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Experiments were designed to determine whether cannabinoids affect salivary gland function. For this purpose, the effect of anandamide on cAMP accumulation, amylase release and Na+-K+-ATPase activity was studied in rat parotid glands. Anandamide induced a concentration-dependent increase in cAMP and led to amylase release but inhibited Na+-K+-ATPase activity. These effects were blocked by the CB1 cannabinoid receptor antagonist, AM281. The inhibition of adenylyl cyclase activity by SQ 22536 impaired amylase release and Na+-K+-ATPase inhibition. The effect of anandamide on cAMP accumulation significantly correlated with its action either on amylase release or on Na+-K+-ATPase activity. Such correlation strongly supports the view that the effect of anandamide on amylase release and Na+-K+-ATPase activity is the result of cAMP accumulation. The relative potencies of the CB1 cannabinoid receptor antagonist, AM281, to block these three functional responses were similar, supporting the view that anandamide actions in parotid glands were achieved through a single receptor subtype, the CB1. Binding studies using the selective cannabinoid CB1 receptor antagonist, [3H]SR141716A, indicated the presence of the specific binding site. It may be concluded that in parotid glands the endogenous cannabinoid anandamide, bound to the CB1 cannabinoid receptor subtype, induces cAMP accumulation which in turn leads to amylase release and Na+-K+-ATPase inhibition.