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Osmoregulation in rat duodenum is dependent on nicotinic acetylcholine receptors
Author(s) -
Sedin John,
Nylander Olof
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1065.4
Subject(s) - hexamethonium , duodenum , endocrinology , medicine , chemistry , motility , acetylcholine , mecamylamine , nicotinic agonist , secretion , receptor , biology , microbiology and biotechnology
We have recently shown that the responsiveness of the duodenum to luminal hypertonicity is markedly enhanced in COX‐2 inhibited rats. Compared to control rats, COX‐2 inhibited ones respond to perfusion with 700 mosmol/kg NaCl with an increase in mucosal permeability, a greater fluid secretion, inhibition of duodenal motility and a better capability to adjust luminal osmolality. The aim of this study was to elucidate whether the hypertonicity‐induced changes of duodenal functions are affected by hexamethonium (HM) and mecamylamine (M), two known nicotinic acetylcholine receptor (nAChR) antagonists, in COX‐2 inhibited rats. The proximal duodenum of anesthetized rats were perfused in situ for 60 min with 700 mosmol/kg NaCl and the effects on mucosal permeability, fluid secretion, motility, luminal fluid osmolality and arterial blood pressure (MAP) studied in the absence and presence of intravenous HM (10 mg/kg, h) or luminal M [10 −4 M]. Results HM and M significantly attenuated the hypertonicity‐induced increase in permeability, fluid secretion and the capability to decrease luminal osmolality. Both HM and M decreased duodenal motility but only HM decreased MAP. Conclusions The capability of the duodenum to adjust luminal hypertonicity depends on enteric neural activity involving nAChR. Uppsala University.

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