Increase nitric oxide synthase activity in parotid glands from rats with experimental periodontitis.
OBJECTIVE
In this study we investigated the activity of the nitric oxide synthase (NOS) in parotid glands from rats with experimental periodontitis and controls.


METHODS
Periodontitis was produced by a ligature placed around the cervix of the two lower first molar. Experiments were carried out 22 days after the ligature.


RESULTS
Ligation caused an increase in parotid NOS activity. The selective blocker of the inducible isoform of the enzyme partially inhibited its activity in parotid glands from rat with ligature. In controls, the activity was partially inhibited by the antagonists of the selective neural and endothelial isoforms. NOS activity in rats with ligature was cyclic adenosine monophosphate (cAMP)-dependent while in controls it was calcium-dependent. Prostaglandin E₂ concentration was increased in parotid gland from rats with ligature. The inhibitor of prostaglandin production, FR 122047, diminished both, prostaglandin production and NOS activity. In rats with ligature unstimulated amylase released is increased. Both, prostaglandin and NOS were involved in the increment of amylase release.


CONCLUSIONS
It can be concluded that in parotid glands from ligated rats, prostaglandin E₂ production is increased and, through cAMP accumulation, activates the inducible NOS isoform. The increment of nitric oxide production participates in the increase in basal amylase release.
Miozza
V
V
Cátedra de Farmacología, Facultad de Odontología, Universidad de Buenos Aires, Buenos Aires, Argentina.
Borda
E
E
S-Borda
L
L
Busch
L
L
D000225:Adenine / Q000031:analogs & derivatives / Q000494:pharmacology; D000681:Amylases / Q000378:metabolism; D000818:Animals; D002118:Calcium / Q000494:pharmacology; D054751:Cyclic AMP-Dependent Protein Kinase Catalytic Subunits / Q000037:antagonists & inhibitors / Q000494:pharmacology; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D015232:Dinoprostone / Q000037:antagonists & inhibitors / Q000378:metabolism; D004195:Disease Models, Animal; D004533:Egtazic Acid / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006146:Guanidines / Q000494:pharmacology; D007191:Indazoles / Q000494:pharmacology; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism*; D052248:Nitric Oxide Synthase Type I / Q000037:antagonists & inhibitors; D052247:Nitric Oxide Synthase Type II / Q000037:antagonists & inhibitors; D052250:Nitric Oxide Synthase Type III / Q000037:antagonists & inhibitors; D009929:Organ Size; D009952:Ornithine / Q000031:analogs & derivatives / Q000494:pharmacology; D010306:Parotid Gland / Q000187:drug effects / Q000201:enzymology*; D010518:Periodontitis / Q000201:enzymology*; D010879:Piperazines / Q000494:pharmacology; D011451:Prostaglandin-Endoperoxide Synthases / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D012471:Salivary Proteins and Peptides / Q000187:drug effects / Q000378:metabolism*; D013844:Thiazoles / Q000494:pharmacology; D019323:omega-N-Methylarginine / Q000494:pharmacology
C106731:3-bromo-7-nitroindazole; D016861:Cyclooxygenase Inhibitors; D004791:Enzyme Inhibitors; D006146:Guanidines; D007191:Indazoles; D010879:Piperazines; D012471:Salivary Proteins and Peptides; D013844:Thiazoles; C085131:1-((4,5-bis(4-methoxyphenyl)-2-thiazoyl)carbonyl)-4-methylpiperazine; C017759:9-(tetrahydro-2-furyl)-adenine; D019323:omega-N-Methylarginine; C065027:N(G)-iminoethylornithine; D004533:Egtazic Acid; D009952:Ornithine; D019001:Nitric Oxide Synthase; D052248:Nitric Oxide Synthase Type I; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III; C496318:Nos2 protein, rat; C496316:Nos3 protein, rat; D011451:Prostaglandin-Endoperoxide Synthases; D054751:Cyclic AMP-Dependent Protein Kinase Catalytic Subunits; D000681:Amylases; D000225:Adenine; D015232:Dinoprostone; C004479:pimagedine; D002118:Calcium; D007213:Indomethacin