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Reversal of mitochondrial Na/Ca exchange during metabolic inhibition in rat cardiomyocytes
Author(s) -
Griffiths Elinor J
Publication year - 1999
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(99)00726-7
Subject(s) - uniporter , mitochondrion , biophysics , chemistry , myocyte , ruthenium red , calcium , membrane potential , sodium calcium exchanger , ion transporter , efflux , biochemistry , hypoxia (environmental) , cytosol , microbiology and biotechnology , biology , oxygen , enzyme , membrane , intracellular , organic chemistry
During hypoxia of isolated cardiomyocytes, Ca 2+ entry into mitochondria may occur via the Na/Ca exchanger, the normal efflux pathway, and not the Ca‐uniporter, the normal influx route. If this is the case, then depletion of myocyte Na + should inhibit Ca 2+ uptake, and collapse of the mitochondrial membrane potential (Δψ m ) would inhibit the uniporter. To test these hypotheses, isolated rat myocytes were exposed to metabolic inhibition, to mimic hypoxia, and [Ca 2+ ] m and [Ca 2+ ] c determined by selective loading of indo‐1 into these compartments. Δψ m was determined using rhodamine 123. Following metabolic inhibition, [Ca 2+ ] m was significantly lower in Na‐depleted cells than controls ( P <0.001), [Ca 2+ ] c was approximately the same in both groups, and mitochondria depolarised completely. Thus Na‐depletion inhibited mitochondrial Ca 2+ uptake, suggesting that Ca 2+ entry occurred via Na/Ca exchange, and the collapse of Δψ m during metabolic inhibition is consistent with inactivity of the Ca‐uniporter.