Enhancement of carbachol-induced amylase secretion in parotid glands from rats with experimental periodontitis

Abstract Objective In a previous study we observed that parotid glands from rats with experimental periodontitis showed an increase in basal amylase release as a result of an increase in cAMP accumulation induced by PGE 2 production. The aim of this work was to study whether this change in amylase release influences the secretory effect of carbachol. Design Experimental periodontitis was induced through placing a black thread around the cervix of the two lower first molars. Experiments were done 22 days after ligature induced periodontitis. Amylase release was evaluated in vitro and determined using a colorimetric method which uses starch as substrate. Results The effect of carbachol was increased in parotid glands from periodontitis rats. The effect of 10 −6  M carbachol was inhibited by 4-DAMP (10 −6  M), U-73122 (5 × 10 −6  M) and trifluoperazine (5 × 10 −6  M) in both groups. No changes were observed in the binding sites and affinity in parotid membranes from rats with experimental periodontitis. The inhibition of the adenylyl cyclase and the cyclooxygenase induced a right shift of the carbachol concentration–response curve in periodontitis group whilst the opposite effect was observed in control group in the presence of db-cAMP and PGE 2 . Conclusions Parotid glands from rats with experimental periodontitis release more amylase in response to carbachol suggesting an interaction between Ca 2+ and cAMP in the fusion/exocytosis step of secretory vesicles.