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The characteristics of mitochondrial Ca 2+ dynamics in single permeabilized ventricular myocytes of rat
Author(s) -
Leem Chae Hun,
Ha Jeong Mi,
Seol Chang Ahn,
Jung Jin Hee,
Koh Eun A,
Youm Jae Boum,
Choe Han,
Jang Yeon Jin
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1181.13
Subject(s) - cytosol , depolarization , mitochondrion , biophysics , membrane potential , chemistry , myocyte , inner mitochondrial membrane , calcium , fura 2 , biochemistry , biology , microbiology and biotechnology , enzyme , organic chemistry
We would like to study the characteristics of the mitochondrial Ca 2+ dynamics in permeabilized rat ventricular myocytes. We monitored NADH, Ca 2+ with Fura‐2‐FF and the mitochondrial membrane potential (ψ m ) with TMRE, simultaneously. We also developed a new correction method for correcting signal interference between NADH and Fura‐2‐FF. The application of 1 μM Ca 2+ without cytosolic Na + could increase intramitochondial Ca 2+ upto 8 μM, which is far less than electrochemical equilibrium. The increase and loading kinetics of Ca 2+ were strongly affected by the cytosolic Ca 2+ concentration itself and completely blocked by RuR. The Ca 2+ efflux from the mitochondria was strongly affected by the cytosolic Na + concentration, suggested the major role of mitochondrial Na + ‐Ca 2+ exchange (mito‐NCX) in the Ca 2+ efflux from the mitocondria. We found the cytosolic K + was an obligatory ion to activate Ca 2+ efflux through mito‐NCX. Cytosolic Cl − did not affect the mitochondrial Ca 2+ dynamics. Cytosolic phosphate in addition to Ca 2+ strongly inhibited Ca 2+ loading and depolarized ψ m . This depolarization was not blocked by CsA or 5‐HD. The increase phosphate with the increase of the cytocolic Ca 2+ probably plays an important role in the degradation of mitochondrial function. This mechanism must be closely related to the post‐ischemic reperfusion injury of the heart. Supported by the grant (No. R01‐2004‐000‐10374‐0) from KOSEF