Activation of the basolateral Cl− conductance by cAMP in rabbit renal proximal tubule S3 segments
Abstract The regulatory mechanism of basolateral Cl− conductance in rabbit renal proximal tubule S3 segments was investigated with conventional and Cl− sensitive microelectrodes. After the basolateral Cl−/HCO 3 − exchanger was blocked by 4,4′-diisothiocyanatostilbene-2, 2′-disulphonic acid (DIDS) we...
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E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
1995 |
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| Umfang: |
8 |
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| Reproduktion: |
Springer Online Journal Archives 1860-2002 |
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| Übergeordnetes Werk: |
in: Pflügers Archiv - 1868, 430(1995) vom: Jan., Seite 88-95 |
| Übergeordnetes Werk: |
volume:430 ; year:1995 ; month:01 ; pages:88-95 ; extent:8 |
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NLEJ201004526 |
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| 245 | 1 | 0 | |a Activation of the basolateral Cl− conductance by cAMP in rabbit renal proximal tubule S3 segments |
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| 520 | |a Abstract The regulatory mechanism of basolateral Cl− conductance in rabbit renal proximal tubule S3 segments was investigated with conventional and Cl− sensitive microelectrodes. After the basolateral Cl−/HCO 3 − exchanger was blocked by 4,4′-diisothiocyanatostilbene-2, 2′-disulphonic acid (DIDS) we increased the bath K+ concentration from 5 mmol/l to 20 mmol/l, which depolarized the cells and thereby increased intracellular Cl− activity ([Cl−]i). This [Cl−]i response was enhanced by +63% in the presence of forskolin (20 μmol/l), by +40% in the presence of dibutyryl adenosine 3′,5′-cyclic monophosphate (db-cAMP) (1 mmol/l) and by +44% in the presence of parathyroid hormone (PTH, 10 nmol/l), whereas it was inhibited by a Cl− channel blocker, indanyl-oxyacetic acid (IAA-94, 0.3 mmol/l). In addition, forskolin, PTH and chlorophenylthio-cAMP enhanced the electrogenic response to removal of bath Cl− after the blockade of K+ conductance, and this activation was also sensitive to IAA-94. On the other hand, 2 μmol/l ionomycin and 0.5 μmol/l phorbol myristate failed to activate the [Cl−]i response to elevation of bath K+ concentration and the electrogenic response to Cl− removal, and ionomycin had no effect even in the absence of DIDS. These results indicate that this basolateral Cl− conductance can be activated by cAMP, while neither the increase in cytosolic Ca2+ nor the activation of protein kinase C has direct effects on this conductance. | ||
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| 700 | 1 | |a Uwatoko, Shu |4 oth | |
| 700 | 1 | |a Suzuki, Keiji |4 oth | |
| 700 | 1 | |a Kurokawa, Kiyoshi |4 oth | |
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(DE-627)NLEJ201004526 DE-627 ger DE-627 rakwb eng Activation of the basolateral Cl− conductance by cAMP in rabbit renal proximal tubule S3 segments 1995 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract The regulatory mechanism of basolateral Cl− conductance in rabbit renal proximal tubule S3 segments was investigated with conventional and Cl− sensitive microelectrodes. After the basolateral Cl−/HCO 3 − exchanger was blocked by 4,4′-diisothiocyanatostilbene-2, 2′-disulphonic acid (DIDS) we increased the bath K+ concentration from 5 mmol/l to 20 mmol/l, which depolarized the cells and thereby increased intracellular Cl− activity ([Cl−]i). This [Cl−]i response was enhanced by +63% in the presence of forskolin (20 μmol/l), by +40% in the presence of dibutyryl adenosine 3′,5′-cyclic monophosphate (db-cAMP) (1 mmol/l) and by +44% in the