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Received October 24, 2005
Accepted on February 6, 2006

BASIC SCIENCE: Cell and Transport Physiology

Distal Colonic K⁺ Secretion Occurs via BK Channels

Matthias Sausbier ^*, Joana E. Matos , Ulrike Sausbier ^*, Golo Beranek ^*, Claudia Arntz ^*, Winfried Neuhuber , Peter Ruth ^*, and Jens Leipziger ¹

*Pharmakologie und Toxikologie, Pharmazeutisches Institut, Universität Tübingen, Tübingen, Germany; Institute of Physiology and Biophysics, The Water and Salt Research Center, University of Aarhus, Aarhus C, Denmark; and Anatomisches Institut, Universität Erlangen-Nürnberg, Erlangen, Germany

¹ To whom correspondence should be addressed. E-mail: leip{at}fi.au.dk.

	Abstract

K+ secretion in the kidney and distal colon is a main determinant of K+ homeostasis. This study investigated the identity of the relevant luminal secretory K+ ion channel in distal colon. An Ussing chamber was used to measure ion transport in the recently generated BK channel-deficient (BK-/-) mice. BK-/- mice display a significant colonic epithelial phenotype with (1) lack of Ba²⁺-sensitive resting K+ secretion, (2) absence of K+ secretion stimulated by luminal P2Y₂ and P2Y₄ receptors, (3) absence of luminal Ca²⁺ ionophore (A23187)-stimulated K+ secretion, (4) reduced K+ and increased Na+ contents in feces, and (5) an increased colonic Na+ absorption. In contrast, resting and uridine triphosphate (UTP)-stimulated K+ secretion was not altered in mice that were deficient for the intermediate conductance Ca²⁺-activated K+ channel SK4. BK channels localize to the luminal membrane of crypt, and reverse transcription-PCR results confirm the expression of the BK channel -subunit in isolated distal colonic crypts. It is concluded that BK channels are the responsible K+ channels for resting and stimulated Ca²⁺-activated K+ secretion in mouse distal colon.

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