Insulin stimulated Na" transport is mediated by increase of apical Na' channels and not open probability in control and aldosterone prestimulated A6 EP1thelia

Insulin-sensitive A6 epithelia grown on Transwell tissue-culture treated inserts were studied using a non-invasive Na' channel blocker pulse inhibition method II-'ASEB J. 9:A64,1995) to determine apical membrane single channel current (iNa), channel density (Nr) and open probability (PJ. 2.7 uM aldosterone (N=6) increased amiloride-sensitive short-circuit currents (INa) from 1.51±0.26 (N=5) to 6.20±0.42 liA/cm' due to increase of Nr (I7.6±4.1 to 57.9±7.2 million channels/cm-', respectively). 20 nM insulin caused maximal increases of Na1 transport within 30 min (control, 264%) and 10 min (aldosterone, 198%). In both control and aldosterone stimulated tissues, the increase of Na" transport was due to increase of N, (49.8±10.1 and 168.9± 19.4 million channels/cm', respectively). iNa was decreased slightly ( 10-20%) from control values averaging near 0.38 pA due to expected changes of fractional transcellular resistance. P remained unchanged in control tissues (0.27±0.01) but was decreased in aldosterone stimulated tissues (0.320.02 to 0.23±0.01). We conclude that both insulin and aldosterone stimulate Na transport by increase of N_T. However, the mechanisms are separate and distinct.