Paper Information

Title: 

H2S AS AN IMPORTANT MOTILITY INHIBITOR IN MICE SMALL INTESTINE

Type: POSTER
Author(s): RAHMATI R.*
 
 *DEPT. OF PHYSIOLOGY AND PHARMACOLOGY, GOLESTAN UNIVERSITY OF MEDICAL SCIENCES
 
Name of Seminar: IRANIAN CONGRESS OF PHYSIOLOGY AND PHARMACOLOGY
Type of Seminar:  CONGRESS
Sponsor:  PHYSIOLOGY AND PHARMACOLOGY SOCIETY, MASHHAD UNIVERSITY OF MEDICAL SCIENCE
Date:  2007Volume 18
 
 
Abstract: 

Introduction: Although the physiology and pharmacology of gaseous neurotransmitters such as NO have been extensively studied over many years, the biological and pharmacological activity of another biologically active gas, H2S, in various parts of the body is not entirely clear. The main aim was to examine the effects of NaHS (i.e. sodium hydrogen sulphide, as H2S donor) on contractions of the small intestine of mice.
Methods: Experiments were performed on mice intestine and contractile activity was recorded from in vitro segments of jejunum 4-5cm in length. Furthermore, using vanilloid receptor 1 deficient mice (VR 1- /-) we tested hypothesis that extrinsic sensory nerves mediated alterations in contractile responses in the presence of H2S.
Results: Serosal application of NaHS produced a dose-dependent inhibition of motor activity that are not significantly different between VR 1- /- and VR 1 + /+ mice (n=5, p>0.05). The effects of NaHS were not affected by L-NAME a competitive inhibitor of NO synthase (100μM) and PPADS as a P2 antagonist (P>0.05). In the presence of TTX (1μM) NaHS (300µM) caused a reduction in basal tone (19.5%, p<0.05 n=5) and inhibited the contraction evoked by 30µM bethanechol by 55% (n=4, p<0.05).
Conclusion: These results demonstrate that H2S is an important motility inhibitor in mice intestine and suggest that the VR1 receptor, NO and ATP were not involved in the inhibitory effect of H2S on motility and a direct action on smooth muscle can be involved in this regard. This finding may be relevant to intestinal function in health and disease, particularly with regard to mucosa damage and altered H2S production seen in conditions such as inflammatory bowel disease.

 
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