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ATP-sensitive K+ channels in renal mitochondria
Douglas V Cancherini1, Leonardo G Trabuco, Nancy A Rebouças
1Departamento de Fisiologia e Biofísica, Instituto de Ciências Biomédicas, Instituto de Química, Universidade de São Paulo, Av. Prof. Lineu Prestes 748, Cidade Universitária, 05508-900 São Paulo, Brazil.
American Journal of Physiology. Renal Physiology
|September 4, 2003
Summary
Kidney mitochondria possess ATP-sensitive potassium (K+) channels that regulate mitochondrial volume and respiration. These channels, inhibited by ATP, may prevent mitochondrial ATP hydrolysis.
Area of Science:
- Mitochondrial Physiology
- Ion Transport
- Renal Cell Biology
Background:
- Mitochondria play crucial roles in cellular energy metabolism and homeostasis.
- ATP-sensitive potassium (K+) channels are known to exist in mitochondria of various tissues, including heart, liver, and brain.
Purpose of the Study:
- To investigate the presence and function of ATP-sensitive K+ channels in isolated kidney mitochondria.
- To characterize the physiological effects of K+ transport on mitochondrial function.
Main Methods:
- Incubation of isolated kidney mitochondria in hyposmotic solutions containing K+ salts.
- Assessment of mitochondrial swelling, respiration, inner membrane potential, and ATP hydrolysis.
- Pharmacological manipulation using ATP, ADP, 5-hydroxydecanoate, glibenclamide, GTP, and diazoxide.
Main Results:
- Kidney mitochondria exhibit swelling in response to K+ salts, inhibited by ATP and stimulated by GTP and diazoxide, suggesting ATP-sensitive K+ channels.
- Renal mitochondrial ATP-sensitive K+ uptake rates were measured at approximately 140 nmol/min/mg protein.
- K+ transport led to a slight increase in respiration, a decrease in inner membrane potential, and reduced ATP hydrolysis via F0F1 ATP synthase.
Conclusions:
- An ATP-sensitive K+ transport pathway exists in kidney mitochondria.
- This pathway influences mitochondrial volume, respiration, and membrane potential.
- The identified pathway may play a protective role against mitochondrial ATP hydrolysis.