had much larger currents when the animals were fed a low-sodium diet or infused with aldosterone. Collectively, the data indicated that mineralocorticoid regulation of ENaC was maintained, even potentiated in the mouse model of Liddle’s syndrome. 21 In the colon, 22 aldosterone responsiveness of the ENaC in colon was also increased but may differ from that of the kidney in 2 aspects: ex vivo measurements of colonic tissues show a very significant increase in baseline currents, unlike the ex vivo cortical collecting duct patched tubules. Dysregulation of ENaC in colon may thus also have an impact on sodium balance. This may be pathophysiologically relevant in patients with Liddle’s syndrome, in particular on a high-salt diet, when suppression of plasma aldosterone is likely to be insufficient to reduce sodium absorption to an appropriate level both in kidney and colon.