Prolactin stimulates K+ secretion in isolated rat distal colon

The effect of prolactin (PRL) on ion transport across the rat colonic epithelium was investigated using the Ussing chamber technique. PRL induced a sustained decrease in basal short circuit current (Isc) by 5–35% depending on the colonic segment: a maximum response in the distal colon and less in the proximal colon. In the distal colon, PRL decreased Isc in a concentration dependent manner with an IC 50 value of 140 ng/ml. The PRL‐induced decrease in Isc was not affected in the presence of Na + channel blocker amiloride, but showed higher response in the presence of Cl − channel blocker NPPB or glibenclamide added to the apical solution. In contrast, the PRL response was inhibited in the presence of Na + ‐K + ‐2Cl − transporter inhibitor bumetanide or K + channel blocker BaCl 2 , but not other K + channel blocker apamin, clotrimazole or 293B added serosally. Among K + channel blockers, only 293B added apically partially diminished the PRL response. In addition, the carbachol or forskolin‐activated Cl − secretion remained unchanged in the presence of PRL. Thus in the rat distal colon, PRL stimulates K + secretion through barium‐sensitive basolateral K + channel and bumetanide‐sensitive pathway, with no effect on Na + or Cl − transport. This work was supported by The Srinakharinwirot University Research Grant (325/2552).