The mechanism of the halothane-dependent efflux of calcium from rat-liver mitochondria.
The halothane-dependent, calcium-induced loss of respiratory control in rat liver mitochondria [1, 2] is Mg2plus -dependent and is accompanied by an enhanced mitochondrial swelling. It is suggested that this swelling reflects an increase in calcium activity in the matrix space, due to a decrease in binding of the accumulated cation. This change in the partition of intramitochondrial calcium is correlated with an inhibition by halothane of energy-independent, calcium-induced swelling. The enhanced swelling associated with the active accumulation of calcium in the presence of halothane does not lead to a marked increase in permeability to other ions. Nevertheless, under conditions of energised calcium uptake, and in the presence of Mg2plus, a halothane-dependent, ruthenium red-insensitive efflux of calcium is observed. This is consistent with the proposed halothane-dependent increase in the matrix activity of accumulated Ca2plus. It is suggested that this mechanism accounts for the previously postulated [2] futile cycle of calcium uptake and release induced by halothane in rat liver mitochondria.
D000818:Animals; D002118:Calcium / Q000378:metabolism* / Q000494:pharmacology; D006221:Halothane / Q000494:pharmacology*; D006863:Hydrogen-Ion Concentration; D008274:Magnesium / Q000494:pharmacology; D008930:Mitochondria, Liver / Q000187:drug effects / Q000378:metabolism*; D008933:Mitochondrial Swelling / Q000187:drug effects; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D012430:Ruthenium Red / Q000494:pharmacology; D014634:Valinomycin / Q000494:pharmacology
D012430:Ruthenium Red; D014634:Valinomycin; D008274:Magnesium; D011188:Potassium; D002118:Calcium; D006221:Halothane