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Am J Physiol Renal Physiol (September 2, 2003). doi:10.1152/ajprenal.00103.2003
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Submitted on March 13, 2003
Accepted on August 26, 2003

ATP-Sensitive K+ Channels in Renal Mitochondria

Douglas V. Cancherini1, Leonardo G. Trabuco1, Nancy A. Reboucas1, and Alicia J. Kowaltowski2*

1 Departamento de Fisiologia e Biofisica, Instituto de Ciencias Biomedicas, Universidade de Sao Paulo, Sao Paulo, SP, Brazil
2 Departamento de Bioquimica, Instituto de Quimica, Universidade de Sao Paulo, Sao Paulo, SP, Brazil

* To whom correspondence should be addressed. E-mail: alicia{at}iq.usp.br.

Isolated kidney mitochondria swell when incubated in hyposmotic solutions containing K+ salts in a manner inhibited by ATP, ADP, 5-hydroxydecanoate and glibenclamide, and stimulated by GTP and diazoxide. These results suggest the existence of ATP-sensitive K+ channels in these mitochondria, similar to those previously described in heart, liver and brain. Renal mitochondrial ATP-sensitive K+ uptake rates are approximately 140 nmol . min-1 . (mg protein)-1. This K+ transport results in a slight increase in respiration and decrease in the inner membrane potential. In addition, the activation of ATP-inhibited K+ uptake using diazoxide leads to a decrease of ATP hydrolysis through the reverse activity of the FOF1 ATP synthase when respiration is inhibited. In conclusion, we characterize an ATP-sensitive K+ transport pathway in kidney mitochondria which affects volume, respiration and membrane potential, and may have a role in the prevention of mitochondrial ATP hydrolysis.




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