EFFECTS OF DOPAMINE ON ADENYLYL-CYCLASE ACTIVITY AND AMYLASE SECRETION IN RAT PAROTID TISSUE

Several previous studies have shown that dopamine causes amylase secre tion from rat parotid tissue. However, the mechanism of this dopamine action is still unclear. The present study was designed to characteriz e dopamine action in rat parotid gland tissue by examining the effects of dopamine on cyclic AMP accumulation, adenylyl cyclase activity, an d amylase release. Dopamine significantly enhanced accumulation of cyc lic AMP in parotid slices and stimulated adenylyl cyclase activity in parotid membrane preparations. It also significantly stimulated amylas e release from parotid slices. The stimulatory effects of dopamine on cyclic AMP accumulation, adenylyl cyclase activity, and amylase releas e were effectively blocked with propranolol, a beta-adrenergic antagon ist, but not by either SCH 23390, a preferential D-1 antagonist, or bu taclamol, a preferential D-2 antagonist. No substantial specific bindi ng sites for D-1 receptors were detectable by [H-3]SCH 23390 binding i n parotid membranes. These results suggest that the stimulatory effect of dopamine on amylase secretion in rat parotid tissue is not mediate d through specific D-1 dopamine receptors but rather through beta-adre nergic receptors.