| First Author | Sausbier M | Year | 2006 |
| Journal | J Am Soc Nephrol | Volume | 17 |
| Issue | 5 | Pages | 1275-82 |
| PubMed ID | 16571783 | Mgi Jnum | J:135743 |
| Mgi Id | MGI:3794391 | Doi | 10.1681/ASN.2005101111 |
| Citation | Sausbier M, et al. (2006) Distal colonic K(+) secretion occurs via BK channels. J Am Soc Nephrol 17(5):1275-82 |
| abstractText | 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 Ba(2+)-sensitive resting K(+) secretion, (2) absence of K(+) secretion stimulated by luminal P2Y(2) and P2Y(4) receptors, (3) absence of luminal Ca(2+) 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 Ca(2+)-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 alpha-subunit in isolated distal colonic crypts. It is concluded that BK channels are the responsible K(+) channels for resting and stimulated Ca(2+)-activated K(+) secretion in mouse distal colon. |
