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Am J Physiol Heart Circ Physiol (March 11, 2005). doi:10.1152/ajpheart.01296.2004
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Submitted on December 23, 2004
Accepted on March 10, 2005

K+ Dependent Regulation of Matrix Volume Improves Mitochondrial Function Under Conditions Mimicking Ischemia-Reperfusion

Paavo Korge1*, Henry M Honda1, and James N Weiss1

1 Medicine (Cardiology) and Physiology, School of Medicine at UCLA, Los Angeles, CA, USA

* To whom correspondence should be addressed. E-mail: PKorge{at}mednet.ucla.edu.

To delineate the role of mitochondrial K+ fluxes in cardioprotection, we investigated the effect of extramitochondrial K+ on the ability of mitochondria to support membrane potential ({Delta}{Psi}), regulate matrix volume, consume oxygen and phosphorylate ADP under conditions mimicking key elements of ischemia/reperfusion. Isolated energized mitochondria responded to ADP addition with depolarization, increased O2 consumption and matrix shrinkage. The time required for full recovery of {Delta}{Psi}, signaling the completion of ADP phosphorylation, was used to evaluate the rate of ATP synthesis during repeated ADP pulses. In mitochondria with decreased ability to support {Delta}{Psi}, the rate of ADP phosphorylation was significantly improved by extramitochondrial K+ > Na+ > Li+, especially at higher buffer osmolarity which promotes matrix shrinkage. K+-induced improvement in {Delta}{Psi} recovery after ADP pulses was accompanied by more rapid and complete matrix volume recovery and enhanced O2 consumption. Manipulations expected to affect matrix swelling by regulating K+ fluxes or water distribution indicate that matrix volume regulation by external factors becomes increasingly important in mitochondria with decreased ability to support {Delta}{Psi} in the face of a high ADP load. Under these conditions, opening of K+ influx pathways improved mitochondrial function and delayed failure. This may be an important factor in the mechanism of diaxozide-induced cardioprotection.




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