italic><jats:sub>Ca,L</jats:sub></jats:styled-content> rapidly inactivated by about 50 %; during the plateau phase inactivation proceeded to 95 %. Later, during repolarization, the L‐type channels recovered up to 25 %.</jats:p></jats:list-item> <jats:list-item><jats:p>The voltage‐dependent component of inactivation during an action potential was determined from measurements of L‐type current carried by monovalent cations. This component of inactivation proceeded rather slowly and contributed only a little to <jats:italic>f</jats:italic><jats:sub>AP</jats:sub>. <jats:styled-content><jats:italic>I</jats:italic><jats:sub>Ca,L</jats:sub></jats:styled-content> during an action potential is thus mainly controlled by Ca<jats:sup>2+</jats:sup>‐dependent inactivation.</jats:p></jats:list-item> <jats:list-item><jats:p>In order to investigate the source of the Ca<jats:sup>2+</jats:sup> controlling <jats:italic>f</jats:italic><jats:sub>AP</jats:sub>, internal Ca<jats:sup>2+</jats:sup> homeostasis was manipulated by the use of Ca<jats:sup>2+</jats:sup> buffers (EGTA, BAPTA), by blocking Na<jats:sup>+</jats:sup>−Ca<jats:sup>2+</jats:sup> exchange, or by blocking Ca<jats:sup>2+</jats:sup> release from the sarcoplasmic reticulum (SR). Internal BAPTA markedly reduced the L‐type channel inactivation during the entire action potential, whereas EGTA affected <jats:italic>f</jats:italic><jats:sub>AP</jats:sub> only during the middle and late plateau phases. Inhibition of Na<jats:sup>+</jats:sup>−Ca<jats:sup>2+</jats:sup> exchange markedly increased inactivation of L‐type channels. Although blocking SR Ca<jats:sup>2+</jats:sup> release decreased the fura‐2‐measured cytoplasmic Ca<jats:sup>2+</jats:sup> concentration ([Ca<jats:sup>2+</jats:sup>]<jats:sub>i</jats:sub>) transient by about 90 %, it reduced L‐type channel inactivation only during the initial 50 ms of the action potential. Thus, it is Ca<jats:sup>2+</jats:sup> entering the cell through the L‐type channels that controls the inactivation process for the majority of the action potential. Nevertheless, SR Ca<jats:sup>2+</jats:sup>‐release contributes 40–50 % to L‐type channel inactivation during the initial period of the action potential. However, the maximum extent of inactivation reached during the plateau is independent of Ca<jats:sup>2+</jats:sup> released from the SR.</jats:p></jats:list-item> <jats:list-item><jats:p>For the first time, the actual time course of L‐type channel inactivation has been directly determined during an action potential under various defined [Ca<jats:sup>2+</jats:sup>]<jats:sub>i</jats:sub> conditions. Thereby, the relative contribution to <jats:styled-content><jats:italic>I</jats:italic><jats:sub>Ca,L</jats:sub></jats:styled-content> inactivation of voltage, Ca<jats:sup>2+</jats:sup> entering through L‐type channels, and Ca<jats:sup>2+</jats:sup> being released from the SR could be directly demonstrated.</jats:p></jats:list-item> </jats:list> </jats:p> Control of L‐type calcium current during the action potential of guinea‐pig ventricular myocytes The Journal of Physiology |
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10.1111/j.1469-7793.1998.425bb.x |
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Biologie |
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linz1998controlofltypecalciumcurrentduringtheactionpotentialofguineapigventricularmyocytes |
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1998 |
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Wiley |
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ai |
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ai |
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The Journal of Physiology |
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49 |
| title |
Control of L‐type calcium current during the action potential of guinea‐pig ventricular myocytes |
| title_unstemmed |
