Abstract:
:Relevant Ca(2+) pools and fluxes in H9c2 cells have been studied using fluorescent indicators and Ca(2+)-mobilizing agents. Vasopressin produced a cytoplasmic Ca(2+) peak with half-maximal effective concentration of 6 nM, whereas thapsigargin-induced Ca(2+) increase showed half-maximal effect at 3 nM. Depolarization of the mitochondrial inner membrane by protonophore was also associated with an increase in cytoplasmic Ca(2+). Ionomycin induced a small and sustained depolarization, while thapsigargin had a small but transient effect. The thapsigargin-sensitive Ca(2+) pool was also sensitive to ionomycin, whereas the protonophore-sensitive Ca(2+) pool was not. The vasopressin-induced cytoplasmic Ca(2+) signal, which caused a reversible discharge of the sarco-endoplasmic reticulum Ca(2+) pool, was sensed as a mitochondrial Ca(2+) peak but was unaffected by the permeability transition pore inhibitor cyclosporin A. The mitochondrial Ca(2+) peak was affected by cyclosporin A when the Ca(2+) signal was induced by irreversible discharge of the intracellular Ca(2+) pool, i.e., adding thapsigargin. These observations indicate that the mitochondria interpret the cytoplasmic Ca(2+) signals generated in the reticular store.
journal_name
J Bioenerg Biomembrjournal_title
Journal of bioenergetics and biomembranesauthors
Lax A,Soler F,Fernández-Belda Fdoi
10.1007/s10863-005-6635-zkeywords:
subject
Has Abstractpub_date
2005-08-01 00:00:00pages
249-59issue
4eissn
0145-479Xissn
1573-6881journal_volume
37pub_type
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journal_title:Journal of bioenergetics and biomembranes
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journal_title:Journal of bioenergetics and biomembranes
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