Mechanism of aldosterone-induced increase of K+ conductance in early distal renal tubule cells of the frog

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Abstract
Isolated early distal tubule cells (EDC) of frog kidney were incubated for 20–28 hr in the presence of aldosterone and then whole-cell K+ currents were measured at constant intracellular pH by the whole-cell voltage-clamp technique. Aldosterone increased barium-inhibitable whole-cell K+ conductance (gK+) threefold. This effect was reduced by amiloride and totally abolished by ouabain. However, aldosterone could still raisegK+ in ouabain-treated cells in the presence of furosemide. We tested whether changes in intracellular pH (pH i ) could be a signal for cells to regulategK+. After removal of aldosterone, the increase ingK+ was preserved by subsequent incubation for 8 hr at pH 7.6 but abolished at pH 6.6. In the complete absence of aldosterone, incubation of cells at pH 8.0 for 20–28 hr raised pH i and doubledgK+. Using the patch-clamp technique, three types of K+-selective channels were identified, which had conductances of 24, 45 and 59 pS. Aldosterone had no effect on the conductance or open probability (P o) of any of the three types of channels. However, the incidence of observing type II channels was increased from 4 to 22%. Type II channels were also found to be pH sensitive,P o was increased by raising pH. These results indicate that prolonged aldosterone treatment raises pH i and increasesgK+ by promoting insertion of K+ channels into the cell membrane. Channel insertion is itself triggered by raising both pH i and increasing the activity of the Na+/K+ pump in early distal cells of frog kidney.