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Related Experiment Videos

Endotoxin can decrease isolated rat parotid acinar cell amylase secretion in a nitric oxide-independent manner.

Adrienn Barta1, Ildikó Tarján, Agnes Kittel

  • 1Department of Pediatrics and Orthodontics, Faculty of Dentistry, Semmelweis University, Budapest, Hungary.

European Journal of Pharmacology
|October 29, 2005
PubMed
Summary

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Bacterial endotoxin reduces amylase secretion in rat parotid acinar cells. This effect is not mediated by nitric oxide (NO), suggesting other pathways are involved in regulating salivary amylase release.

Area of Science:

  • Salivary gland physiology
  • Immunology
  • Biochemistry

Background:

  • Salivary mucus and amylase possess antibacterial properties.
  • Bacterial endotoxins are known to impair mucus secretion via nitric oxide pathways.
  • The impact of endotoxins on amylase secretion remains less understood.

Purpose of the Study:

  • To investigate the effect of bacterial endotoxin on amylase-secreting cells in rat parotid glands.
  • To determine the role of endogenous nitric oxide in mediating endotoxin's actions on amylase secretion.

Main Methods:

  • Induction of nitric oxide synthase 2 (NOS2) by Escherichia coli lipopolysaccharide (endotoxin) in rat parotid tissue and isolated acinar cells.
  • Assessment of NOS2 induction using Western blot, citrulline assay, and immunohistochemistry.

Related Experiment Videos

  • Measurement of basal and acetylcholine-stimulated amylase secretion in isolated parotid acinar cells.
  • Inhibition of nitric oxide synthase using N(G)-nitro-L-arginine methyl ester.

    • Main Results:

    • Endotoxin administration led to NOS2 induction in parotid tissue and acinar cells.
    • Endotoxin significantly reduced both basal and acetylcholine-stimulated amylase secretion.
    • Inhibition of nitric oxide synthase did not alter amylase secretion in either control or endotoxin-treated cells.

    Conclusions:

    • Endotoxin impairs amylase secretion from rat parotid acinar cells.
    • Endogenous nitric oxide does not appear to modulate basal, acetylcholine-stimulated, or endotoxin-decreased amylase secretion.
    • Alternative mechanisms may be responsible for the endotoxin-induced reduction in salivary amylase secretion.