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|Title:||Site-specific regulation of ion transport by prolactin in rat colon epithelium|
ethylene glycol 1,2 bis(2 aminophenyl) ether n,n,n',n' tetraacetic acid
n benzyl 2 cyano 3 (3,4 dihydroxyphenyl)acrylamide
phosphatidylinositol 3 kinase
sodium potassium chloride cotransporter
MAP Kinase Signaling System
Potassium Channel Blockers
Sodium Channel Blockers
|Abstract:||The effect of prolactin (PRL) on ion transport across the rat colon epithelium was investigated using Ussing chamber technique. PRL (1 μg/ml) induced a sustained decrease in short-circuit current (I sc) in the distal colon with an EC 50 value of 100 ng/ml and increased I sc in the proximal colon with an EC 50 value of 49 ng/ml. In the distal colon, the PRL-induced decrease in I sc was not affected by Na + channel blocker amiloride or Cl - channel blockers, NPPB, DPC, or DIDS, added mucosally. However, the response was inhibited by mucosal application of K + channel blockers glibenclamide, quinidine, and chromanol 293B, whereas other K + channel blockers, Ba 2+, tetraethylammonium, clotrimazole, and apamin, failed to have effects. The PRL-induced decrease in I sc was also inhibited by Na +-K +-2Cl - transporter inhibitor bumetanide, Ba 2+, and chromanol 293B applied serosally. In the transverse and proximal colon, the PRL-induced increase in I sc was suppressed by DPC, glibenclamide, and bumetanide, but not by NPPB, DIDS, or amiloride. The PRL-induced changes in I sc in both distal and proximal colon were abolished by JAK2 inhibitor AG490, but not BAPTA-AM, the Ca 2+ chelating agent, or phosphatidylinositol 3-kinase inhibitor wortmannin. These results suggest a segment-specific effect of PRL in rat colon, by activation of K + secretion in the distal colon and activation of Cl - secretion in the transverse and proximal colon. Both PRL actions are mediated by JAK-STAT-dependent pathway, but not phosphatidylinositol 3-kinase pathway or Ca 2+ mobilization. These findings suggest a role of PRL in the regulation of electrolyte transport in mammalian colon. © 2012 the American Physiological Society.|
|Appears in Collections:||Scopus 1983-2021|
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