Control of L‐type calcium current during the action potential of guinea‐pig ventricular myocytes |
| title_full |
Control of L‐type calcium current during the action potential of guinea‐pig ventricular myocytes |
| title_fullStr |
Control of L‐type calcium current during the action potential of guinea‐pig ventricular myocytes |
| title_full_unstemmed |
Control of L‐type calcium current during the action potential of guinea‐pig ventricular myocytes |
| title_short |
Control of L‐type calcium current during the action potential of guinea‐pig ventricular myocytes |
| title_sort |
control of l‐type calcium current during the action potential of guinea‐pig ventricular myocytes |
| topic |
Physiology |
| url |
http://dx.doi.org/10.1111/j.1469-7793.1998.425bb.x |
| publishDate |
1998 |
| physical |
425-442 |
| description |
<jats:p>
<jats:list list-type="explicit-label">
<jats:list-item><jats:p>During an action potential the L‐type Ca<jats:sup>2+</jats:sup> current (<jats:styled-content><jats:italic>I</jats:italic><jats:sub>Ca,L</jats:sub></jats:styled-content>) activates rapidly, then partially declines leading to a sustained inward current during the plateau phase. The reason for the sustained part of <jats:styled-content><jats:italic>I</jats:italic><jats:sub>Ca,L</jats:sub></jats:styled-content> has been investigated here.</jats:p></jats:list-item>
<jats:list-item><jats:p>In the present study the mechanisms controlling the <jats:styled-content><jats:italic>I</jats:italic><jats:sub>Ca,L</jats:sub></jats:styled-content> during an action potential were investigated quantitatively in isolated guinea‐pig ventricular myocytes by whole‐cell patch clamp. To measure the actual time courses of <jats:styled-content><jats:italic>I</jats:italic><jats:sub>Ca,L</jats:sub></jats:styled-content> and the corresponding L‐type channel inactivation (<jats:styled-content><jats:italic>f</jats:italic><jats:sub>AP</jats:sub></jats:styled-content>) during an action potential, action potential‐clamp protocols combined with square pulses were applied.</jats:p></jats:list-item>
<jats:list-item><jats:p>Within the first 10 ms of the action potential the <jats:styled-content><jats:italic>I</jats:italic><jats:sub>Ca,L</jats:sub></jats:styled-content> rapidly inactivated by about 50 %; during the plateau phase inactivation proceeded to 95 %. Later, during repolarization, the L‐type channels recovered up to 25 %.</jats:p></jats:list-item>
<jats:list-item><jats:p>The voltage‐dependent component of inactivation during an action potential was determined from measurements of L‐type current carried by monovalent cations. This component of inactivation proceeded rather slowly and contributed only a little to <jats:italic>f</jats:italic><jats:sub>AP</jats:sub>. <jats:styled-content><jats:italic>I</jats:italic><jats:sub>Ca,L</jats:sub></jats:styled-content> during an action potential is thus mainly controlled by Ca<jats:sup>2+</jats:sup>‐dependent inactivation.</jats:p></jats:list-item>
<jats:list-item><jats:p>In order to investigate the source of the Ca<jats:sup>2+</jats:sup> controlling <jats:italic>f</jats:italic><jats:sub>AP</jats:sub>, internal Ca<jats:sup>2+</jats:sup> homeostasis was manipulated by the use of Ca<jats:sup>2+</jats:sup> buffers (EGTA, BAPTA), by blocking Na<jats:sup>+</jats:sup>−Ca<jats:sup>2+</jats:sup> exchange, or by blocking Ca<jats:sup>2+</jats:sup> release from the sarcoplasmic reticulum (SR). Internal BAPTA markedly reduced the L‐type channel inactivation during the entire action potential, whereas EGTA affected <jats:italic>f</jats:italic><jats:sub>AP</jats:sub> only during the middle and late plateau phases. Inhibition of Na<jats:sup>+</jats:sup>−Ca<jats:sup>2+</jats:sup> exchange markedly increased inactivation of L‐type channels. Although blocking SR Ca<jats:sup>2+</jats:sup> release decreased the fura‐2‐measured cytoplasmic Ca<jats:sup>2+</jats:sup> concentration ([Ca<jats:sup>2+</jats:sup>]<jats:sub>i</jats:sub>) transient by about 90 %, it reduced L‐type channel inactivation only during the initial 50 ms of the action potential. Thus, it is Ca<jats:sup>2+</jats:sup> entering the cell through the L‐type channels that controls the inactivation process for the majority of the action potential. Nevertheless, SR Ca<jats:sup>2+</jats:sup>‐release contributes 40–50 % to L‐type channel inactivation during the initial period of the action potential. However, the maximum extent of inactivation reached during the plateau is independent of Ca<jats:sup>2+</jats:sup> released from the SR.