Abstract
SUMMARY: 1. The effects of metabolic inhibitors and ionic changes on the short-circuit current across the toad's bladder have been studied both in the presence and absence of vasopressin. 2. The effects of metabolic inhibitors indicate that the energy for short-circuit current is derived from both glycolysis and oxidative metabolism. 3. Divalent ions play an important part in the maintenance of the resting short-circuit current and of its response to vasopressin. Ca++ or Sr++ are necessary for the former and Ca++ for the latter. 4. Increased concentration of Ca++, Sr++, Mg++ or Ba++ did not inhibit the increment in short-circuit current produced by vasopressin, in contrast to the effect of these ions on water transport. 5. Increase and decrease in potassium concentration inhibited the short-circuit current whether vasopressin was present or not. 6. The correct concentration of sodium on the serosal side of the bladder was necessary to maintain the short-circuit current, but the increment seen when vasopressin was added was not affected by 50% substitution of choline for sodium.