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Calcium-sensing receptor abrogates secretagogue- induced increases in intestinal net fluid secretion by enhancing

John Geibel1, Kumudesh Sritharan, Rainer Geibel

  • 1Department of Cellular and Molecular Physiology, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06520, USA. john.geibel@yale.edu

Proceedings of the National Academy of Sciences of the United States of America
|June 9, 2006
PubMed

Insights

The calcium-sensing receptor (CaSR) in the colon regulates intestinal fluid transport by degrading cyclic nucleotides. CaSR activation reverses fluid secretion caused by toxins, suggesting potential therapies for secretory diarrheas.

Area of Science:

  • Gastroenterology
  • Cell Biology
  • Physiology

Background:

  • The calcium-sensing receptor (CaSR) detects extracellular solute changes in various cells.
  • CaSR's function in the intestinal tract, particularly its response to solute variations, is largely unexplored.

Purpose of the Study:

  • To investigate the role of CaSR signaling in colonic epithelial cells.
  • To determine CaSR's effect on intestinal fluid and electrolyte transport.
  • To explore potential therapeutic applications of CaSR agonists for secretory diarrheas.

Main Methods:

  • Investigated CaSR signaling pathways in colonic cells.
  • Assessed the impact of CaSR activation on cyclic nucleotide levels.
  • Examined the effects of CaSR agonists on fluid secretion induced by cholera toxin and E. coli STa.

Main Results:

  • Colonic CaSR signaling promotes cyclic nucleotide degradation via phosphodiesterases.
  • CaSR activation counteracts the fluid and electrolyte secretion stimulated by cAMP- and cGMP-generating agents.
  • A small-molecule CaSR agonist reversed fluid secretion induced by cholera toxin and STa.

Conclusions:

  • CaSR plays a key role in regulating intestinal fluid transport by modulating secretagogue actions.
  • CaSR activation offers a potential therapeutic strategy for managing secretory diarrheas.

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