ATP-Sensitive Potassium Channel Currents in Eccentrically Hypertrophied Cardiac Myocytes of Volume-Overloaded Rats
ATP-sensitive potassium channels (KATP) protect the myocardium from hypertrophy induced by pressure-overloading. In this study, we determined the effects of these channels in volume-overloading. We compared the effects of a KATP agonist and a KATP antagonist on sarcolemmal transmembrane current dens...
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| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Wiley
2011-01-01
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| Series: | International Journal of Cell Biology |
| Online Access: | http://dx.doi.org/10.1155/2011/838951 |
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| Summary: | ATP-sensitive potassium channels (KATP) protect the myocardium from hypertrophy induced by pressure-overloading. In this study, we determined the effects of these channels in volume-overloading. We compared the effects of a KATP agonist and a KATP antagonist on sarcolemmal transmembrane current density (pA/pF) clamped at 20 mV increments of membrane potential from −80 to +40 mV in ventricular cardiac myocytes. The basal outward potassium pA/pF in myocytes of volume-overloaded animals was significantly smaller than that in the myocytes of sham-operated controls. Treatment of the control myocytes with the KATP agonist cromakalim increased pA/pF significantly. This increase was blocked by the KATP antagonist glibenclamide. Treatment of the hypertrophied myocytes from volume-overloaded animals with cromakalim and in the presence and absence of glibenclamide did not change pA/pF significantly. These findings suggest that eccentrically hypertrophied cardiac myocytes from volume-overloading may be unresponsive to specific activation/inactivation of KATP and that dysfunctional KATP may fail to protect the myocardium from left ventricular hypertrophy associated with volume-overloading. |
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| ISSN: | 1687-8876 1687-8884 |