Is the Beneficial Effect of Calcium Channel Blockers Against Cyclosporine A Toxicity Related to a Restoration of ATP Synthesis?
Abstract ATP synthesis inhibited by Cyclosporine A is restored by calcium channel blockers: nifedipine, verapamil, bepridil, diltiazem. ATP synthesis was estimated using liver mitochondria by measuring the rate of respiration during state 3 and a measure of the yield of ATP synthesis, the P/O ratio....
Ausführliche Beschreibung
Gespeichert in:
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
1995 |
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| Umfang: |
5 |
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| Reproduktion: |
Springer Online Journal Archives 1860-2002 |
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| Übergeordnetes Werk: |
in: Pharmaceutical research - 1984, 12(1995) vom: Apr., Seite 518-522 |
| Übergeordnetes Werk: |
volume:12 ; year:1995 ; month:04 ; pages:518-522 ; extent:5 |
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NLEJ198392613 |
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| 520 | |a Abstract ATP synthesis inhibited by Cyclosporine A is restored by calcium channel blockers: nifedipine, verapamil, bepridil, diltiazem. ATP synthesis was estimated using liver mitochondria by measuring the rate of respiration during state 3 and a measure of the yield of ATP synthesis, the P/O ratio. The study of calcium fluxes through mitochondrial membrane indicates that calcium channel blockers counteract the mitochondrial calcium storage induced by Cyclosporine A. If the restoration of ATP synthesis observed in vitro also occurred in vivo, the increase in ATP pool might contribute to a better functioning of the Ca2+ extrusion pumps of the cells, thereby maintaining the cytosolic calcium concentration (Cai) in the normal range. The nephrotoxicity of Cyclosporine A appears to be due to a vasoconstrictive effect related to an increased Cai This result may account for the reduction of clinical Cyclosporine A toxicity by calcium channel blockers. Verapamil appears to be the most efficient in restoring ATP synthesis. | ||
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| 700 | 1 | |a Berland, Yvon F. |4 oth | |
| 700 | 1 | |a Crevat, Aimé D. |4 oth | |
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(DE-627)NLEJ198392613 DE-627 ger DE-627 rakwb eng Is the Beneficial Effect of Calcium Channel Blockers Against Cyclosporine A Toxicity Related to a Restoration of ATP Synthesis? 1995 5 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract ATP synthesis inhibited by Cyclosporine A is restored by calcium channel blockers: nifedipine, verapamil, bepridil, diltiazem. ATP synthesis was estimated using liver mitochondria by measuring the rate of respiration during state 3 and a measure of the yield of ATP synthesis, the P/O ratio. The study of calcium fluxes through mitochondrial membrane indicates that calcium channel blockers counteract the mitochondrial calcium storage induced by Cyclosporine A. If the restoration of ATP synthesis observed in vitro also occurred in vivo, the increase in ATP pool might contribute to a better functioning of the Ca2+ extrusion pumps of the cells, thereby maintaining the cytosolic calcium concentration (Cai) in the normal range. The nephrotoxicity of Cyclosporine A appears to be due to a vasoconstrictive effect related to an increased Cai This result may account for the reduction of clinical Cyclosporine A toxicity by calcium channel blockers. Verapamil appears to be the most efficient in restoring ATP synthesis. Springer Online Journal Archives 1860-2002 Salducci, Marie D. oth Chauvet-Monges, Anne M. oth Dussol, Bertrand M. oth Berland, Yvon F. oth Crevat, Aimé D. oth in Pharmaceutical research 1984 12(1995) vom: Apr., Seite 518-522 (DE-627)NLEJ188988084 (DE-600)2036232-8 1573-904X nnns volume:12 year:1995 month:04 pages:518-522 extent:5 http://dx.doi.org/10.1023/A:1016293627487 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 12 1995 4 518-522 5 |
