Urea movement across the toad bladder was measured with [14C]urea and by determining the amount of water flow obligated to urea movement along a urea concentration gradient from mucosa to serosa. This “urea-linked volume flux” was measured gravimetrically. Both the urea-linked volume flux and the [14C]urea transport were stimulated by vasopressin and reversibly inhibited by 0.1 mM amiloride by about 50%. Amiloride had no effect on vasopressin-stimulated osmotic water flux across the bladder wall. Calculations on the amount of water obligated to urea movement indicate that the mucosal urea solution becomes concentrated during its passage through the bladder wall in the presenlce of vasopressin. This concentrating effect of the permeability barrier is less pronounced in the presence of amiloride. It is postulated that amiloride blocks specific urea channels in the rate-limiting barrier, channels which are capable of selectively enhancing urea movement and retarding water flow. Since amiloride is also a well-known inhibitor of sodium transport in this tissue, the present study raises the question as to whether amiloride acts on two different sets of channels or blocks only one which is shared by both sodium and urea.