The ethanol-induced stimulation of rat duodenal mucosal bicarbonate secretion in vivo is critically dependent on luminal Cl

Autor: Markus Sjöblom, Wan Salman Wan Saudi, Olof Nylander, Anna Sommansson
Rok vydání: 2013
Předmět:
Male
Physiology
Digestive Physiology
lcsh:Medicine
Cystic Fibrosis Transmembrane Conductance Regulator
Stimulation
Nicotinic Antagonists
Receptors
Nicotinic
Antiporters
Rats
Sprague-Dawley
chemistry.chemical_compound
Intestinal mucosa
Integrative Physiology
Medicine and Health Sciences
Intestinal Mucosa
lcsh:Science
Mammals
Multidisciplinary
Systems Biology
Gastrointestinal Motility Disorders
Animal Models
Body Fluids
medicine.anatomical_structure
Sulfate Transporters
Paracellular transport
Vertebrates
Small Intestine
Hexamethonium
Chlorine
Anatomy
Capsazepine
Neurovetenskaper
Research Article
medicine.medical_specialty
Duodenum
Bicarbonate
Anion Transport Proteins
Gastroenterology and Hepatology
Biology
Research and Analysis Methods
Rodents
Gastric Acid
Model Organisms
Internal medicine
medicine
Animals
Digestive Functions
Ethanol
lcsh:R
Neurosciences
Organisms
Veterinary Anatomy
Biology and Life Sciences
Rats
Gastrointestinal Tract
Bicarbonates
Endocrinology
chemistry
Gastric acid
lcsh:Q
Veterinary Science
Hydrochloric Acid
Fluid Physiology
Capsaicin
Physiological Processes
Digestive System
Zdroj: PLoS ONE
PLoS ONE, Vol 9, Iss 7, p e102654 (2014)
ISSN: 1932-6203
Popis: Alcohol may induce metabolic and functional changes in gastrointestinal epithelial cells, contributing to impaired mucosal barrier function. Duodenal mucosal bicarbonate secretion (DBS) is a primary epithelial defense against gastric acid and also has an important function in maintaining the homeostasis of the juxtamucosal microenvironment. The aim in this study was to investigate the effects of the luminal perfusion of moderate concentrations of ethanol in vivo on epithelial DBS, fluid secretion and paracellular permeability. Under thiobarbiturate anesthesia, a similar to 30-mm segment of the proximal duodenum with an intact blood supply was perfused in situ in rats. The effects on DBS, duodenal transepithelial net fluid flux and the blood-to-lumen clearance of Cr-51-EDTA were investigated. Perfusing the duodenum with isotonic solutions of 10% or 15% ethanol-by-volume for 30 min increased DBS in a concentration-dependent manner, while the net fluid flux did not change. Pre-treatment with the CFTR inhibitor CFTRinh172 (i.p. or i.v.) did not change the secretory response to ethanol, while removing Cl- from the luminal perfusate abolished the ethanol-induced increase in DBS. The administration of hexamethonium (i.v.) but not capsazepine significantly reduced the basal net fluid flux and the ethanol-induced increase in DBS. Perfusing the duodenum with a combination of 1.0 mM HCl and 15% ethanol induced significantly greater increases in DBS than 15% ethanol or 1.0 mM HCl alone but did not influence fluid flux. Our data demonstrate that ethanol induces increases in DBS through a mechanism that is critically dependent on luminal Cl- and partly dependent on enteric neural pathways involving nicotinic receptors. Ethanol and HCl appears to stimulate DBS via the activation of different bicarbonate transporting mechanisms.
Databáze: OpenAIRE
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