</jats:p></jats:list-item>
<jats:list-item><jats:p>For the first time, the actual time course of L‐type channel inactivation has been directly determined during an action potential under various defined [Ca<jats:sup>2+</jats:sup>]<jats:sub>i</jats:sub> conditions. Thereby, the relative contribution to <jats:styled-content><jats:italic>I</jats:italic><jats:sub>Ca,L</jats:sub></jats:styled-content> inactivation of voltage, Ca<jats:sup>2+</jats:sup> entering through L‐type channels, and Ca<jats:sup>2+</jats:sup> being released from the SR could be directly demonstrated.</jats:p></jats:list-item>
</jats:list>
</jats:p> |
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| description | <jats:p> <jats:list list-type="explicit-label"> <jats:list-item><jats:p>During an action potential the L‐type Ca<jats:sup>2+</jats:sup> current (<jats:styled-content><jats:italic>I</jats:italic><jats:sub>Ca,L</jats:sub></jats:styled-content>) activates rapidly, then partially declines leading to a sustained inward current during the plateau phase. The reason for the sustained part of <jats:styled-content><jats:italic>I</jats:italic><jats:sub>Ca,L</jats:sub></jats:styled-content> has been investigated here.</jats:p></jats:list-item> <jats:list-item><jats:p>In the present study the mechanisms controlling the <jats:styled-content><jats:italic>I</jats:italic><jats:sub>Ca,L</jats:sub></jats:styled-content> during an action potential were investigated quantitatively in isolated guinea‐pig ventricular myocytes by whole‐cell patch clamp. To measure the actual time courses of <jats:styled-content><jats:italic>I</jats:italic><jats:sub>Ca,L</jats:sub></jats:styled-content> and the corresponding L‐type channel inactivation (<jats:styled-content><jats:italic>f</jats:italic><jats:sub>AP</jats:sub></jats:styled-content>) during an action potential, action potential‐clamp protocols combined with square pulses were applied.</jats:p></jats:list-item> <jats:list-item><jats:p>Within the first 10 ms of the action potential the <jats:styled-content><jats:italic>I</jats:italic><jats:sub>Ca,L</jats:sub></jats:styled-content> rapidly inactivated by about 50 %; during the plateau phase inactivation proceeded to 95 %. Later, during repolarization, the L‐type channels recovered up to 25 %.</jats:p></jats:list-item> <jats:list-item><jats:p>The voltage‐dependent component of inactivation during an action potential was determined from measurements of L‐type current carried by monovalent cations. This component of inactivation proceeded rather slowly and contributed only a little to <jats:italic>f</jats:italic><jats:sub>AP</jats:sub>. <jats:styled-content><jats:italic>I</jats:italic><jats:sub>Ca,L</jats:sub></jats:styled-content> during an action potential is thus mainly controlled by Ca<jats:sup>2+</jats:sup>‐dependent inactivation.