Steroid hormone-dependent expression of blockersensitive ENaCs in apical membranes of A6 epithelia

Weak channel blocker-induced noise analysis wasused to determine the way in which the steroids aldosterone andcorticosterone stimulated apical membraneNa⁺ entry into the cells oftissue-cultured A6 epithelia. Among groups of tissues grown on avariety of substrates, in a variety of growth media, and with cells atpassages 73-112, the steroidsstimulated both amiloride-sensitive and amiloride-insensitiveNa⁺ transport as measured byshort-circuit currents in chambers perfused with either growth mediumor a Ringer solution. From baseline rates of blocker-sensitiveshort-circuit current between 2 and 7 µA/cm², transport was stimulatedabout threefold in all groups of experiments. Single channel currentsaveraged near 0.3 pA (growth medium) and 0.5 pA (Ringer) and weredecreased 6-20% from controls by steroid due to the expecteddecreases of fractional transcellular resistance. Irrespective ofbaseline transport rates, the steroids in all groups of tissuesstimulated transport by increase of the density of blocker-sensitiveepithelial Na⁺ channels (ENaCs).Channel open probability was the same in control and stimulatedtissues, averaging ~0.3 in all groups of tissues. Accordingly,steroid-mediated increases of open channel density responsible forstimulation of Na⁺ transport aredue to increases of the apical membrane pool of functional channels andnot their open probability.