Distal colonic K+ excretion is determined by the balance of K+ absorption and K+ secretion by the enterocytes. This presentation addresses the current knowledge of the cellular mechanism for colonic K+ secretion, with focus on the luminal secretory K+ channel. Several recent observations highlight the unique role of the large conductance, Ca2+-activated KCa1.1 (BK, KCNMA) channel as the functionally relevant luminal K+ efflux pathway in mouse distal colonic crypts. This conclusion is based on functional studies in BK channel α-subunit knock-out mice. Several relevant issues will be presented: 1. BK channels mediate the resting distal colonic K+ secretion, 2. they are acutely stimulated by luminal nucleotide receptor activation and an intracellular Ca2+ increase, 3. BK channels are up-regulated by aldosterone, 4. Also the cAMP-stimulated distal colonic K+ secretion is mediated via BK channels, 5. and finally aldosterone was found to specifically up-regulate the ZERO (e.g. cAMP activated) C-terminal splice variant of the BK channel. We propose the BK channel as the sole exit pathway for transcellular K+ secretion in mammalian distal colon, which is the target for short term intracellular Ca2+ and cAMP activation and long term aldosterone regulation.