Summary. Urea transport across amphibian membranes is influenced by interactionswith the membrane, the solvent and other solutes. One case of solute interaction, that in which the two species are chemically identical, is investigated here. Because of the effects of hypertonic urea on permeability, the demonstration of interaction required consideration of the ratio r of bidirectional tracer permeabilities. Mucosal-to-serosal (M ~ S) and serosal-to-mucosal (M ~ S) tracer urea fluxes were determined in paired toad urinary bladders, in the absence and presence of abundant urea. In the control state, r was 1.0. Addition of 0.3 M urea to M increased r, and to S decreased r. These results indicate coupling of abundant and tracer urea flows (isotope interaction), probably occurring in specialized regions. The effects persisted after the addition of antidiuretic hormone, despite the opposing influence of osmotic water flow. Quantitatively different effects of mucosal and serosal hypertonicity, both with and without antidiuretic hormone, are explicable in terms of heterogeneous parallel and series permeability barriers.Because of the importance of urea in the renal concentrating system, the mechanism of its transport is of considerable interest. Amphibian epithelia are useful model systems for the study of this process and have directed attention to three types of interactions.First, interaction of urea or its congeners with the membrane, evaluated by tracer permeability in the frog skin and toad bladder, has allowed speculation as to the mechanism of permeation [2,15,17,19]. Second, interaction with water (solvent drag) has been cited as evidence that these compounds share a common pathway with water [2,17]. A third type of interaction, that of urea with other solute particles, has been observed in the frog skin and toad skin [3,10,12,22,23].

Experiments were carried out in rats and isolated turtle bladders to study the defect in H+ transport induced by LiCl. After 3-4 days of intraperitoneal LiCl, rats developed urinary findings of "distal" renal tubular acidosis. Proximal tubular fluid pH measured in situ by glass microelectrodes was higher in lithium-treated rats than in acidotic controls. Proximal fluid total CO2 [tCO2] was also higher, and the fraction of tCO2 leaving the proximal tubule was 14 vs. 7% (P less than 0.001). Impaired acidification was also apparent beyond distal convoluted tubules, as judged by normal distal tCO2 reabsorption but increased HCO3(-) in the urine. During NaHCO3 loading, the proximal defect was ameliorated but not the distal. Turtle bladder studies showed that mucosal lithium inhibits H+ secretion secondary to reducing transepithelial electrical potential, presumably by hyperpolarization of the luminal membrane. A similar mechanism may be responsible for lithium's effect on the distal nephron. Inhibition of proximal tubular HCO3(-) reabsorption is probably not attributable to electrical potential changes but might be due to interference of luminal membrane Na+ entry by Li+ and reduced (Na+ + Li+)-H+ exchange.

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