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Am J Physiol Heart Circ Physiol (December 2, 2004). doi:10.1152/ajpheart.00589.2004
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Submitted on June 15, 2004
Accepted on November 18, 2004

Mitochondrial Membrane Potential Modulates Ragulation of Mitochondrial Ca2+ in Skinned Rat Ventricular Myocytes

Masao Saotome1, Hideki Katoh1*, Hiroshi Satoh1, Shiro Nagasaka1, Shu Yoshihara1, Hajime Terada1, and Hideharu Hayashi1

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 ({Delta}{Psi}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 {Delta}{Psi}m When {Delta}{Psi}m was partially depolarized by FCCP (0.01 - 0.1 µM), there were dose-dependent decreases in [Ca2+]m. When the complete {Delta}{Psi}m 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 {Delta}{Psi}mdissipation by FCCP accelerated calcein leakage from mitochondria in a cyclosporin A (CsA)-sensitive manner, indicating that the {Delta}{Psi}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 {Delta}{Psi}m and 7.6 mM in the {Delta}{Psi}m dissipation. We conclude that 1) the mitochondrial Ca2+ uniporter accumulates Ca2+ {Delta}{Psi}m dependently at the physiological range of [Ca2+]c, 2) the {Delta}{Psi}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 {Delta}{Psi}m, dissipation.




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