RESUMO
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.
