Friederich-Persson 2013 Abstract MiP2013: Difference between revisions
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{{Abstract | {{Abstract | ||
|title=Friederich-Persson M, Hansell P, Wilcox CS, Palm F(2013) Potassium controls rat mitochondria function | |title=Friederich-Persson M, Hansell P, Wilcox CS, Palm F(2013) Potassium controls rat mitochondria function: ''In vivo'' and ''in vitro'' considerations. Mitochondr Physiol Network 18.08. | ||
|authors=Friederich-Persson M, Hansell P, Wilcox CS, Palm F | |authors=Friederich-Persson M, Hansell P, Wilcox CS, Palm F | ||
|year=2013 | |year=2013 | ||
|event=MiP2013 | |event=MiP2013 | ||
|abstract= | |abstract=The intracellular potassium concentration, [K+], varies depending on tissue type and is about 60 mM in kidney proximal tubular cells whereas it is approximately 120 mM in cardiac myocytes. Intracellular [K+] may therefore affect mitochondria function. | ||
Β | |||
By measuring the respiratory function and swelling of mitochondria isolated from kidney cortex and heart at [K+] ranging from 15 mM to 146 mM we showed that [K+] controls mitochondria function in the heart. Increasing [K+] resulted in increased resting state respiration and decreased respiratory control ratio (RCR) in kidney cortex mitochondria. The reduced RCR corresponded with mitochondria swelling, indicating failing mitochondria. The effects of K+ in kidney mitochondria was prevented by inhibitors of ATP-sensitive K+-channels and voltage-gated K+-channels (glibenclamide and by 4-aminopyridine, respectively). On the contrary, RCR in heart mitochondria increased with increasing [K+] and was unaffected by K+channel inhibitors. | |||
Β | |||
These results demonstrate [K+] control of mitochondria function in rat kidney and heart. | |||
Β | |||
|mipnetlab=SE Uppsala Liss P | |||
}} | |||
{{Labeling | |||
|instruments=Oxygraph-2k | |||
|tissues=Kidney | |||
|preparations=Isolated Mitochondria | |||
}} | }} | ||
__TOC__ | __TOC__ | ||
Revision as of 19:45, 13 July 2013
Friederich-Persson M, Hansell P, Wilcox CS, Palm F(2013) Potassium controls rat mitochondria function: In vivo and in vitro considerations. Mitochondr Physiol Network 18.08. |
Link:
Friederich-Persson M, Hansell P, Wilcox CS, Palm F (2013)
Event: MiP2013
The intracellular potassium concentration, [K+], varies depending on tissue type and is about 60 mM in kidney proximal tubular cells whereas it is approximately 120 mM in cardiac myocytes. Intracellular [K+] may therefore affect mitochondria function.
By measuring the respiratory function and swelling of mitochondria isolated from kidney cortex and heart at [K+] ranging from 15 mM to 146 mM we showed that [K+] controls mitochondria function in the heart. Increasing [K+] resulted in increased resting state respiration and decreased respiratory control ratio (RCR) in kidney cortex mitochondria. The reduced RCR corresponded with mitochondria swelling, indicating failing mitochondria. The effects of K+ in kidney mitochondria was prevented by inhibitors of ATP-sensitive K+-channels and voltage-gated K+-channels (glibenclamide and by 4-aminopyridine, respectively). On the contrary, RCR in heart mitochondria increased with increasing [K+] and was unaffected by K+channel inhibitors.
These results demonstrate [K+] control of mitochondria function in rat kidney and heart.
β’ O2k-Network Lab: SE Uppsala Liss P
Labels:
Tissue;cell: Kidney Preparation: Isolated Mitochondria"Isolated Mitochondria" is not in the list (Intact organism, Intact organ, Permeabilized cells, Permeabilized tissue, Homogenate, Isolated mitochondria, SMP, Chloroplasts, Enzyme, Oxidase;biochemical oxidation, ...) of allowed values for the "Preparation" property.
HRR: Oxygraph-2k
Affiliations and author contributions
1 - Dept of Medical Cell Biology, Uppsala University, Sweden
2 - Dept of Medicine, Division of Hypertension and Nephrology, Georgetown University Medical Center, Washington DC, USA;
3 - Dept of Medical and Health Sciences, LinkΓΆping University, Sweden;
4 - Center for Medical Image Science and Visualization, LinkΓΆping University, Sweden.
Email: [email protected]