Inhibition of the Na +–H + exchanger with cariporide abolishes stretch-induced calcium but not sodium accumulation in mouse ventricular myocytes
We address the question whether activation of the sodium–proton exchanger (NHE) does contribute to the stretch-induced accumulation of intracellular sodium and calcium in mouse ventricular myocytes. NHE-blocker cariporide (10 μM) were applied to the bath for 10 min. Axial stretch was applied for 2 m...
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Published in | Cell calcium (Edinburgh) Vol. 37; no. 1; pp. 69 - 80 |
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Language | English |
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Abstract | We address the question whether activation of the sodium–proton exchanger (NHE) does contribute to the stretch-induced accumulation of intracellular sodium and calcium in mouse ventricular myocytes.
NHE-blocker cariporide (10
μM) were applied to the bath for 10
min. Axial stretch was applied for 2
min by increasing the distance between an adherent glass stylus and the patch pipette by 20%. Myocytes (stimulated at 3
Hz) were shock-frozen in diastole and the membrane currents monitored till cryofixation. Controls were treated identically, but not stretched. Total sodium and calcium concentrations ([Na], [Ca] = sum of free and bound Na and Ca) were measured by electron probe microanalysis (EPMA) in peripheral and central cytosol, mitochondria, nucleus and nuclear envelope.
Cariporide did not reduce the stretch-activated negative current. The stretch-induced rise in [Na] was not different in the presence and in the absence of cariporide. Cariporide significantly reduced diastolic [Ca] in the cytosol of stretched myocytes.
Since cariporide does not prevent the stretch-induced [Na] accumulation, we suggest that not NHE but the stretch-activated streptomycin-sensitive current
I
SAC causes the well documented stretch-induced [Na] accumulation. The discovery that cariporide prevents the stretch-induced rise in cytosolic [Ca] demonstrates an important additional effect of the drug on calcium handling. |
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AbstractList | We address the question whether activation of the sodium–proton exchanger (NHE) does contribute to the stretch-induced accumulation of intracellular sodium and calcium in mouse ventricular myocytes.
NHE-blocker cariporide (10
μM) were applied to the bath for 10
min. Axial stretch was applied for 2
min by increasing the distance between an adherent glass stylus and the patch pipette by 20%. Myocytes (stimulated at 3
Hz) were shock-frozen in diastole and the membrane currents monitored till cryofixation. Controls were treated identically, but not stretched. Total sodium and calcium concentrations ([Na], [Ca] = sum of free and bound Na and Ca) were measured by electron probe microanalysis (EPMA) in peripheral and central cytosol, mitochondria, nucleus and nuclear envelope.
Cariporide did not reduce the stretch-activated negative current. The stretch-induced rise in [Na] was not different in the presence and in the absence of cariporide. Cariporide significantly reduced diastolic [Ca] in the cytosol of stretched myocytes.
Since cariporide does not prevent the stretch-induced [Na] accumulation, we suggest that not NHE but the stretch-activated streptomycin-sensitive current
I
SAC causes the well documented stretch-induced [Na] accumulation. The discovery that cariporide prevents the stretch-induced rise in cytosolic [Ca] demonstrates an important additional effect of the drug on calcium handling. We address the question whether activation of the sodium-proton exchanger (NHE) does contribute to the stretch-induced accumulation of intracellular sodium and calcium in mouse ventricular myocytes. NHE-blocker cariporide (10 microM) were applied to the bath for 10 min. Axial stretch was applied for 2 min by increasing the distance between an adherent glass stylus and the patch pipette by 20%. Myocytes (stimulated at 3 Hz) were shock-frozen in diastole and the membrane currents monitored till cryofixation. Controls were treated identically, but not stretched. Total sodium and calcium concentrations ([Na], [Ca]=sum of free and bound Na and Ca) were measured by electron probe microanalysis (EPMA) in peripheral and central cytosol, mitochondria, nucleus and nuclear envelope. Cariporide did not reduce the stretch-activated negative current. The stretch-induced rise in [Na] was not different in the presence and in the absence of cariporide. Cariporide significantly reduced diastolic [Ca] in the cytosol of stretched myocytes. Since cariporide does not prevent the stretch-induced [Na] accumulation, we suggest that not NHE but the stretch-activated streptomycin-sensitive current I(SAC) causes the well documented stretch-induced [Na] accumulation. The discovery that cariporide prevents the stretch-induced rise in cytosolic [Ca] demonstrates an important additional effect of the drug on calcium handling. |
Author | Kondratev, Denis Christ, Andreas Gallitelli, Maria Fiora |
Author_xml | – sequence: 1 givenname: Denis surname: Kondratev fullname: Kondratev, Denis – sequence: 2 givenname: Andreas surname: Christ fullname: Christ, Andreas – sequence: 3 givenname: Maria Fiora surname: Gallitelli fullname: Gallitelli, Maria Fiora email: maria.gallitelli@medizin.uni-halle.de |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/15541465$$D View this record in MEDLINE/PubMed |
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Cites_doi | 10.1113/jphysiol.2003.051888 10.1161/01.RES.83.8.775 10.1111/j.1469-7793.1999.0433p.x 10.1161/01.CIR.0000093277.20968.C7 10.1016/S0008-6363(00)00166-8 10.1161/01.CIR.101.23.2749 10.1016/B978-0-12-185257-3.50013-6 10.1006/jmcc.1999.1029 10.1113/jphysiol.1982.sp014221 10.1111/j.1365-2818.1979.tb00236.x 10.1161/01.CIR.102.25.3032 10.1016/S0143-4160(03)00084-8 10.1016/S0008-6363(00)00208-X 10.1016/S0008-6363(02)00830-1 10.1113/jphysiol.1996.sp021243 10.1152/ajpcell.1978.235.5.C147 10.1016/S0008-6363(96)88579-8 10.1016/S0008-6363(02)00768-X 10.1016/S0079-6107(03)00004-X 10.1016/S0014-2999(96)00755-8 10.1161/01.RES.85.8.716 |
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Keywords | HOE642 Stretched cardiomyocytes Sodium–proton exchange Elecron probe microanalysis Cariporide Intracellular sodium Intracellular calcium depletion |
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Snippet | We address the question whether activation of the sodium–proton exchanger (NHE) does contribute to the stretch-induced accumulation of intracellular sodium and... We address the question whether activation of the sodium-proton exchanger (NHE) does contribute to the stretch-induced accumulation of intracellular sodium and... |
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SubjectTerms | Animals Anti-Arrhythmia Agents - pharmacology Calcium - metabolism Calcium Signaling - drug effects Calcium Signaling - physiology Cariporide Cell Nucleus - drug effects Cell Nucleus - metabolism Cells, Cultured Cytoplasm - drug effects Cytoplasm - metabolism Diastole - drug effects Diastole - physiology Elecron probe microanalysis Guanidines - pharmacology Heart Ventricles - cytology HOE642 Intracellular calcium depletion Intracellular Fluid - drug effects Intracellular Fluid - metabolism Intracellular sodium Membrane Potentials - drug effects Membrane Potentials - physiology Mice Mitochondria - drug effects Mitochondria - metabolism Muscle Contraction - drug effects Muscle Contraction - physiology Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism Patch-Clamp Techniques Sodium - metabolism Sodium-Hydrogen Exchangers - antagonists & inhibitors Sodium-Hydrogen Exchangers - metabolism Sodium–proton exchange Stress, Mechanical Stretched cardiomyocytes Sulfones - pharmacology |
Title | Inhibition of the Na +–H + exchanger with cariporide abolishes stretch-induced calcium but not sodium accumulation in mouse ventricular myocytes |
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