Vasoactive intestinal polypeptide in cholinergic neurons of exocrine glands: Functional significance of coexisting transmitters for vasodilation and secretion

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Abstract
A combination of the indirect immunofluorescence technique with acetylcholinesterase (acetylcholine acetylhydrolase, EC 3.1.1.7) staining, showed that vasoactive intestinal polypeptide (VIP) is present in cholinergic (acetylcholinesterase-rich) neurons involved in control of secretion and vasodilation in exocrine glands of cat. The submandibular salivary gland was used as a functional model. Preganglionic nerve stimulation induced an atropine-resistant, hexamethonium-sensitive vasodilation and release of VIP into the venous outflow from the gland and an atropine- and hexamethonium-sensitive secretion. Infusion of VIP antiserum reduced both the vasodilation and secretion. Infusion of VIP caused vasodilation only, whereas acetylcholine [ACh] caused both vasodilation and secretion. Simultaneous infusion of VIP and acetylcholine in low doses resulted in a marked potentiation of both vasodilation and secretion. The present morphological and functional data support the following hypothesis for regulation of vasodilation and secretion in exocrine glands. Preganglionic cholinergic nerves activate, via nicotinic receptors, postganglionic neurons, causing concomitant release from the same nerve endings of 2 coexisting putative transmitters, ACh and VIP. ACh produces mainly secretion by a muscarinic action and VIP causes mainly vasodilation, but the 2 substances seem to cooperate directly or indirectly in both types of response. The coexistence of 2 putative neurotransmitters, VIP and ACh in 1 neuron may explain the dual effector response (i.e., the cholinergic secretion and the atropine-resistant vasodilation) caused by nerve stimulation in exocrine glands.