title: Endotoxin can decrease isolated rat parotid acinar cell amylase secretion in a nitric oxide-independent manner.
abstract: Salivary mucus and amylase have an anti-bacterial nature. Bacterial endotoxin is considered to decrease mucus secreting cell activity by nitric oxide-dependent mechanisms. In this study, the actions of endotoxin on amylase secreting cell activity have been studied. Endotoxin (Escherichia coli lipopolysaccharide; 3 mg/kg, i.v., 5 h) evoked nitric oxide synthase 2 (NOS2) induction in the rat whole parotid tissue (assessed by Western blot and the citrulline assay) and in rat isolated parotid acinar cells (assessed by Western blot and immunohistochemistry), and reduced basal and acetylcholine-stimulated amylase secretion from these isolated cells. However, N(G)-nitro-L-arginine methyl ester (0.1 mg/ml, 4 days in drinking water, yielding a dose of 25 mg/kg/day) did not affect amylase release under basal or acetylcholine-stimulated conditions, either in control acinar cells or those from endotoxin challenged rats. Thus, basal, acetylcholine-evoked or endotoxin-decreased cellular amylase secretion from rat isolated parotid acinar cells does not appear to be modulated by endogenous nitric oxide.
authors.affiliation: Department of Pediatrics and Orthodontics, Faculty of Dentistry, Semmelweis University, Budapest, Hungary.
authors.forename: Adrienn
authors.initials: A
authors.lastname: Barta
authors.forename: Ildikó
authors.initials: I
authors.lastname: Tarján
authors.forename: Agnes
authors.initials: A
authors.lastname: Kittel
authors.forename: Krisztina
authors.initials: K
authors.lastname: Horváth
authors.forename: Anikó
authors.initials: A
authors.lastname: Pósa
authors.forename: Ferenc
authors.initials: F
authors.lastname: László
authors.forename: Attila
authors.initials: A
authors.lastname: Kovács
authors.forename: Gábor
authors.initials: G
authors.lastname: Varga
authors.forename: Tivadar
authors.initials: T
authors.lastname: Zelles
authors.forename: Brendan J R
authors.initials: BJ
authors.lastname: Whittle
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000681:Amylases / Q000378:metabolism*; D000818:Animals; D002118:Calcium / Q000378:metabolism; D002478:Cells, Cultured; D004305:Dose-Response Relationship, Drug; D004487:Edema / Q000378:metabolism / Q000473:pathology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D007150:Immunohistochemistry; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism*; D052247:Nitric Oxide Synthase Type II / Q000037:antagonists & inhibitors / Q000378:metabolism; D010306:Parotid Gland / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar
chemical_list: D004791:Enzyme Inhibitors; D008070:Lipopolysaccharides; D009569:Nitric Oxide; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat; D000681:Amylases; D000109:Acetylcholine; D002118:Calcium; D019331:NG-Nitroarginine Methyl Ester