presence of parathyroid hormone (PTH, 10 nmol/l), whereas it was inhibited by a Cl− channel blocker, indanyl-oxyacetic acid (IAA-94, 0.3 mmol/l). In addition, forskolin, PTH and chlorophenylthio-cAMP enhanced the electrogenic response to removal of bath Cl− after the blockade of K+ conductance, and this activation was also sensitive to IAA-94. On the other hand, 2 μmol/l ionomycin and 0.5 μmol/l phorbol myristate failed to activate the [Cl−]i response to elevation of bath K+ concentration and the electrogenic response to Cl− removal, and ionomycin had no effect even in the absence of DIDS. These results indicate that this basolateral Cl− conductance can be activated by cAMP, while neither the increase in cytosolic Ca2+ nor the activation of protein kinase C has direct effects on this conductance. Springer Online Journal Archives 1860-2002 Seki, George oth Taniguchi, Shigeo oth Uwatoko, Shu oth Suzuki, Keiji oth Kurokawa, Kiyoshi oth in Pflügers Archiv 1868 430(1995) vom: Jan., Seite 88-95 (DE-627)NLEJ188987363 (DE-600)1463014-x 1432-2013 nnns volume:430 year:1995 month:01 pages:88-95 extent:8 http://dx.doi.org/10.1007/BF00373843 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 430 1995 1 88-95 8 |
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(DE-627)NLEJ201004526 DE-627 ger DE-627 rakwb eng Activation of the basolateral Cl− conductance by cAMP in rabbit renal proximal tubule S3 segments 1995 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract The regulatory mechanism of basolateral Cl− conductance in rabbit renal proximal tubule S3 segments was investigated with conventional and Cl− sensitive microelectrodes. After the basolateral Cl−/HCO 3 − exchanger was blocked by 4,4′-diisothiocyanatostilbene-2, 2′-disulphonic acid (DIDS) we increased the bath K+ concentration from 5 mmol/l to 20 mmol/l, which depolarized the cells and thereby increased intracellular Cl− activity ([Cl−]i). This [Cl−]i response was enhanced by +63% in the presence of forskolin (20 μmol/l), by +40% in the presence of dibutyryl adenosine 3′,5′-cyclic monophosphate (db-cAMP) (1 mmol/l) and by +44% in the presence of parathyroid hormone (PTH, 10 nmol/l), whereas it was inhibited by a Cl− channel blocker, indanyl-oxyacetic acid (IAA-94, 0.3 mmol/l). In addition, forskolin, PTH and chlorophenylthio-cAMP enhanced the electrogenic response to removal of bath Cl− after the blockade of K+ conductance, and this activation was also sensitive to IAA-94. On the other hand, 2 μmol/l ionomycin and 0.5 μmol/l phorbol myristate failed to activate the [Cl−]i response to elevation of bath K+ concentration and the electrogenic response to Cl− removal, and ionomycin had no effect even in the absence of DIDS. These results indicate that this basolateral Cl− conductance can be activated by cAMP, while neither the increase in cytosolic Ca2+ nor the activation of protein kinase C has direct effects on this conductance. Springer Online Journal Archives 1860-2002 Seki, George oth Taniguchi, Shigeo oth Uwatoko, Shu oth Suzuki, Keiji oth Kurokawa, Kiyoshi oth in Pflügers Archiv 1868 430(1995) vom: Jan., Seite 88-95 (DE-627)NLEJ188987363 (DE-600)1463014-x 1432-2013 nnns volume:430 year:1995 month:01 pages:88-95 extent:8 http://dx.doi.org/10.1007/BF00373843 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 430 1995 1 88-95 8 |
