1. Aldosterone- and adrenaline-induced K+ secretion were investigated in rat late distal colon using conductance scanning and Ussing chamber techniques. K+ secretion was unmasked by the K+ channel blocker tetraethylammonium (TEA). Electrogenic Na+ absorption was inhibited by amiloride. Rb+ net fluxes consistently measured about 80% of K+ secretion estimated using change in short-circuit current (delta ISC) measurements. 2. Partial block of K+ absorption by mucosal ouabain did not change TEA-sensitive K+ secretion. Thus, K+ absorption and K+ secretion are not coupled. 3. Additivity of Rb+ fluxes as well as delta ISC caused by 3 nM aldosterone (6 h in vitro incubation) and, subsequently, adrenaline suggested additivity of aldosterone-induced and cAMP-mediated K+ secretion in the presence of amiloride. 4. Conductance scanning under control conditions revealed a small TEA-sensitive K+ conductivity in surface epithelium (0.3 +/- 0.2 mS cm-2) but not in crypts, as well as a small basal K+ secretion in surface epithelium (delta ISC = 0.3 mumol h-1 cm-2), which increased during sham incubation. 5. Aldosterone (3 nM, 6 h in vitro incubation) resulted, after correction for the basal K+ secretion, in a K+ secretion of delta ISC = 0.9 mumol h-1 cm-2. Aldosterone induced a TEA-sensitive conductivity of 1.1 +/- 0.3 mS cm-2 in surface epithelium, but not in crypts. 6. Adrenaline (5 microM) caused, in fresh tissue, a K+ secretion of delta ISC = 1.2 mumol h-1 cm-2 and equal conductivity changes in crypts (0.7 +/- 0.2 mS cm-2) and surface epithelium (0.7 +/- 0.1 mS cm-2). 7. We conclude that K+ secretion induced by aldosterone in physiological concentration is restricted to surface epithelium, whereas cAMP-mediated K+ secretion is located equally in crypts and surface epithelium.