PILOCARPINE-INDUCED SALIVARY SECRETION, KININ SYSTEM AND NITRIC-OXIDE IN RATS

In anaesthetized rats, intraperitoneal injection of pilocarpine (0.1 to 1 mg.Kg(-1)) induced a dose-dependent flow of saliva. During salivation by pilocarpine (0.5 mg.Kg(-1)), the blood content of submaxillary glands was not significantly increased but the blood volume of the animals was reduced. The salivary flow rate induced by pilocarpine was similar in normal and kininogen-deficient rats. L-N-G-nitro-arginine (L-NOARG, 35 mg.Kg(-1)), a nitric oxide synthesis inhibitor, increased the salivary flow elicited by pilocarpine (0.5 mg.Kg(-1)). L-NOARG did not modify the blood volume loss but decreased the blood content of the submaxillary glands. The volume of salivary secretion induced by isoproterenol (250 mg.Kg(-1)) was lower in kininogen-deficient rats than in normal rats. It was significantly reduced by HOE 140 (2 mg.Kg(-1)), a bradykinin antagonist. L-NOARG increased the salivary flow induced by isoproterenol during the ten first minutes of collection but suppressed it thereafter. We concluded that kinins are not involved in the stimulating effect of pilocarpine on rat salivary glands but these peptides would participate to the development of the salivation induced by isoproterenol in rats. Nitric oxide contributes to the control of the vascular tone in rat salivary glands. The influce of L-NOARG on salivation would be explained by its effects on blood pressure and vascular resistances.