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(DE-627)NLEJ201004526 DE-627 ger DE-627 rakwb eng Activation of the basolateral Cl− conductance by cAMP in rabbit renal proximal tubule S3 segments 1995 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract The regulatory mechanism of basolateral Cl− conductance in rabbit renal proximal tubule S3 segments was investigated with conventional and Cl− sensitive microelectrodes. After the basolateral Cl−/HCO 3 − exchanger was blocked by 4,4′-diisothiocyanatostilbene-2, 2′-disulphonic acid (DIDS) we increased the bath K+ concentration from 5 mmol/l to 20 mmol/l, which depolarized the cells and thereby increased intracellular Cl− activity ([Cl−]i). This [Cl−]i response was enhanced by +63% in the presence of forskolin (20 μmol/l), by +40% in the presence of dibutyryl adenosine 3′,5′-cyclic monophosphate (db-cAMP) (1 mmol/l) and by +44% in the presence of parathyroid hormone (PTH, 10 nmol/l), whereas it was inhibited by a Cl− channel blocker, indanyl-oxyacetic acid (IAA-94, 0.3 mmol/l). In addition, forskolin, PTH and chlorophenylthio-cAMP enhanced the electrogenic response to removal of bath Cl− after the blockade of K+ conductance, and this activation was also sensitive to IAA-94. On the other hand, 2 μmol/l ionomycin and 0.5 μmol/l phorbol myristate failed to activate the [Cl−]i response to elevation of bath K+ concentration and the electrogenic response to Cl− removal, and ionomycin had no effect even in the absence of DIDS. These results indicate that this basolateral Cl− conductance can be activated by cAMP, while neither the increase in cytosolic Ca2+ nor the activation of protein kinase C has direct effects on this conductance. Springer Online Journal Archives 1860-2002 Seki, George oth Taniguchi, Shigeo oth Uwatoko, Shu oth Suzuki, Keiji oth Kurokawa, Kiyoshi oth in Pflügers Archiv 1868 430(1995) vom: Jan., Seite 88-95 (DE-627)NLEJ188987363 (DE-600)1463014-x 1432-2013 nnns volume:430 year:1995 month:01 pages:88-95 extent:8 http://dx.doi.org/10.1007/BF00373843 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 430 1995 1 88-95 8 |
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(DE-627)NLEJ201004526 DE-627 ger DE-627 rakwb eng Activation of the basolateral Cl− conductance by cAMP in rabbit renal proximal tubule S3 segments 1995 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract The regulatory mechanism of basolateral Cl− conductance in rabbit renal proximal tubule S3 segments was investigated with conventional and Cl− sensitive microelectrodes. After the basolateral Cl−/HCO 3 − exchanger was blocked by 4,4′-diisothiocyanatostilbene-2, 2′-disulphonic acid (DIDS) we increased the bath K+ concentration from 5 mmol/l to 20 mmol/l, which depolarized the cells and thereby increased intracellular Cl− activity ([Cl−]i). This [Cl−]i response was enhanced by +63% in the presence of forskolin (20 μmol/l), by +40% in the presence of dibutyryl adenosine 3′,5′-cyclic monophosphate (db-cAMP) (1 mmol/l) and by +44% in the presence of parathyroid hormone (PTH, 10 nmol/l), whereas it was inhibited by a Cl− channel blocker, indanyl-oxyacetic acid (IAA-94, 0.3 mmol/l). In addition, forskolin, PTH and chlorophenylthio-cAMP enhanced the electrogenic response to removal of bath Cl− after the blockade of K+ conductance, and this activation was also sensitive to IAA-94. On the other hand, 2 μmol/l ionomycin and 0.5 μmol/l phorbol myristate failed to activate the [Cl−]i response to elevation of bath K+ concentration and the electrogenic response to Cl− removal, and ionomycin had no effect even in the absence of DIDS. These results indicate that this basolateral Cl− conductance can be activated by cAMP, while neither the increase in cytosolic Ca2+ nor the activation of protein kinase C has direct effects on this conductance. Springer Online Journal Archives 1860-2002 Seki, George oth Taniguchi, Shigeo oth Uwatoko, Shu oth Suzuki, Keiji oth Kurokawa, Kiyoshi oth in Pflügers Archiv 1868 430(1995) vom: Jan., Seite 88-95 (DE-627)NLEJ188987363 (DE-600)1463014-x 1432-2013 nnns volume:430 year:1995 month:01 pages:88-95 extent:8 http://dx.doi.org/10.1007/BF00373843 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 430 1995 1 88-95 8 |
