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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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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author | Zikiar V. Alvin Richard M. Millis Wissam Hajj-Mousssa Georges E. Haddad |
author_facet | Zikiar V. Alvin Richard M. Millis Wissam Hajj-Mousssa Georges E. Haddad |
author_sort | Zikiar V. Alvin |
collection | DOAJ |
description | 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. |
format | Article |
id | doaj-art-f84229c3185a4839ad43a0d9ce2c3773 |
institution | Kabale University |
issn | 1687-8876 1687-8884 |
language | English |
publishDate | 2011-01-01 |
publisher | Wiley |
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series | International Journal of Cell Biology |
spelling | doaj-art-f84229c3185a4839ad43a0d9ce2c37732025-02-03T05:46:14ZengWileyInternational Journal of Cell Biology1687-88761687-88842011-01-01201110.1155/2011/838951838951ATP-Sensitive Potassium Channel Currents in Eccentrically Hypertrophied Cardiac Myocytes of Volume-Overloaded RatsZikiar V. Alvin0Richard M. Millis1Wissam Hajj-Mousssa2Georges E. Haddad3Department of Physiology & Biophysics, College of Medicine, Howard University, Washington, DC 20059, USADepartment of Physiology & Biophysics, College of Medicine, Howard University, Washington, DC 20059, USADepartment of Physiology & Biophysics, College of Medicine, Howard University, Washington, DC 20059, USADepartment of Physiology & Biophysics, College of Medicine, Howard University, Washington, DC 20059, USAATP-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.http://dx.doi.org/10.1155/2011/838951 |
spellingShingle | Zikiar V. Alvin Richard M. Millis Wissam Hajj-Mousssa Georges E. Haddad ATP-Sensitive Potassium Channel Currents in Eccentrically Hypertrophied Cardiac Myocytes of Volume-Overloaded Rats International Journal of Cell Biology |
title | ATP-Sensitive Potassium Channel Currents in Eccentrically Hypertrophied Cardiac Myocytes of Volume-Overloaded Rats |
title_full | ATP-Sensitive Potassium Channel Currents in Eccentrically Hypertrophied Cardiac Myocytes of Volume-Overloaded Rats |
title_fullStr | ATP-Sensitive Potassium Channel Currents in Eccentrically Hypertrophied Cardiac Myocytes of Volume-Overloaded Rats |
title_full_unstemmed | ATP-Sensitive Potassium Channel Currents in Eccentrically Hypertrophied Cardiac Myocytes of Volume-Overloaded Rats |
title_short | ATP-Sensitive Potassium Channel Currents in Eccentrically Hypertrophied Cardiac Myocytes of Volume-Overloaded Rats |
title_sort | atp sensitive potassium channel currents in eccentrically hypertrophied cardiac myocytes of volume overloaded rats |
url | http://dx.doi.org/10.1155/2011/838951 |
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