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ATP-sensitive K⁺ channels in renal mitochondria

¹Departamento de Fisiologia e Biofísica, Instituto de Ciências Biomédicas, and ²Departamento de Bioquímica, Instituto de Química, Universidade de São Paulo, 05508-900 São Paulo, Brazil

Submitted 13 March 2003 ; accepted in final form 26 August 2003

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 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 F₀F₁ ATP synthase when respiration is inhibited. In conclusion, we characterize an ATP-sensitive K⁺ transport pathway in kidney mitochondria that affects volume, respiration, and membrane potential and may have a role in the prevention of mitochondrial ATP hydrolysis.

kidney mitochondria; K⁺ transport; ischemic preconditioning; uncoupling

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