Subcellular heterogeneity in mitochondrial red-ox responses to KATP channel agonists in freshly isolated rabbit cardiomyocytes

@article{Ojeda2004SubcellularHI,
  title={Subcellular heterogeneity in mitochondrial red-ox responses to KATP channel agonists in freshly isolated rabbit cardiomyocytes},
  author={C. Ojeda and P. Joseph and V. Saks and V. Piriou and Y. Tourneur},
  journal={Molecular and Cellular Biochemistry},
  year={2004},
  volume={256-257},
  pages={367-377}
}
We have used the technique of fluorescent microscopy imaging supplemented with the refined analysis of temporal cartography of the cell fluorescence to investigate the mechanisms of regulation of mitochondrial function and its red-ox state in cardiac cells in vivo. Autofluorescence of flavoproteins of the respiratory chain in the isolated rabbit cardiomyocytes was registered before and after application of mitochondrial KATP channel opener diazoxide (100 and 400 μM). Diazoxide addition resulted… Expand
1 Citations
Non-beating HL-1 cells for confocal microscopy: application to mitochondrial functions during cardiac preconditioning.
TLDR
Cardiac pharmacological preconditioning by K(ATP) channel openers might involve other routes than mitochondrial K channels targeting, and no mitochondrial depolarization could be detected when the membrane potential was measured by using very low light photomultiplier and confocal fluorescence imaging under the K(ATOR) channel opener diazoxide. Expand

References

SHOWING 1-10 OF 50 REFERENCES
Do Modulators of the Mitochondrial KATP Channel Change the Function of Mitochondria in Situ?*
TLDR
At a cardioprotective dose, the main functional effect of diazoxide depends on respiratory substrates and seems not to be related to KATP channel activity. Expand
Mitochondrial ATP-dependent potassium channels: novel effectors of cardioprotection?
TLDR
The results demonstrate that diazoxide targets mitochondrial but not sarcolemmal KATP channels and imply that mitochondrial KatP channels may mediate the protection from KATp channel openers. Expand
Fluctuations in mitochondrial membrane potential caused by repetitive gating of the permeability transition pore.
TLDR
It is suggested that under conditions of prolonged oxidative stress and/or cellular Ca(2+) overload, short openings of MTP might serve as an emergency mechanism allowing the partial dissipation of DeltaPsi(m), the fast release of accumulated Ca( 2+) ions and the decreased generation of endogenous oxygen radicals. Expand
Regulation of mitochondrial respiration in heart cells analyzed by reaction-diffusion model of energy transfer.
TLDR
The model shows that workload-dependent alteration of ADP concentration in the compartmentalized creatine kinase system may be taken, together with the changes in P(i) concentration, to be among the major components of the metabolic feedback signal for regulation of respiration in muscle cells. Expand
Effects of cardiac work on electrical potential gradient across mitochondrial membrane in perfused rat hearts.
TLDR
Both NADH-generating reactions and the ATP synthase-catalyzed reaction are important in causing the increase in respiration that accompanies increased work, which indicates that the myocardium responds to alterations in cardiac work by changing its rate of O2 consumption. Expand
Imaging the permeability pore transition in single mitochondria.
TLDR
It is concluded that the spontaneous depolarizations were caused by repeated stochastic openings and closings of the transition pore, demonstrating a much more dynamic regulation of membrane permeability at the level of a single organelle than predicted from ensemble behavior of mitochondrial populations. Expand
Metabolic compartmentation and substrate channelling in muscle cells
TLDR
It is proposed that in muscle cells feed-back signal between contraction and mitochondrial respiration may be conducted by metabolic wave (propagation of oscillations of local concentration of ADP and creatine) through cytoplasmic equilibrium creatine and adenylate kinases and is amplified by coupled creatine kinase reaction in mitochondria. Expand
Modulation of mitochondrial ATP-dependent K+ channels by protein kinase C.
TLDR
Potentiation of mitoKATP channel opening by PKC provides a direct mechanistic link between the signal transduction of ischemic preconditioning and pharmacological cardioprotection targeted at ATP-dependent K+ channels. Expand
Functional complexes of mitochondria with Ca,MgATPases of myofibrils and sarcoplasmic reticulum in muscle cells.
TLDR
It is concluded that in oxidative muscle cells mitochondria behave as if they were incorporated into functional complexes with adjacent ADP producing systems - with the MgATPases in myofibrils and Ca,MgAtPases of sarcoplasmic reticulum. Expand
Mitochondrial ATP-sensitive K+ channels modulate cardiac mitochondrial function.
TLDR
In isolated cardiac mitochondria, KATP channel openers depolarized the membrane, accelerated respiration, slowed ATP production, released accumulated Ca2+, produced swelling, and stimulated efflux of intermembrane proteins. Expand
...
1
2
3
4
5
...