Lack of nitric oxide-mediated regulation of amylase secretion stimulated by VIP in parotid glands of NOD mice.

Content Provider	Semantic Scholar
Author	Roca, Valeria Rosignoli, Florencia Calafat, Mario Jose Leirós, Claudia Pérez
Copyright Year	2004
Abstract	The non-obese diabetic (NOD) mouse is chosen among other experimental models to study autoimmune sialadenitis resembling Sjögren's syndrome (SS), because of its unique characteristic of developing salivary dysfunction. Based on the deep loss of nitric oxide synthase (NOS) activity in parotid glands of NOD mice observed from early stages of disease and the inhibitory effect of nitric oxide (NO) donors on amylase secretion in normal salivary glands, our goal was to investigate whether parotid glands from NOD mice lacking NOS activity presented this regulatory mechanism of amylase secretion. We found that parotid glands from NOD mice lack nitric oxide-mediated regulation of amylase secretion in response to VIP stimulation. The lack of regulation might be assigned to the loss of NOS activity as derived from the results with NOS inhibitors and increasing concentrations of VIP. These functional differences observed in NOD vs. BALB/c parotid glands occur in the absence of immune infiltrates in exocrine tissue, and it is not related to cAMP accumulation. NO-mediated regulation of amylase secretion was not observed in BALB/c submandibular glands to the same extent as described in parotid glands and was absent in submandibular glands of NOD mice.
File Format	PDF HTM / HTML
DOI	10.1016/j.intimp.2004.08.004
PubMed reference number	15531299
Journal	Medline
Volume Number	4
Issue Number	14
Alternate Webpage(s)	http://digital.bl.fcen.uba.ar/Download/paper/paper_15675769_v4_n14SPEC.ISS._p1837_Roca.pdf
Alternate Webpage(s)	https://doi.org/10.1016/j.intimp.2004.08.004
Journal	International immunopharmacology
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article