Relationship of transient electrical properties to active sodium transport by toad urinary bladder

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Abstract
Application of voltage pulses of 10 mV for periods of 9 sec across toad urinary bladder elicits a rapid deflection in transepithelial current. Frequently, the current decays back towards its baseline value during the course of the polarizing pulse. This transient phenomenon can be induced, or its magnitude increased, by raising the mucosal or serosal Na+ concentration. The transient can be abolished by sufficiently hyperpolarizing the tissue (rendering serosa positive to mucosa), by inhibiting transcellular Na+ transport with amiloride or ouabain, and by increasing the serosal K+ concentration. Vasopressin increases net Na+ movement across toad bladder but does not elicit these transients. It is proposed as a working hypothesis for further study that the transient behavior characterized in this study reflects: (1) the partition of Na+ between the apical plasma membrane and contiguous fluid layers, (2) the partition of K+ between the basolateral plasma membrane and adjacent submucosal fluid layer, and (3) the negative feedback interaction between intracellular Na+ activity and Na+ permeability of the apical plasma membrane of the transporting cells.