Friederich-Persson 2013 Abstract MiP2013: Difference between revisions

From Bioblast
No edit summary
No edit summary
Line 1: Line 1:
{{Abstract
{{Abstract
|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.
|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=Text
|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
}}
}}
{{Labeling}}
__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]

Cookies help us deliver our services. By using our services, you agree to our use of cookies.