</jats:p></jats:list-item> <jats:list-item><jats:p>In order to investigate the source of the Ca<jats:sup>2+</jats:sup> controlling <jats:italic>f</jats:italic><jats:sub>AP</jats:sub>, internal Ca<jats:sup>2+</jats:sup> homeostasis was manipulated by the use of Ca<jats:sup>2+</jats:sup> buffers (EGTA, BAPTA), by blocking Na<jats:sup>+</jats:sup>−Ca<jats:sup>2+</jats:sup> exchange, or by blocking Ca<jats:sup>2+</jats:sup> release from the sarcoplasmic reticulum (SR). Internal BAPTA markedly reduced the L‐type channel inactivation during the entire action potential, whereas EGTA affected <jats:italic>f</jats:italic><jats:sub>AP</jats:sub> only during the middle and late plateau phases. Inhibition of Na<jats:sup>+</jats:sup>−Ca<jats:sup>2+</jats:sup> exchange markedly increased inactivation of L‐type channels. Although blocking SR Ca<jats:sup>2+</jats:sup> release decreased the fura‐2‐measured cytoplasmic Ca<jats:sup>2+</jats:sup> concentration ([Ca<jats:sup>2+</jats:sup>]<jats:sub>i</jats:sub>) transient by about 90 %, it reduced L‐type channel inactivation only during the initial 50 ms of the action potential. Thus, it is Ca<jats:sup>2+</jats:sup> entering the cell through the L‐type channels that controls the inactivation process for the majority of the action potential. Nevertheless, SR Ca<jats:sup>2+</jats:sup>‐release contributes 40–50 % to L‐type channel inactivation during the initial period of the action potential. However, the maximum extent of inactivation reached during the plateau is independent of Ca<jats:sup>2+</jats:sup> released from the SR.</jats:p></jats:list-item> <jats:list-item><jats:p>For the first time, the actual time course of L‐type channel inactivation has been directly determined during an action potential under various defined [Ca<jats:sup>2+</jats:sup>]<jats:sub>i</jats:sub> conditions. Thereby, the relative contribution to <jats:styled-content><jats:italic>I</jats:italic><jats:sub>Ca,L</jats:sub></jats:styled-content> inactivation of voltage, Ca<jats:sup>2+</jats:sup> entering through L‐type channels, and Ca<jats:sup>2+</jats:sup> being released from the SR could be directly demonstrated.</jats:p></jats:list-item> </jats:list> </jats:p> |
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| imprint | Wiley, 1998 |
| imprint_str_mv | Wiley, 1998 |
| institution | DE-Brt1, DE-Zwi2, DE-D161, DE-Gla1, DE-Zi4, DE-15, DE-Pl11, DE-Rs1, DE-105, DE-14, DE-Ch1, DE-L229, DE-D275, DE-Bn3 |
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| match_str | linz1998controlofltypecalciumcurrentduringtheactionpotentialofguineapigventricularmyocytes |
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| physical | 425-442 |
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| spelling | Linz, Klaus W. Meyer, Rainer 0022-3751 1469-7793 Wiley Physiology http://dx.doi.org/10.1111/j.1469-7793.1998.425bb.x <jats:p> <jats:list list-type="explicit-label"> <jats:list-item><jats:p>During an action potential the L‐type Ca<jats:sup>2+</jats:sup> current (<jats:styled-content><jats:italic>I</jats:italic><jats:sub>Ca,L</jats:sub></jats:styled-content>) activates rapidly, then partially declines leading to a sustained inward current during the plateau phase. The reason for the sustained part of <jats:styled-content><jats:italic>I</jats:italic><jats:sub>Ca,L</jats:sub></jats:styled-content> has been investigated here.</jats:p></jats:list-item> <jats:list-item><jats:p>In the present study the mechanisms controlling the <jats:styled-content><jats:italic>I</jats:italic><jats:sub>Ca,L</jats:sub></jats:styled-content> during an action potential were investigated quantitatively in isolated guinea‐pig ventricular myocytes by whole‐cell patch clamp. To measure the actual time courses of <jats:styled-content><jats:italic>I</jats:italic><jats:sub>Ca,L</jats:sub></jats:styled-content> and the corresponding L‐type channel inactivation (<jats:styled-content><jats:italic>f</jats:italic><jats:sub>AP</jats:sub></jats:styled-content>) during an action potential, action potential‐clamp protocols combined with square pulses were applied.</jats:p></jats:list-item> <jats:list-item><jats:p>Within the first 10 ms of the action potential the <jats:styled-content><jats:italic>I</jats:italic><jats:sub>Ca,L</jats:sub></jats:styled-content> rapidly inactivated by about 50 %; during the plateau phase inactivation proceeded to 95 %. Later, during repolarization, the L‐type channels recovered up to 25 %.