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1 Internal Medicine III, Hamamatsu University School of Medicine, Hamamatsu, Japan
* To whom correspondence should be addressed. E-mail: hkatoh{at}hama-med.ac.jp.
Although recent studies focused on the contribution of mitochondrial Ca2+ for the mechanisms of ischemia/reperfusion injury, the regulation of mitochondrial Ca2+ under the pathophysiological condition remains largely unclear. By using saponin-permeabilized rat myocytes, we measured mitochondrial membrane potential (A
m) and mitochondrial Ca2+ concentration ([Ca2+]m) at the physiological range of cytosolic Ca2+ concentration ([Ca2+]c= 300 nM), and investigated the regulation of [Ca2+]m both in the normal and dissipated Am When 
m was partially depolarized by FCCP (0.01 - 0.1 µM), there were dose-dependent decreases in [Ca2+]m. When the complete Am dissipation was achieved by FCCP (0.3 - 1 µM), [Ca2+]m remained at the half of control level, in spite of no Ca2+ influx via the Ca2+ uniporter. The Amdissipation by FCCP accelerated calcein leakage from mitochondria in a cyclosporin A (CsA)-sensitive manner, indicating that the m dissipation opened mitochondrial permeability transition pore (mPTP). While the inhibition of mPTP by CsA caused further [Ca2+]m reduction after FCCP, the inhibition of mitochondrial Na+/Ca2+ exchange (mitoNCX) by a Na+-free solution abolished the [Ca2+]m reduction after FCCP. The cytosolic Na+ concentrations, which give a half-maximal activity of mitoNCX, were 3.6 mM in the normal m and 7.6 mM in the m dissipation. We conclude that 1) the mitochondrial Ca2+ uniporter accumulates Ca2+ m dependently at the physiological range of [Ca2+]c, 2) the m dissipation opens mPTP, resulting in a Ca2+ influx into mitochondria, 3) although the activity of mitoNCX is impaired, mitoNCX extrudes Ca2+ from matrix even after the m, dissipation.
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