Aldosterone control of the density of sodium channels in the toad urinary bladder.

Near-instantaneous current-voltage relationships and shot-noise analysis of amiloride-induced current fluctuations were used to estimate apical membrane permeability to Na (PNa), intraepithelial Na activity (Nac), 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 voltage-clamping of the apical membrane, the serosal plasma membranes were depolarized by substitution of a high KCl (85 mM) sucrose (50 mM) medium for the conventional Na-Ringer's solution on the serosal side. Aldosterone (5 X 10(-7) M, serosal side only) elicited proportionate increases in the Na-specific current (INa and in PNa, with no significant change in the dependence of PNa on mucosal Na (Nao). PNa and the control of PNa by aldosterone were substrate-dependent: In substrate-depleted bladders, pretreatment with aldosterone markedly augmented the response to pyruvate (7.5 X 10(-3) M) which evoked coordinate and equivalent increases in INa and PNa. The aldosterone-dependent increase in PNa 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.