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(DE-627)NLEJ198392613 DE-627 ger DE-627 rakwb eng Is the Beneficial Effect of Calcium Channel Blockers Against Cyclosporine A Toxicity Related to a Restoration of ATP Synthesis? 1995 5 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract ATP synthesis inhibited by Cyclosporine A is restored by calcium channel blockers: nifedipine, verapamil, bepridil, diltiazem. ATP synthesis was estimated using liver mitochondria by measuring the rate of respiration during state 3 and a measure of the yield of ATP synthesis, the P/O ratio. The study of calcium fluxes through mitochondrial membrane indicates that calcium channel blockers counteract the mitochondrial calcium storage induced by Cyclosporine A. If the restoration of ATP synthesis observed in vitro also occurred in vivo, the increase in ATP pool might contribute to a better functioning of the Ca2+ extrusion pumps of the cells, thereby maintaining the cytosolic calcium concentration (Cai) in the normal range. The nephrotoxicity of Cyclosporine A appears to be due to a vasoconstrictive effect related to an increased Cai This result may account for the reduction of clinical Cyclosporine A toxicity by calcium channel blockers. Verapamil appears to be the most efficient in restoring ATP synthesis. Springer Online Journal Archives 1860-2002 Salducci, Marie D. oth Chauvet-Monges, Anne M. oth Dussol, Bertrand M. oth Berland, Yvon F. oth Crevat, Aimé D. oth in Pharmaceutical research 1984 12(1995) vom: Apr., Seite 518-522 (DE-627)NLEJ188988084 (DE-600)2036232-8 1573-904X nnns volume:12 year:1995 month:04 pages:518-522 extent:5 http://dx.doi.org/10.1023/A:1016293627487 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 12 1995 4 518-522 5 |
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(DE-627)NLEJ198392613 DE-627 ger DE-627 rakwb eng Is the Beneficial Effect of Calcium Channel Blockers Against Cyclosporine A Toxicity Related to a Restoration of ATP Synthesis? 1995 5 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract ATP synthesis inhibited by Cyclosporine A is restored by calcium channel blockers: nifedipine, verapamil, bepridil, diltiazem. ATP synthesis was estimated using liver mitochondria by measuring the rate of respiration during state 3 and a measure of the yield of ATP synthesis, the P/O ratio. The study of calcium fluxes through mitochondrial membrane indicates that calcium channel blockers counteract the mitochondrial calcium storage induced by Cyclosporine A. If the restoration of ATP synthesis observed in vitro also occurred in vivo, the increase in ATP pool might contribute to a better functioning of the Ca2+ extrusion pumps of the cells, thereby maintaining the cytosolic calcium concentration (Cai) in the normal range. The nephrotoxicity of Cyclosporine A appears to be due to a vasoconstrictive effect related to an increased Cai This result may account for the reduction of clinical Cyclosporine A toxicity by calcium channel blockers. Verapamil appears to be the most efficient in restoring ATP synthesis. Springer Online Journal Archives 1860-2002 Salducci, Marie D. oth Chauvet-Monges, Anne M. oth Dussol, Bertrand M. oth Berland, Yvon F. oth Crevat, Aimé D. oth in Pharmaceutical research 1984 12(1995) vom: Apr., Seite 518-522 (DE-627)NLEJ188988084 (DE-600)2036232-8 1573-904X nnns volume:12 year:1995 month:04 pages:518-522 extent:5 http://dx.doi.org/10.1023/A:1016293627487 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 12 1995 4 518-522 5 |
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(DE-627)NLEJ198392613 DE-627 ger DE-627 rakwb eng Is the Beneficial Effect of Calcium Channel Blockers Against Cyclosporine A Toxicity Related to a Restoration of ATP Synthesis? 1995 5 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract ATP synthesis inhibited by Cyclosporine A is restored by calcium channel blockers: nifedipine, verapamil, bepridil, diltiazem. ATP synthesis was estimated using liver mitochondria by measuring the rate of respiration during state 3 and a measure of the yield of ATP synthesis, the P/O ratio. The study of calcium fluxes through mitochondrial membrane indicates that calcium channel blockers counteract the mitochondrial calcium storage induced by Cyclosporine A. If the restoration of ATP synthesis observed in vitro also occurred in vivo, the increase in ATP pool might contribute to a better functioning of the Ca2+ extrusion pumps of the cells, thereby maintaining the cytosolic calcium concentration (Cai) in the normal range. The nephrotoxicity of Cyclosporine A appears to be due to a vasoconstrictive effect related to an increased Cai This result may account for the reduction of clinical Cyclosporine A toxicity by calcium channel blockers. Verapamil appears to be the most efficient in restoring ATP synthesis. Springer Online Journal Archives 1860-2002 Salducci, Marie D. oth Chauvet-Monges, Anne M. oth Dussol, Bertrand M. oth Berland, Yvon F. oth Crevat, Aimé D. oth in Pharmaceutical research 1984 12(1995) vom: Apr., Seite 518-522 (DE-627)NLEJ188988084 (DE-600)2036232-8 1573-904X nnns volume:12 year:1995 month:04 pages:518-522 extent:5 http://dx.doi.org/10.1023/A:1016293627487 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 12 1995 4 518-522 5 |
