Near-instantaneous current-voltage relationships and shot-noise analysis of amiloride-induced current fluctuations were used to estimate apical membrane permeability to Na (P_Na), intraepithelial Na activity (Na_c), single-channel Na currents (i) and the number of open (conducting) apical Na channels (N₀), in the urinary bladder of the toad (Bufo marinus). To facilitate voltageclamping of the apical membrane, the serosal plasma membranes were depolarized by substitution of a high KCl (85mm) sucrose (50mm) medium for the conventional Na-Ringer's solution on the serosal side. Aldosterone (5×10⁻⁷m, serosal side only) elicited proportionate increases in the Na-specific current (I_Na and inP_Na, with no significant change in the dependence ofP_Na on mucosal Na (Na_o).P_Na and the control ofP_Na by aldosterone were substrate-dependent: In substrate-depleted bladders, pretreatment with aldosterone markedly augmented the response to pyruvate (7.5×10⁻³m) which evoked coordinate and equivalent increases inI_Na andP_Na. The aldosterone-dependent increase inP_Na was a result of an equivalent increase in the area density of conducting apical Na channels. The computed single-channel current did not change. We propose that, following aldosterone-induced protein synthesis, there is a reversible metabolically-dependent recruitment of preexisting Na channels from a reservoir of electrically undetectable channels. The results do not exclude the possibility of a complementary induction of Na-channel synthesis.

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