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Oxidant stress inhibits Na-Ca-exchange current in cardiac myocytes: mediation by sulfhydryl groups?

Oxidant stress inhibits Na-Ca-exchange current in cardiac myocytes: mediation by sulfhydryl groups? in cardiac AND DAVID J. HEARSE St. Thomas’ Hospital, FREE OXYGEN RADICALS and/or oxidative stress cause cellular injury that is thought, in part at least, to be mediated by increased cytosolic Ca2+ levels (18). Disturbances of a variety of mechanisms that normally maintain intracellular Ca2+ homeostasis occur during oxidant stress. For example, hypochlorous acid causes an increase of cytosolic Ca2+ concentration (Ca2+), a change that is independent of extracellular Ca2+ concentration ([Ca”+],> and can be abolished by pretreatment with caffeine (lZ>, suggesting that oxidant stress modifies the activity of internal Ca2+ stores. An increased Ca2+ permeability, as a consequence of oxidant stress, also occurs in mitochondria and sarcoplasmic reticular vesicles (30). Furthermore, a depressed Ca2+ uptake and an inhibition of sarcoplasmic reticular Ca2+-adenosine triphosphatase activity occurs under conditions of oxidant stress (22). Oxidant stress therefore not only promotes the release, but also impairs Ca2+-uptake mechanisms into internal stores with a consequent increased cytosolic Ca2+ levels. Sarcolemmal ion translocation pathways are known to be influenced by oxidant stress. Specific membrane channels in the sarcolemma that are known to be inhibited include the calcium current, sodium current, delayed rectifier, inward rectifier and Na+ -K+-pump current (3,5,6,25,33,35). Sarcolemmal Ca2+-extruding pathways are http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Heart and Circulatory Physiology The American Physiological Society

Oxidant stress inhibits Na-Ca-exchange current in cardiac myocytes: mediation by sulfhydryl groups?

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Publisher
The American Physiological Society
Copyright
Copyright © 1994 the American Physiological Society
ISSN
0363-6135
eISSN
1522-1539
Publisher site
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Abstract

in cardiac AND DAVID J. HEARSE St. Thomas’ Hospital, FREE OXYGEN RADICALS and/or oxidative stress cause cellular injury that is thought, in part at least, to be mediated by increased cytosolic Ca2+ levels (18). Disturbances of a variety of mechanisms that normally maintain intracellular Ca2+ homeostasis occur during oxidant stress. For example, hypochlorous acid causes an increase of cytosolic Ca2+ concentration (Ca2+), a change that is independent of extracellular Ca2+ concentration ([Ca”+],> and can be abolished by pretreatment with caffeine (lZ>, suggesting that oxidant stress modifies the activity of internal Ca2+ stores. An increased Ca2+ permeability, as a consequence of oxidant stress, also occurs in mitochondria and sarcoplasmic reticular vesicles (30). Furthermore, a depressed Ca2+ uptake and an inhibition of sarcoplasmic reticular Ca2+-adenosine triphosphatase activity occurs under conditions of oxidant stress (22). Oxidant stress therefore not only promotes the release, but also impairs Ca2+-uptake mechanisms into internal stores with a consequent increased cytosolic Ca2+ levels. Sarcolemmal ion translocation pathways are known to be influenced by oxidant stress. Specific membrane channels in the sarcolemma that are known to be inhibited include the calcium current, sodium current, delayed rectifier, inward rectifier and Na+ -K+-pump current (3,5,6,25,33,35). Sarcolemmal Ca2+-extruding pathways are

Journal

AJP - Heart and Circulatory Physiology – The American Physiological Society

Published: Mar 1, 1994

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