The interaction of two different vasodilator mechanisms in the chorda-tympani activated submandibular salivary gland.

The vasodilatation caused by stimulation of the chordo-lingual nerve has been studied in the cat submandibular salivary gland perfused under conditions of constant volume inflow, at a rate equal to the flow existing in the resting organ. When a perfusate of red cells suspended in normal plasma was used at perfusion pressures of 55–120 mm Hg, a typical two-phasic and long-lasting vasodilatation was observed as a response to nerve stimulation. This vasodilator pattern was maintained when repeated nerve stimulations were carried out during a single perfusion period. Wlien the gland was perfused continuously with red cells suspended in a kininogen-free solution then one of two different response patterns could be seen, When a low perfusion pressure prevailed (below 55 mm Hg), then the chorda-mediated vasodilatation was reduced or abolished on repeated nerve stimulation. At conditions with a higher perfusion pressure (60–120 mm Hg) there developed on chorda stimulation a one-phasic, short-lasting vasodilatation, which was not reduced on repeated stimulations. In another series of experiments the kinin-destroying activity of a perfusate of red cells in normal plasma was increased by addition of carboxypeptidase-B. Chorda stimulation then caused a short-lasting vasodilatation of the type seen when a red cell perfusate containing no kininogen was used. It is concluded from these findings that functional vasodilatation in the submandibular salivary gland is probably initiated by the effect of vasodilator nerve fibres and supported and maintained by the action of kinins formed in the activated gland.