The redox state of pyridine nucleotides controls permeability of uncoupled mitochondria to K+

The results suggest that a latent pathway for K+-permeability is present in the membrane, that it can be opened and closed reversibly, and that it reflects, either directly or indirectly, the redox status of mitochondrial pyridine nucleotides.

Abstract

Heart mitochondria respiring in the presence of Pi release endogenous K+ to a sucrose medium when an uncoupler is added. The uncoupled mitochondria retain K+, however, if the oxidation of NAD(P)H is prevented by the addition of rotenone or antimycin. Addition of rotenone, once the uncoupler-dependent K+-efflux has been initiated, results in a rapid reduction of NAD(P) and a simultaneous decrease in permeability to K+. These changes are independent of respiration. The results suggest that a latent pathway for K+-permeability is present in the membrane, that it can be opened and closed reversibly, and that it reflects, either directly or indirectly, the redox status of mitochondrial pyridine nucleotides. The possible relationship of this putative pathway to those available for Ca2+ uptake and release is considered.