STEROID HORMONE-DEPENDENT EXPRESSION OF BLOCKER-SENSITIVE ENACS IN APICAL MEMBRANES OF A6 EPITHELIA

Weak channel blocker-induced noise analysis was used to determine the way in which the steroids aldosterone and corticosterone stimulated ap ical membrane Na+ entry into the cells of tissue-cultured A6 epithelia . Among groups of tissues grown on a variety of substrates, in a varie ty of growth media, and with cells at passages 73-112, the steroids st imulated both amiloride-sensitive and amiloride-insensitive Naf transp ort as measured by short-circuit currents in chambers perfused with ei ther growth medium or a Ringer solution. From baseline rates of blocke r-sensitive short-circuit current between 2 and 7 mu A/cm(2), transpor t was stimulated about threefold in all groups of experiments. Single channel currents averaged near 0.3 pA (growth medium) and 0.5 pA (Ring er) and were decreased 6-20% from controls by steroid due to the expec ted decreases of fractional transcellular resistance. Irrespective of baseline transport rates, the steroids in all groups of tissues stimul ated transport by increase of the density of blocker-sensitive epithel ial Na+ channels (ENaCs). Channel open probability was the same in con trol and stimulated tissues, averaging similar to 0.3 in all groups of tissues. Accordingly, steroid-mediated increases of open channel dens ity responsible for stimulation of Na+ transport are due to increases of the apical membrane pool of functional channels and not their open probability.