Experimental Periodontitis Induces a cAMP-dependent Increase in Amylase Activity in Parotid Glands from Male Rats

It is known that subjects with periodontitis show enhanced amylase concentration in saliva. Our purpose was to analyze the release of amylase in parotid glands from rats with experimental periodontitis and controls. We present evidence that periodontitis induces an increase in resting amylase activity and release without changes in isoproterenol-induced amylase secretion. Changes in amylase were reverted by the inhibition of the adenylyl cyclase by SQ 22536, the cyclooxygenase type 1 by FR 122047 and by blocking the vasoactive intestinal peptide (VIP) receptor with VIP 6–28. Parotid glands from rats with periodontitis showed an increase in cAMP levels that was also reverted in the presence of SQ 22536, FR 122047 and VIP 6–28. We concluded that both PGE2 and VIP are produced in parotid glands from rats with periodontitis and, by activating their own receptors in acinar cells, induce cAMP accumulation leading to an increase in amylase basal secretion.