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Modulation of electrogenic transport processes in the porcine proximal colon by enteric neurotransmitters

The aim of our study was to evaluate the involvement of essential pro‐ and antisecretory neurotransmitters in regulation of secretion in porcine proximal colon. Choline acetyltransferase (ChAT), nitric oxide synthase (NOS), vasoactive intestinal peptide (VIP), substance P (SP), somatostatin (SOM) an...

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Published in:Journal of animal physiology and animal nutrition 2012-06, Vol.96 (3), p.482-493
Main Authors: Pfannkuche, H, Mauksch, A, Gäbel, G
Format: Article
Language:English
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Summary:The aim of our study was to evaluate the involvement of essential pro‐ and antisecretory neurotransmitters in regulation of secretion in porcine proximal colon. Choline acetyltransferase (ChAT), nitric oxide synthase (NOS), vasoactive intestinal peptide (VIP), substance P (SP), somatostatin (SOM) and neuropeptide Y (NPY) were located immunohistochemically in the epithelium and subepithelial layer. Modulation of epithelial secretion was studied in Ussing chambers. Application of carbachol (CA), sodium nitroprussid (SNP), VIP and SP but not of NPY or SOM resulted in a chloride dependent increase in short circuit current (Isc). Isc increase induced by CA, VIP or SNP was not altered by preincubation with tetrodotoxin or indomethacin. In contrast, SP‐induced Isc increase was diminished by preincubation with tetrodotoxin, indomethacin, l‐nitro‐arginin‐methyl‐ester, and atropine but not hexamethonium. Simultaneous application of CA and VIP, or CA and SNP increased the Isc stronger as expected. Applying SP/CA led to a smaller increase in Isc as calculated. It is concluded that mainly prosecretory neurotransmitters are involved in regulation of colonic secretion. Cross‐potentiations of acetylcholine and nitric oxide and acetylcholine and VIP suggest activation of different intracellular cascades. Similar intracellular pathways may be stimulated by acetylcholine and SP, thus preventing an additive effect of the transmitters.
ISSN:0931-2439
1439-0396
DOI:10.1111/j.1439-0396.2011.01168.x