</jats:p></jats:list-item> <jats:list-item><jats:p>The voltage‐dependent component of inactivation during an action potential was determined from measurements of L‐type current carried by monovalent cations. This component of inactivation proceeded rather slowly and contributed only a little to <jats:italic>f</jats:italic><jats:sub>AP</jats:sub>. <jats:styled-content><jats:italic>I</jats:italic><jats:sub>Ca,L</jats:sub></jats:styled-content> during an action potential is thus mainly controlled by Ca<jats:sup>2+</jats:sup>‐dependent inactivation.</jats:p></jats:list-item> <jats:list-item><jats:p>In order to investigate the source of the Ca<jats:sup>2+</jats:sup> controlling <jats:italic>f</jats:italic><jats:sub>AP</jats:sub>, internal Ca<jats:sup>2+</jats:sup> homeostasis was manipulated by the use of Ca<jats:sup>2+</jats:sup> buffers (EGTA, BAPTA), by blocking Na<jats:sup>+</jats:sup>−Ca<jats:sup>2+</jats:sup> exchange, or by blocking Ca<jats:sup>2+</jats:sup> release from the sarcoplasmic reticulum (SR). Internal BAPTA markedly reduced the L‐type channel inactivation during the entire action potential, whereas EGTA affected <jats:italic>f</jats:italic><jats:sub>AP</jats:sub> only during the middle and late plateau phases. Inhibition of Na<jats:sup>+</jats:sup>−Ca<jats:sup>2+</jats:sup> exchange markedly increased inactivation of L‐type channels. Although blocking SR Ca<jats:sup>2+</jats:sup> release decreased the fura‐2‐measured cytoplasmic Ca<jats:sup>2+</jats:sup> concentration ([Ca<jats:sup>2+</jats:sup>]<jats:sub>i</jats:sub>) transient by about 90 %, it reduced L‐type channel inactivation only during the initial 50 ms of the action potential. Thus, it is Ca<jats:sup>2+</jats:sup> entering the cell through the L‐type channels that controls the inactivation process for the majority of the action potential. Nevertheless, SR Ca<jats:sup>2+</jats:sup>‐release contributes 40–50 % to L‐type channel inactivation during the initial period of the action potential. However, the maximum extent of inactivation reached during the plateau is independent of Ca<jats:sup>2+</jats:sup> released from the SR.</jats:p></jats:list-item> <jats:list-item><jats:p>For the first time, the actual time course of L‐type channel inactivation has been directly determined during an action potential under various defined [Ca<jats:sup>2+</jats:sup>]<jats:sub>i</jats:sub> conditions. Thereby, the relative contribution to <jats:styled-content><jats:italic>I</jats:italic><jats:sub>Ca,L</jats:sub></jats:styled-content> inactivation of voltage, Ca<jats:sup>2+</jats:sup> entering through L‐type channels, and Ca<jats:sup>2+</jats:sup> being released from the SR could be directly demonstrated.</jats:p></jats:list-item> </jats:list> </jats:p> Control of L‐type calcium current during the action potential of guinea‐pig ventricular myocytes The Journal of Physiology |
| spellingShingle | Linz, Klaus W., Meyer, Rainer, The Journal of Physiology, Control of L‐type calcium current during the action potential of guinea‐pig ventricular myocytes, Physiology |
| title | Control of L‐type calcium current during the action potential of guinea‐pig ventricular myocytes |
| title_full | Control of L‐type calcium current during the action potential of guinea‐pig ventricular myocytes |
| title_fullStr | Control of L‐type calcium current during the action potential of guinea‐pig ventricular myocytes |
| title_full_unstemmed | Control of L‐type calcium current during the action potential of guinea‐pig ventricular myocytes |
| title_short | Control of L‐type calcium current during the action potential of guinea‐pig ventricular myocytes |
| title_sort | control of l‐type calcium current during the action potential of guinea‐pig ventricular myocytes |
| title_unstemmed | Control of L‐type calcium current during the action potential of guinea‐pig ventricular myocytes |
| topic | Physiology |
| url | http://dx.doi.org/10.1111/j.1469-7793.1998.425bb.x |