1. Potassium secretion by the distal colon before and during intravenous infusion of a potassium load was measured in vivo in groups of rats treated in various ways: A, normal control; B, adrenalectomized; C, sodium depleted; D, on potassium-rich diet for 7 days; E, after 72 h aldosterone (1 microgram/h); F, after 72 h aldosterone (10 micrograms/h). 2. Potassium infusion produced no increase of secretion in the adrenalectomized rats but in all the other groups it increased by 2- to 3-fold. Secretion during infusion correlated well with the basal (pre-infusion) rate and in groups C and D reached 140 +/- 15 and 173 +/- 17 nmol min-1 cm-1 respectively compared with 28 +/- 6 nmol min-1 cm-1 in the controls (A). The passive paracellular pathway for potassium was unaffected by the infusion. Amiloride (100 mumol/l) did not significantly affect potassium secretion rate either before or during the acute potassium infusion. The potassium channel blocker, tetraethylammonium chloride, reduced both basal and the secretion rate during infusion. 3. Transepithelial potential difference (PD), active sodium absorption and sodium fluxes were similar in normal controls and rats fed the potassium-rich diet. However, the PD was partially amiloride sensitive in the latter group although amiloride insensitive in the normal group. In sodium-depleted rats, the PD was elevated and totally amiloride insensitive. 4. In both aldosterone-treated groups (E and F), basal potassium secretion rate was high and similar, and during potassium infusion rose 3-fold to 114 +/- 24 (E) and 105 +/- 5 (F) nmol min-1 cm-1. However, the PD was not elevated significantly in group E and was only partially amiloride sensitive, whereas in those infused at the higher rate (F) the PD was increased and was totally amiloride sensitive. 5. The high potassium secretion rates developed by this epithelium in sodium-restricted and potassium-enriched dietary states appear to depend on the presence of an amiloride-insensitive transcellular potassium pathway which is induced at a lower level of aldosterone stimulation than is the amiloride-sensitive transcellular sodium pathway.