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Inhibition of salivary secretion by lipopolysaccharide: possible role of prostaglandins
Ist Teil von
American journal of physiology: endocrinology and metabolism, 2001-08, Vol.281 (2), p.E405-E411
Ort / Verlag
United States
Erscheinungsjahr
2001
Quelle
MEDLINE
Beschreibungen/Notizen
1 Cátedra de Fisiología, Faculta de
Odontología, Universidad de Buenos Aires, 1122;
2 Centro de Estudios Farmacológicos y Botánicos
Consejo Nacional de Investigaciones Científicas y
Técnicas, 1414 Buenos Aires, Argentina; and 3 Pennington
Biomedical Research Center, Louisiana State University, Baton
Rouge, Louisiana 70808-4124
Inducible (calcium-independent) nitric oxide
synthase (iNOS) and cyclooxygenase-2 (COX-2) are important in
the regulation of the function of different organs during infection. A
single dose of lipopolysaccharide (LPS; 5 mg/kg ip) within 6 h
increased NOS activity (20%) and prostaglandin E (PGE) content (100%)
in submandibular glands (SMG) and blocked stimulated salivary secretion in adult male rats. The administration of an iNOS synthesis inhibitor, aminoguanidine (AG), with LPS decreased NOS activity and PGE content. Furthermore, the administration of meloxicam (MLX), an inhibitor of
COX-2, blocked the increase in PGE and the production of NO. The
incubation of slices of SMG in the presence of 3-morpholinosydnonimine, a donor of NO, increased the release of PGE highly significantly. The
incubation of SMG in the presence of a PGE 1 analog
(alprostadil) increased the production of NO. These results indicate
that LPS activates NOS, leading to NO release, which activates COX,
generating PGEs that act back to further activate NOS, causing further
generation of PGEs by activation of COX. Because the alprostadil
administration inhibited stimulated salivation, LPS-induced inhibition
of salivation appears to be caused by increased PGE production.
Diminished salivary secretion produces poor oral health; thus the use
of COX-2 inhibitors to counteract the effects of inhibited salivation
should be considered.
nitric oxide synthase; cyclooxygenase; noradrenaline; methacholine; endotoxemia