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Implications of Tachykinins and Calcitonin Gene-Related Peptide in Inflammatory Bowel Disease

Holzer P.

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Department of Experimental and Clinical Pharmacology, University of Graz, Austria

Corresponding Author

Dr. Peter Holzer

Department of Experimental and Clinical Pharmacology

University of Graz, Universitätsplatz 4

A–8010 Graz (Austria)

Tel. +43 (316) 380 4500, Fax +43 (316) 380 9645, E-Mail peter.holzer@kfunigraz.ac.at

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Digestion 1998;59:269–283

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Calcitonin gene-related peptide (CGRP) and the preprotachykinin A gene-derived peptides substance P (SP) and neurokinin A (NKA) are expressed in extrinsic primary afferent nerve fibres and intrinsic enteric neurons of the gut. The actions of tachykinins on the digestive effector systems are mediated by three different types of tachykinin receptor, termed NK1, NK2 and NK3 receptors, while the gastro-intestinal actions of CGRP are brought about by CGRP1 and possibly other CGRP receptors. These neuropeptide transmitters are expressed by enteric neurons, intestinal muscle, epithelium and vascular system in a cell-specific manner and enable SP, NKA and CGRP to influence motility, electrolyte and fluid secretion, vascular and immune functions in a peptide- and region-specific fashion. Inflammatory disorders of various aetiology involve changes in the peptidergic innervation of the gut, and inflammatory bowel disease is associated with NK1 receptor upregulation in intestinal blood vessels and lymphoid structures. Some of these alterations are reproduced in experimental models of gastro-intestinal disease, and there is mounting evidence that an imbalanced function of peptidergic neurons contributes to motor, secretory, vascular and immunological disturbances in intestinal anaphylaxis, infection and inflammation. In a therapeutic perspective it seems conceivable that tachykinin and CGRP receptors antagonists can be employed as spasmolytic, antidiarrhoeal, anti-inflammatory and antinociceptive drugs.

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Abstract of Review

Published online: August 03, 1998
Issue release date: July – August

Number of Print Pages: 15
Number of Figures: 0
Number of Tables: 0

ISSN: 0012-2823 (Print)
eISSN: 1421-9867 (Online)

For additional information: http://www.karger.com/DIG

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