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(DE-627)NLEJ198392613 DE-627 ger DE-627 rakwb eng Is the Beneficial Effect of Calcium Channel Blockers Against Cyclosporine A Toxicity Related to a Restoration of ATP Synthesis? 1995 5 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract ATP synthesis inhibited by Cyclosporine A is restored by calcium channel blockers: nifedipine, verapamil, bepridil, diltiazem. ATP synthesis was estimated using liver mitochondria by measuring the rate of respiration during state 3 and a measure of the yield of ATP synthesis, the P/O ratio. The study of calcium fluxes through mitochondrial membrane indicates that calcium channel blockers counteract the mitochondrial calcium storage induced by Cyclosporine A. If the restoration of ATP synthesis observed in vitro also occurred in vivo, the increase in ATP pool might contribute to a better functioning of the Ca2+ extrusion pumps of the cells, thereby maintaining the cytosolic calcium concentration (Cai) in the normal range. The nephrotoxicity of Cyclosporine A appears to be due to a vasoconstrictive effect related to an increased Cai This result may account for the reduction of clinical Cyclosporine A toxicity by calcium channel blockers. Verapamil appears to be the most efficient in restoring ATP synthesis. Springer Online Journal Archives 1860-2002 Salducci, Marie D. oth Chauvet-Monges, Anne M. oth Dussol, Bertrand M. oth Berland, Yvon F. oth Crevat, Aimé D. oth in Pharmaceutical research 1984 12(1995) vom: Apr., Seite 518-522 (DE-627)NLEJ188988084 (DE-600)2036232-8 1573-904X nnns volume:12 year:1995 month:04 pages:518-522 extent:5 http://dx.doi.org/10.1023/A:1016293627487 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 12 1995 4 518-522 5 |
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Is the Beneficial Effect of Calcium Channel Blockers Against Cyclosporine A Toxicity Related to a Restoration of ATP Synthesis? |
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Abstract ATP synthesis inhibited by Cyclosporine A is restored by calcium channel blockers: nifedipine, verapamil, bepridil, diltiazem. ATP synthesis was estimated using liver mitochondria by measuring the rate of respiration during state 3 and a measure of the yield of ATP synthesis, the P/O ratio. The study of calcium fluxes through mitochondrial membrane indicates that calcium channel blockers counteract the mitochondrial calcium storage induced by Cyclosporine A. If the restoration of ATP synthesis observed in vitro also occurred in vivo, the increase in ATP pool might contribute to a better functioning of the Ca2+ extrusion pumps of the cells, thereby maintaining the cytosolic calcium concentration (Cai) in the normal range. The nephrotoxicity of Cyclosporine A appears to be due to a vasoconstrictive effect related to an increased Cai This result may account for the reduction of clinical Cyclosporine A toxicity by calcium channel blockers. Verapamil appears to be the most efficient in restoring ATP synthesis. |
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Abstract ATP synthesis inhibited by Cyclosporine A is restored by calcium channel blockers: nifedipine, verapamil, bepridil, diltiazem. ATP synthesis was estimated using liver mitochondria by measuring the rate of respiration during state 3 and a measure of the yield of ATP synthesis, the P/O ratio. The study of calcium fluxes through mitochondrial membrane indicates that calcium channel blockers counteract the mitochondrial calcium storage induced by Cyclosporine A. If the restoration of ATP synthesis observed in vitro also occurred in vivo, the increase in ATP pool might contribute to a better functioning of the Ca2+ extrusion pumps of the cells, thereby maintaining the cytosolic calcium concentration (Cai) in the normal range. The nephrotoxicity of Cyclosporine A appears to be due to a vasoconstrictive effect related to an increased Cai This result may account for the reduction of clinical Cyclosporine A toxicity by calcium channel blockers. Verapamil appears to be the most efficient in restoring ATP synthesis. |
