L-arginine/nitric oxide pathway and interaction with lead acetate on rat submandibular gland function.

The effects of lead acetate, L-arginine (nitric oxide precursor) and L-NAME (nitric oxide synthesis inhibitor) on rat submandibular secretory function were studied. Pure submandibular saliva was collected intraorally from anaesthetized rats by a micro polyethylene cannula using pilocarpine as secretagogue. Treatment for twenty-eight days with three doses of lead acetate (0.01%, 0.04%, 0.05% w/v) in drinking water caused significant alterations on salivary function. Salivary flow rate was decreased by lead at all doses used. The total protein concentration and amylase activity of saliva were both decreased by lead (0.04% and 0.05%). All doses of lead decreased saliva calcium concentrations. Two weeks' treatment of rats by L-arginine (2.25% w/v) and L-NAME (0.7% w/v) in drinking water also affected the saliva secretory function. L-Arginine caused increase in submandibular gland weight. The saliva flow rate was reduced by L-NAME. The total protein concentration of saliva was increased by L-arginine and decreased by L-NAME. Amylase activity was reduced by L-arginine treatment. Calcium concentration was reduced by L-arginine and increased by L-NAME. Concurrent L-arginine treatment with lead acetate recovered lead-induced reduction of flow rate but L-NAME potentiated it. Concurrent therapy of lead and L-NAME resulted in greater reduction of protein concentration when compared to that of lead. L-Arginine showed a preventive effect on lead-induced decrease of protein concentration. Both L-arginine and L-NAME prevented lead-induced reduction in calcium concentration. It is concluded that nitric oxide plays a role in salivary gland function. Also lead acetate inhibitory effect on submandibular function is somewhat diminished by L-arginine and partially increased by L-NAME. It seems that lead acetate interacts with nitric oxide modulatory role in salivary gland.