© 1999 by European Society of Cardiology
Copyright © 1999, European Society of Cardiology
The mitochondrial permeability transition and the calcium, oxygen and pH paradoxes: one paradox after another
Department of Cell Biology and Anatomy, University of North Carolina at Chapel Hill, Room 236, Taylor Hall, Chapel Hill, NC 27599-7090, USA
* Tel.: +1-919-966-5507; fax: +1-919-966-1856 lemaster@med.unc.edu
accepted 13 October 1999
| The first 150 words of the full text of this article appear below. |
See article by Ban et al. [3] (pages 556–567) in this issue.
In the calcium paradox, Ca2+-free incubation produces Na+ loading of cardiac myocytes largely mediated by Na+ influx via L-type Ca2+ channels. Subsequent exposure to normal extracellular Ca2+ activates sarcolemmal Na+/Ca2+ exchange operating in the reverse mode. As a consequence, cytosolic free Ca2+ rapidly increases causing an abrupt and apparently irreversible contracture of the myocytes [1]. The calcium paradox has many parallels to the oxygen paradox of anoxia/reoxygenation and ischemia/reperfusion injuries where Na+ loading occurs during anoxia/ischemia, which is followed by Ca2+ overload and irreversible contracture after reoxygenation/reperfusion [2].
The interesting and provocative paper by Ban et al. in this issue of Cardiovascular Research [3] addresses mitochondrial changes occurring during the calcium paradox. After Ca2+ repletion following a Ca2+-free incubation, mitochondria of isolated guinea pig cardiac myocytes depolarized completely after a delay of 60–90
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