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(DE-627)NLEJ201004526 DE-627 ger DE-627 rakwb eng Activation of the basolateral Cl− conductance by cAMP in rabbit renal proximal tubule S3 segments 1995 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract The regulatory mechanism of basolateral Cl− conductance in rabbit renal proximal tubule S3 segments was investigated with conventional and Cl− sensitive microelectrodes. After the basolateral Cl−/HCO 3 − exchanger was blocked by 4,4′-diisothiocyanatostilbene-2, 2′-disulphonic acid (DIDS) we increased the bath K+ concentration from 5 mmol/l to 20 mmol/l, which depolarized the cells and thereby increased intracellular Cl− activity ([Cl−]i). This [Cl−]i response was enhanced by +63% in the presence of forskolin (20 μmol/l), by +40% in the presence of dibutyryl adenosine 3′,5′-cyclic monophosphate (db-cAMP) (1 mmol/l) and by +44% in the presence of parathyroid hormone (PTH, 10 nmol/l), whereas it was inhibited by a Cl− channel blocker, indanyl-oxyacetic acid (IAA-94, 0.3 mmol/l). In addition, forskolin, PTH and chlorophenylthio-cAMP enhanced the electrogenic response to removal of bath Cl− after the blockade of K+ conductance, and this activation was also sensitive to IAA-94. On the other hand, 2 μmol/l ionomycin and 0.5 μmol/l phorbol myristate failed to activate the [Cl−]i response to elevation of bath K+ concentration and the electrogenic response to Cl− removal, and ionomycin had no effect even in the absence of DIDS. These results indicate that this basolateral Cl− conductance can be activated by cAMP, while neither the increase in cytosolic Ca2+ nor the activation of protein kinase C has direct effects on this conductance. Springer Online Journal Archives 1860-2002 Seki, George oth Taniguchi, Shigeo oth Uwatoko, Shu oth Suzuki, Keiji oth Kurokawa, Kiyoshi oth in Pflügers Archiv 1868 430(1995) vom: Jan., Seite 88-95 (DE-627)NLEJ188987363 (DE-600)1463014-x 1432-2013 nnns volume:430 year:1995 month:01 pages:88-95 extent:8 http://dx.doi.org/10.1007/BF00373843 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 430 1995 1 88-95 8 |
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activation of the basolateral cl− conductance by camp in rabbit renal proximal tubule s3 segments |
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Activation of the basolateral Cl− conductance by cAMP in rabbit renal proximal tubule S3 segments |
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Abstract The regulatory mechanism of basolateral Cl− conductance in rabbit renal proximal tubule S3 segments was investigated with conventional and Cl− sensitive microelectrodes. After the basolateral Cl−/HCO 3 − exchanger was blocked by 4,4′-diisothiocyanatostilbene-2, 2′-disulphonic acid (DIDS) we increased the bath K+ concentration from 5 mmol/l to 20 mmol/l, which depolarized the cells and thereby increased intracellular Cl− activity ([Cl−]i). This [Cl−]i response was enhanced by +63% in the presence of forskolin (20 μmol/l), by +40% in the presence of dibutyryl adenosine 3′,5′-cyclic monophosphate (db-cAMP) (1 mmol/l) and by +44% in the presence of parathyroid hormone (PTH, 10 nmol/l), whereas it was inhibited by a Cl− channel blocker, indanyl-oxyacetic acid (IAA-94, 0.3 mmol/l). In addition, forskolin, PTH and chlorophenylthio-cAMP enhanced the electrogenic response to removal of bath Cl− after the blockade of K+ conductance, and this activation was also sensitive to IAA-94. On the other hand, 2 μmol/l ionomycin and 0.5 μmol/l phorbol myristate failed to activate the [Cl−]i response to elevation of bath K+ concentration and the electrogenic response to Cl− removal, and ionomycin had no effect even in the absence of DIDS. These results indicate that this basolateral Cl− conductance can be activated by cAMP, while neither the increase in cytosolic Ca2+ nor the activation of protein kinase C has direct effects on this conductance. |
