ArticleThe Journal of physiology2003
Ethanol induces fluid hypersecretion from guinea-pig pancreatic duct cells.
Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 48 citations in OpenAlex.
- Review
- TDP-43 regulates early-phase insulin secretion via CaV1.2-mediated exocytosis in islets.The Journal of clinical investigation · 2019Article
- Ca2+ toxicity and mitochondrial damage in acute pancreatitis: translational overview.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2016Review
- CFTR: A New Horizon in the Pathomechanism and Treatment of Pancreatitis.Reviews of physiology, biochemistry and pharmacology · 2016Review
- ATP release, generation and hydrolysis in exocrine pancreatic duct cells.Purinergic signalling · 2015Article
- Alcohol disrupts levels and function of the cystic fibrosis transmembrane conductance regulator to promote development of pancreatitis.Gastroenterology · 2015Article
- Ethanol and its non-oxidative metabolites profoundly inhibit CFTR function in pancreatic epithelial cells which is prevented by ATP supplementation.Pflugers Archiv : European journal of physiology · 2014Article
- Apoptotic damage of pancreatic ductal epithelia by alcohol and its rescue by an antioxidant.PloS one · 2013Article
- Pathogenic mechanisms of acute pancreatitis.Current opinion in gastroenterology · 2012Review
- Physiology and pathophysiology of bicarbonate secretion by pancreatic duct epithelium.Nagoya journal of medical science · 2012Review
- Molecular mechanism of pancreatic and salivary gland fluid and HCO3 secretion.Physiological reviews · 2012Review
- Trypsin reduces pancreatic ductal bicarbonate secretion by inhibiting CFTR Cl⁻ channels and luminal anion exchangers.Gastroenterology · 2011Article
- Molecular mechanisms of pancreatic injury.Current opinion in gastroenterology · 2011Review
- Review
- Pancreatic ductal bicarbonate secretion: challenge of the acinar Acid load.Frontiers in physiology · 2011Article
- High glucose inhibits HCO3(-) and fluid secretion in rat pancreatic ducts.Pflugers Archiv : European journal of physiology · 2009Article
- Effect of herpesvirus infection on pancreatic duct cell secretion.World journal of gastroenterology · 2005Article
- Two components of the human alcohol electro-oculogram.Documenta ophthalmologica. Advances in ophthalmology · 2004Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ethanol is the leading cause of pancreatitis; however, its cellular effects are poorly understood. We examined the direct effects of ethanol in the concentration range 0.1-30 mM, i.e. relevant to usual levels of drinking, on fluid secretion from guinea-pig pancreatic duct cells. Fluid secretion was continuously measured by monitoring the luminal volume of interlobular duct segments isolated from the guinea-pig pancreas. [Ca2+]i was estimated by microfluorometry in duct cells loaded with fura-2. Ethanol at 0.3-30 mM significantly augmented fluid secretion stimulated by physiological (1 pM) or pharmacological (1 nM) concentrations of secretin. It augmented dibutyryl cAMP-stimulated fluid secretion but failed to affect spontaneous or acethylcholine-stimulated secretion. Ethanol at 1 mM shifted the secretin concentration-fluid secretion response curve upwards and raised the maximal secretory response significantly by 41%. In secretin-stimulated ducts, 1 mM ethanol induced a transient increase in [Ca2+]i that was dependent on the presence of extracellular Ca2+. Ethanol failed to augment secretin-stimulated secretion from ducts pretreated with an intracellular Ca2+ buffer (BAPTA) or a protein kinase A inhibitor (H89). In conclusion, low concentrations of ethanol directly augment pancreatic ductal fluid secretion stimulated by physiological and pharmacological concentrations of secretin, and this appears to be mediated by the activation of both the intracellular cAMP pathway and Ca2+ mobilization.
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