Publication:
Site-specific regulation of ion transport by prolactin in rat colon epithelium

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Issued Date

2012

Resource Type

Article

File Type

application/pdf

ISSN

1931857

DOI

10.1152/ajpgi.00143.2011

Other identifier(s)

2-s2.0-84861141161

Rights Holder(s)

Scopus

Bibliographic Citation

American Journal of Physiology - Gastrointestinal and Liver Physiology. Vol 302, No.10 (2012), p.G1199-G1206

Suggested Citation

Deachapunya C., Poonyachoti S., Krishnamra N. Site-specific regulation of ion transport by prolactin in rat colon epithelium. American Journal of Physiology - Gastrointestinal and Liver Physiology. Vol 302, No.10 (2012), p.G1199-G1206. doi:10.1152/ajpgi.00143.2011 Retrieved from: https://hdl.handle.net/20.500.14740/7059

Title

Site-specific regulation of ion transport by prolactin in rat colon epithelium

Author(s)

Deachapunya C.
 Poonyachoti S.
 Krishnamra N.

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.

Subject(s)

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

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URI

https://hdl.handle.net/20.500.14740/7059

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Scopus: Year 1983-2021

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