Please use this identifier to cite or link to this item: http://ir.swu.ac.th/jspui/handle/123456789/14340
Title: Site-specific regulation of ion transport by prolactin in rat colon epithelium
Authors: Deachapunya C.
Poonyachoti S.
Krishnamra N.
Keywords: amiloride
apamin
bumetanide
carbachol
chromanol 293B
clotrimazole
ethylene glycol 1,2 bis(2 aminophenyl) ether n,n,n',n' tetraacetic acid
glibenclamide
isobutylmethylxanthine
n benzyl 2 cyano 3 (3,4 dihydroxyphenyl)acrylamide
phosphatidylinositol 3 kinase
prolactin
quinidine
sodium potassium chloride cotransporter
tetrylammonium
wortmannin
animal experiment
animal tissue
article
ascending colon
calcium mobilization
colon mucosa
concentration response
controlled study
descending colon
electrolyte transport
electrophysiology
ion transport
male
nonhuman
priority journal
rat
signal transduction
sodium absorption
transverse colon
Animals
Chloride Channels
Chlorides
Colon
Enzyme Inhibitors
Intestinal Mucosa
Ion Transport
Male
MAP Kinase Signaling System
Potassium
Potassium Channel Blockers
Prolactin
Rats
Rats, Wistar
Sodium Channel Blockers
Tyrphostins
Issue Date: 2012
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.
URI: https://www.scopus.com/inward/record.uri?eid=2-s2.0-84861141161&doi=10.1152%2fajpgi.00143.2011&partnerID=40&md5=d81c03736704ab3359dde25464f821d6
http://ir.swu.ac.th/jspui/handle/123456789/14340
ISSN: 1931857
Appears in Collections:Scopus 1983-2021

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