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Abstract ATP synthesis inhibited by Cyclosporine A is restored by calcium channel blockers: nifedipine, verapamil, bepridil, diltiazem. ATP synthesis was estimated using liver mitochondria by measuring the rate of respiration during state 3 and a measure of the yield of ATP synthesis, the P/O ratio. The study of calcium fluxes through mitochondrial membrane indicates that calcium channel blockers counteract the mitochondrial calcium storage induced by Cyclosporine A. If the restoration of ATP synthesis observed in vitro also occurred in vivo, the increase in ATP pool might contribute to a better functioning of the Ca2+ extrusion pumps of the cells, thereby maintaining the cytosolic calcium concentration (Cai) in the normal range. The nephrotoxicity of Cyclosporine A appears to be due to a vasoconstrictive effect related to an increased Cai This result may account for the reduction of clinical Cyclosporine A toxicity by calcium channel blockers. Verapamil appears to be the most efficient in restoring ATP synthesis. |
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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">NLEJ198392613</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230506000955.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">070527s1995 xx |||||o 00| ||eng c</controlfield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ198392613</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">Is the Beneficial Effect of Calcium Channel Blockers Against Cyclosporine A Toxicity Related to a Restoration of ATP Synthesis?</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">1995</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">5</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">Abstract ATP synthesis inhibited by Cyclosporine A is restored by calcium channel blockers: nifedipine, verapamil, bepridil, diltiazem. ATP synthesis was estimated using liver mitochondria by measuring the rate of respiration during state 3 and a measure of the yield of ATP synthesis, the P/O ratio. The study of calcium fluxes through mitochondrial membrane indicates that calcium channel blockers counteract the mitochondrial calcium storage induced by Cyclosporine A. If the restoration of ATP synthesis observed in vitro also occurred in vivo, the increase in ATP pool might contribute to a better functioning of the Ca2+ extrusion pumps of the cells, thereby maintaining the cytosolic calcium concentration (Cai) in the normal range. The nephrotoxicity of Cyclosporine A appears to be due to a vasoconstrictive effect related to an increased Cai This result may account for the reduction of clinical Cyclosporine A toxicity by calcium channel blockers. Verapamil appears to be the most efficient in restoring ATP synthesis.</subfield></datafield><datafield tag="533" ind1=" " ind2=" "><subfield code="f">Springer Online Journal Archives 1860-2002</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Salducci, Marie D.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Chauvet-Monges, Anne M.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Dussol, Bertrand M.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Berland, Yvon F.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Crevat, Aimé D.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">in</subfield><subfield code="t">Pharmaceutical research</subfield><subfield code="d">1984</subfield><subfield code="g">12(1995) vom: Apr., Seite 518-522</subfield><subfield code="w">(DE-627)NLEJ188988084</subfield><subfield code="w">(DE-600)2036232-8</subfield><subfield code="x">1573-904X</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:12</subfield><subfield code="g">year:1995</subfield><subfield code="g">month:04</subfield><subfield code="g">pages:518-522</subfield><subfield code="g">extent:5</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1023/A:1016293627487</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-SOJ</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">12</subfield><subfield code="j">1995</subfield><subfield code="c">4</subfield><subfield code="h">518-522</subfield><subfield code="g">5</subfield></datafield></record></collection>
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