Abstract
1. Release of VIP from the submaxillary gland, in response to stimulation of the chorda tympani, and its vasodilator action at the site of release have been investigated in anaesthetised cats. 2. Chorda stimulation at 20 Hz produced an abrupt rise in the concentration of VIP in the submaxillary venous effluent plasma, accompanied by a substantial increase in submaxillary blood flow, in the presence or absence of atropine. 3. Intra-arterial infusions of VIP which reproduced the rise in submaxillary venous plasma concentration that occurred during chorda stimulation at 20 Hz, also produced a rise in submaxillary blood flow of the same order of magnitude. 4. Direct comparison of the responses of the submaxillary vasculature to intraarterial infusions of VIP, ACh and bradykinin showed that the vasodilator potency of VIP far exceeded that of either of the other agonists. 5. Intra-arterial infusion of ACh, sufficient to elicit a maximal submaxillary vasodilator response, caused no detectable release of VIP from the gland. 6. The results are discussed in relation to the proposition that VIP is released from post-ganglionic parasympathetic neurones, in the submaxillary gland of the cat, and acts, as a transmitter, to cause vasodilatation, which is resistant to atropine.