Ionic and metabolic requirements for decamethonium transport in mouse kidney cortex slices.

Decamethonium accumulates in mouse kidney cortex slices incubated in Krebs-Ringer bicarbonate buffer (37 degrees C, pH 7.4) aerated with O2-CO2 95:5 v/v%. Maximum tissue-medium accumulation ratio decreased with increasing external decamethonium concentration. Decamethonium was released from the tissue at a slow rate. The metabolic inhibitor cyanide inhibited accumulation of decamethonium but did not produce release of decamethonium already accumulated in the tissue. Substitution of external Na+ by other cations depressed decamethonium uptake. However, this cannot be ascribed to absence of Na+ since no inhibition occurred when Na+ was substituted by isoosmotic sucrose. Decamethonium uptake is inhibited when active Na+-transport is impaired (omission of K+ or addition of ouabain). The slow onset of this inhibition is compatible with the idea that it may be secondary to changes in the intracellular electrolyte concentrations. Furthermore, decamethonium uptake was depressed in absence of external Ca2+.