{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T04:41:54Z","timestamp":1791175314794,"version":"4.1.0"},"reference-count":50,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Gastrointestinal and Liver Physiology"],"published-print":{"date-parts":[[2009,7]]},"abstract":"<jats:p>High-conductance apical K<jats:sup>+<\/jats:sup>(BK) channels are present in surface colonocytes of mammalian (including human) colon. Their location makes them well fitted to contribute to the excessive intestinal K<jats:sup>+<\/jats:sup>losses often associated with infective diarrhea. Since many channel proteins are regulated by phosphorylation, we evaluated the roles of protein kinase A (PKA) and phosphatases in the modulation of apical BK channel activity in surface colonocytes from rat distal colon using patch-clamp techniques, having first increased channel abundance by chronic dietary K<jats:sup>+<\/jats:sup>enrichment. We found that PKA activation using 50 \u03bcmol\/l forskolin and 5 mmol\/l 3-isobutyl-1-methylxanthine stimulated BK channels in cell-attached patches and the catalytic subunit of PKA (200 U\/ml) had a similar effect in excised inside-out patches. The antidiarrheal peptide somatostatin (SOM; 2 \u03bcmol\/l) had a G protein-dependent inhibitory effect on BK channels in cell-attached patches, which was unaffected by pretreatment with 10 \u03bcmol\/l okadaic acid (an inhibitor of protein phosphatase type 1 and type 2A) but completely prevented by pretreatment with 100 \u03bcmol\/l Na<jats:sup>+<\/jats:sup>orthovanadate and 10 \u03bcmol\/l BpV (inhibitors of phosphoprotein tyrosine phosphatase). SOM also inhibited apical BK channels in surface colonocytes in human distal colon. We conclude that cAMP-dependent PKA activates apical BK channels and may enhance colonic K<jats:sup>+<\/jats:sup>losses in some cases of secretory diarrhea. SOM inhibits apical BK channels through a phosphoprotein tyrosine phosphatase-dependent mechanism, which could form the basis of new antidiarrheal strategies.<\/jats:p>","DOI":"10.1152\/ajpgi.00132.2009","type":"journal-article","created":{"date-parts":[[2009,5,1]],"date-time":"2009-05-01T01:59:41Z","timestamp":1241143181000},"page":"G159-G167","source":"Crossref","is-referenced-by-count":30,"title":["Regulation of colonic apical potassium (BK) channels by cAMP and somatostatin"],"prefix":"10.1152","volume":"297","author":[{"given":"M. D.","family":"Perry","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"G. 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