| abstractGer |
Abstract The regulatory mechanism of basolateral Cl− conductance in rabbit renal proximal tubule S3 segments was investigated with conventional and Cl− sensitive microelectrodes. After the basolateral Cl−/HCO 3 − exchanger was blocked by 4,4′-diisothiocyanatostilbene-2, 2′-disulphonic acid (DIDS) we increased the bath K+ concentration from 5 mmol/l to 20 mmol/l, which depolarized the cells and thereby increased intracellular Cl− activity ([Cl−]i). This [Cl−]i response was enhanced by +63% in the presence of forskolin (20 μmol/l), by +40% in the presence of dibutyryl adenosine 3′,5′-cyclic monophosphate (db-cAMP) (1 mmol/l) and by +44% in the presence of parathyroid hormone (PTH, 10 nmol/l), whereas it was inhibited by a Cl− channel blocker, indanyl-oxyacetic acid (IAA-94, 0.3 mmol/l). In addition, forskolin, PTH and chlorophenylthio-cAMP enhanced the electrogenic response to removal of bath Cl− after the blockade of K+ conductance, and this activation was also sensitive to IAA-94. On the other hand, 2 μmol/l ionomycin and 0.5 μmol/l phorbol myristate failed to activate the [Cl−]i response to elevation of bath K+ concentration and the electrogenic response to Cl− removal, and ionomycin had no effect even in the absence of DIDS. These results indicate that this basolateral Cl− conductance can be activated by cAMP, while neither the increase in cytosolic Ca2+ nor the activation of protein kinase C has direct effects on this conductance. |
| abstract_unstemmed |
Abstract The regulatory mechanism of basolateral Cl− conductance in rabbit renal proximal tubule S3 segments was investigated with conventional and Cl− sensitive microelectrodes. After the basolateral Cl−/HCO 3 − exchanger was blocked by 4,4′-diisothiocyanatostilbene-2, 2′-disulphonic acid (DIDS) we increased the bath K+ concentration from 5 mmol/l to 20 mmol/l, which depolarized the cells and thereby increased intracellular Cl− activity ([Cl−]i). This [Cl−]i response was enhanced by +63% in the presence of forskolin (20 μmol/l), by +40% in the presence of dibutyryl adenosine 3′,5′-cyclic monophosphate (db-cAMP) (1 mmol/l) and by +44% in the presence of parathyroid hormone (PTH, 10 nmol/l), whereas it was inhibited by a Cl− channel blocker, indanyl-oxyacetic acid (IAA-94, 0.3 mmol/l). In addition, forskolin, PTH and chlorophenylthio-cAMP enhanced the electrogenic response to removal of bath Cl− after the blockade of K+ conductance, and this activation was also sensitive to IAA-94. On the other hand, 2 μmol/l ionomycin and 0.5 μmol/l phorbol myristate failed to activate the [Cl−]i response to elevation of bath K+ concentration and the electrogenic response to Cl− removal, and ionomycin had no effect even in the absence of DIDS. These results indicate that this basolateral Cl− conductance can be activated by cAMP, while neither the increase in cytosolic Ca2+ nor the activation of protein kinase C has direct effects on this conductance. |
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GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE |
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Activation of the basolateral Cl− conductance by cAMP in rabbit renal proximal tubule S3 segments |
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http://dx.doi.org/10.1007/BF00373843 |
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Seki, George Taniguchi, Shigeo Uwatoko, Shu Suzuki, Keiji Kurokawa, Kiyoshi |
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2024-07-06T04:31:57.047Z |
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