The essential role of luminal BK channels in distal colonic K+ secretion

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    Distal colonic K+ excretion is determined by the balance of K+ absorption and K+ secretion by the enterocytes. This presentation summarizes the current knowledge of the cellular mechanism for colonic K+ secretion, with focus on the luminal secretory K+ channel. Several recent observations highlight a pivotal role of the large conductance, Ca2+-activated KCa1.1 (BK, KCNM) channel as the functionally relevant luminal K+ efflux pathway in mouse distal colon (1, 2). This conclusion was based on clear cut results from BK 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 regulated by aldosterone, 4. the cAMP-stimulated distal colonic K+ secretion is apparently 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. In summary we suggest that the sole exit pathway for transcellular K+ secretion in mammalian distal colon is the BK channel, which is the target for short term intracellular Ca2+ and cAMP activation and long term aldosterone regulation.


    Literature Cited

       1.   Sausbier M, Matos JE, Sausbier U, Beranek G, Arntz C et al. 2006. Distal Colonic K+ Secretion Occurs via BK Channels J Am Soc Nephrol 17:1275-82

       2.   Sorensen MV, Matos JE, Sausbier M, Sausbier U, Ruth P et al. 2008. Aldosterone increases KCa1.1 (BK)-channel-mediated colonic K+ secretion J Physiol 586:4251-64


    Periode31 jul. 2009
    Begivenhedstitel11th International Symposium on Exocrine Secretion
    PlaceringTokoshima, JapanVis på kort