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Central nervous α1-adrenoceptor stimulation induces duodenal luminal release of melatonin
Uppsala University, Medicinska vetenskapsområdet, Faculty of Medicine, Department of Neuroscience, Physiology.
Manuscript (Other academic)
URN: urn:nbn:se:uu:diva-90656OAI: oai:DiVA.org:uu-90656DiVA: diva2:163097
Available from: 2003-09-09 Created: 2003-09-09 Last updated: 2010-01-13Bibliographically approved
In thesis
1. The Duodenal Mucosal Bicarbonate Secretion: Role of Melatonin in Neurohumoral Control and Cellular Signaling
Open this publication in new window or tab >>The Duodenal Mucosal Bicarbonate Secretion: Role of Melatonin in Neurohumoral Control and Cellular Signaling
2003 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

The duodenal lumen is exposed to aggressive factors with a high potential to cause damage to the mucosa. Bicarbonate secretion by the duodenal mucosa is accepted as the primary important defense mechanism against the hydrochloric acid intermittently expelled from the stomach.

The present thesis concerns the influence of the central nervous system and the effects of the hormone melatonin on bicarbonate secretion in anesthetized rats in vivo. Effects of melatonin on intracellular calcium signaling by duodenal enterocyte in vitro were examined in tissues of both human and rat origin. The main findings were as follows:

Melatonin is a potent stimulant of duodenal mucosal bicarbonate secretion and also seems to be involved in the acid-induced stimulation of the secretion. Stimulation elicited in the central nervous system by the α1-adrenoceptor agonist phenylephrine induced release of melatonin from the intestinal mucosa and a four-fold increase in alkaline secretion. The melatonin antagonist luzindole abolished the duodenal secretory response to administered melatonin and to central nervous phenylephrine but did not influence the release of intestinal melatonin. Central nervous stimulation was also abolished by synchronous ligation of the vagal trunks and the sympathetic chains at the sub-laryngeal level.

Melatonin induced release of calcium from intracellular stores and also influx of extracellular calcium in isolated duodenal enterocytes. Enterocytes in clusters functioned as a syncytium.

Overnight fasting rapidly and profoundly down-regulated the responses to the duodenal secretagogues orexin-A and bethanechol but not those to melatonin or vasoactive intestinal polypeptide.

In conclusion, the results strongly suggest that intestinal melatonin plays an important role in central nervous elicited stimulation of duodenal mucosal bicarbonate secretion. Sensitivity of this alkaline secretion to some peripheral stimulators markedly depends on the feeding status.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2003. 71 p.
Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 0282-7476 ; 1277
Physiology, alkaline secretion, central nervous system, duodenal enterocyte, duodenal ulcer, duodenum, enterochromaffin cell, human, intraarterial, intracellular calcium, intracerebroventricular, melatonin, rat, vagal nerve, Fysiologi
National Category
urn:nbn:se:uu:diva-3521 (URN)91-554-5688-X (ISBN)
Public defence
2003-10-03, B42, BMC, Uppsala, 09:15
Available from: 2003-09-09 Created: 2003-09-09Bibliographically approved

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