Complementary role of vasoactive intestinal polypeptide (VIP) and acetylcholine for cat submandibular gland blood flow and secretion.

The effects of local intraarterial infusions of VIP, acetylcholine (ACh), substance P, isoprenaline and bradykinin on submandibular gland blood flow and salivary secretion were studied in cats. It was found that VIP (10(-14) to 10(-10) mol/min) caused an atropine resistant vasodilation but no salivary secretion. Several hundred fold higher doses of exogenous VIP had to be infused than the amounts of VIP seen in the venous outflow during maximal nerve stimulation at a similar vasodilatory response. ACh infusions (5 X 10(-12) to 5 X 10(-8) mol/min) caused both a muscarinic vasodilation and salivary secretion. ACh was about 100 times less potent than VIP as a vasodilating agent. Both ACh and VIP induced in high doses a vasodilatory response similar to that seen during parasympathetic nerve stimulation at 15 Hz. ACh by itself did in the present doses, however, only induce about 50-60% of the maximal secretory response. Combined infusions of ACh and VIP, had mostly an additive effect on vasodilation. The salivatory volume response to ACh was potentiated by VIP and to a smaller extent also by isoprenaline. This potentiating effect may be due to a direct effect on secretory elements as well as partly to the additional increase in blood flow. Bradykinin was about 1 000 times less potent than VIP as a vasodilating agent. Substance P (10(-9) mol/min) only caused a weak vasodilation. Since there is evidence that ACh and VIP coexist within the same neurons and are both released upon parasympathetic nervous activation, the present findings suggest that the secretory and vasodilatory responses may be caused by an interaction between these two agents.