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Expression of iNOS mRNA associated with suppression of colonic contraction in rat colitis

S Lundberg1, M Holst, P M Hellström

  • 1Department of Medicine, Unit of Gastroenterology and Hepatology, Karolinska University Hospital Solna, Karolinska Institutet, Stockholm, Sweden. Sofie.Lundberg@ki.se

Acta Physiologica (Oxford, England)
|July 27, 2006
PubMed
Abstract

Insights

In experimental colitis, increased inducible nitric oxide synthase (iNOS) expression in the colon leads to reduced contractility. Blocking this enzyme with L-NAME restored normal colonic function, highlighting iNOS

Area of Science:

  • Gastroenterology
  • Physiology
  • Molecular Biology

Background:

  • Inflammatory bowel disease (IBD) is characterized by increased nitric oxide (NO) synthesis and inducible NO synthase (NOS) expression in the colon, correlating with diminished contractility.
  • The specific NOS subtype activated during experimental colitis remains to be fully elucidated.

Purpose of the Study:

  • To investigate the specific subtype of NOS activated in experimental colitis.
  • To determine the role of induced NO in colonic motor dysfunction during inflammation.

Main Methods:

  • Experimental colitis was induced in rats using Escherichia coli endotoxin.
  • Reverse transcriptase-polymerase chain reaction (RT-PCR) was employed to compare NOS subtype expression in normal and inflamed colonic tissues.
  • Isometric contractile responses to acetylcholine (ACh) were assessed in isolated colonic tissues, with and without NOS inhibition (L-NAME) or NO donation.

Main Results:

  • Colonic inflammation significantly reduced contractility and maximal response to ACh.
  • Pre-treatment with the NOS inhibitor L-NAME reversed the decreased contractility and normalized responses to ACh.
  • RT-PCR analysis revealed the presence of inducible NOS (iNOS) mRNA exclusively in endotoxin-treated rats.

Conclusions:

  • Inducible NOS (iNOS) expression is upregulated in inflamed colonic tissue during experimental colitis.
  • The overproduction of NO by iNOS is implicated in the reduced colonic motility observed in colitis.
  • NO appears to exert a suppressive effect on colonic contractility, which can be reversed by inhibiting iNOS.

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